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Journal articles on the topic 'Ischemia'
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1
Lee, Choong-Hyun, Tae-Kyeong Lee, Dae Won Kim, Soon Sung Lim, Il Jun Kang, Ji Hyeon Ahn, Joon Ha Park, et al. "Relationship between Neuronal Damage/Death and Astrogliosis in the Cerebral Motor Cortex of Gerbil Models of Mild and Severe Ischemia and Reperfusion Injury." International Journal of Molecular Sciences 23, no. 9 (May 3, 2022): 5096. http://dx.doi.org/10.3390/ijms23095096.
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Neuronal loss (death) occurs selectively in vulnerable brain regions after ischemic insults. Astrogliosis is accompanied by neuronal death. It can change the molecular expression and morphology of astrocytes following ischemic insults. However, little is known about cerebral ischemia and reperfusion injury that can variously lead to damage of astrocytes according to the degree of ischemic injury, which is related to neuronal damage/death. Thus, the purpose of this study was to examine the relationship between damage to cortical neurons and astrocytes using gerbil models of mild and severe transient forebrain ischemia induced by blocking the blood supply to the forebrain for five or 15 min. Significant ischemia tFI-induced neuronal death occurred in the deep layers (layers V and VI) of the motor cortex: neuronal death occurred earlier and more severely in gerbils with severe ischemia than in gerbils with mild ischemia. Distinct astrogliosis was detected in layers V and VI. It gradually increased with time after both ischemiae. The astrogliosis was significantly higher in severe ischemia than in mild ischemia. The ischemia-induced increase of glial fibrillary acidic protein (GFAP; a maker of astrocyte) expression in severe ischemia was significantly higher than that in mild ischemia. However, GFAP-immunoreactive astrocytes were apparently damaged two days after both ischemiae. At five days after ischemiae, astrocyte endfeet around capillary endothelial cells were severely ruptured. They were more severely ruptured by severe ischemia than by mild ischemia. However, the number of astrocytes stained with S100 was significantly higher in severe ischemia than in mild ischemia. These results indicate that the degree of astrogliosis, including the disruption (loss) of astrocyte endfeet following ischemia and reperfusion in the forebrain, might depend on the severity of ischemia and that the degree of ischemia-induced neuronal damage may be associated with the degree of astrogliosis.
2
Park, Kwon Moo, Ang Chen, and Joseph V. Bonventre. "Prevention of Kidney Ischemia/Reperfusion-induced Functional Injury and JNK, p38, and MAPK Kinase Activation by Remote Ischemic Pretreatment." Journal of Biological Chemistry 276, no. 15 (January 9, 2001): 11870–76. http://dx.doi.org/10.1074/jbc.m007518200.
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MAPK activities, including JNK, p38, and ERK, are markedly enhanced after ischemiain vivoand chemical anoxiain vitro. The relative extent of JNK, p38, or ERK activation has been proposed to determine cell fate after injury. A mouse model was established in which prior exposure to ischemia protected against a second ischemic insult imposed 8 or 15 days later. In contrast to what was observed after 30 min of bilateral ischemia, when a second period of ischemia of 30- or 35-min duration was imposed 8 days later, there was no subsequent increase in plasma creatinine, decrease in glomerular filtration rate, or increase in fractional excretion of sodium. A shorter period of prior ischemia (15 min) was partially protective against subsequent ischemic injury 8 days later. Unilateral ischemia was also protective against a subsequent ischemic insult to the same kidney, revealing that systemic uremia is not necessary for protection. The ischemia-related activation of JNK and p38 and outer medullary vascular congestion were markedly mitigated by prior exposure to ischemia, whereas preconditioning had no effect on post-ischemic activation of ERK1/2. The phosphorylation of MKK7, MKK4, and MKK3/6, upstream activators of JNK and p38, was markedly reduced by ischemic preconditioning, whereas the post-ischemic phosphorylation of MEK1/2, the upstream activator of ERK1/2, was unaffected by preconditioning. Pre- and post-ischemic HSP-25 levels were much higher in the preconditioned kidney. In summary, post-ischemic JNK and p38 (but not ERK1/2) activation was markedly reduced in a model of kidney ischemic preconditioning that was established in the mouse. The reduction in JNK and p38 activation can be accounted for by reduced activation of upstream MAPK kinases. The post-ischemic activation patterns of MAPKs may explain the remarkable protection against ischemic injury observed in this model.
3
Lee, H. Thomas, and Charles W. Emala. "Protective effects of renal ischemic preconditioning and adenosine pretreatment: role of A1 and A3receptors." American Journal of Physiology-Renal Physiology 278, no. 3 (March 1, 2000): F380—F387. http://dx.doi.org/10.1152/ajprenal.2000.278.3.f380.
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Renal ischemia and reperfusion during aortic and renal transplant surgery result in ischemic-reperfusion injury. Ischemic preconditioning and adenosine infusion before ischemia protect against ischemic-reperfusion injury in cardiac and skeletal muscle, but these protective phenomena have not been demonstrated in the kidney. Rats were randomized to sham operation, 45-min renal ischemia, ischemic preconditioning with four cycles of 8-min renal ischemia and 5-min reperfusion followed by 45-min renal ischemia, systemic adenosine pretreatment before 45-min renal ischemia, or pretreatments with selective adenosine receptor subtype agonists or antagonists before 45-min renal ischemia. Forty-five minutes of renal ischemia followed by 24 h of reperfusion resulted in marked rises in blood urea nitrogen and creatinine. Ischemic preconditioning and adenosine pretreatment protected renal function and improved renal morphology. A1 adenosine receptor activation mimics and A1 adenosine antagonism blocks adenosine-induced protection. In addition, A3 adenosine receptor activation before renal ischemia worsens renal ischemic-reperfusion injury, and A3 adenosine receptor antagonism protects renal function. We demonstrate for the first time that rat kidneys can be preconditioned to attenuate ischemic-reperfusion injury and adenosine infusion before ischemic insult protects renal function via A1 adenosine receptor activation. Our data suggest that an A1 adenosine agonist and A3 adenosine antagonist may have clinically beneficial implications where renal ischemia is unavoidable.
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Kanazawa, Masato, Tetsuya Takahashi, Masanori Ishikawa, Osamu Onodera, Takayoshi Shimohata, and Gregory J. del Zoppo. "Angiogenesis in the ischemic core: A potential treatment target?" Journal of Cerebral Blood Flow & Metabolism 39, no. 5 (March 6, 2019): 753–69. http://dx.doi.org/10.1177/0271678x19834158.
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The ischemic penumbra is both a concept in understanding the evolution of cerebral tissue injury outcome of focal ischemia and a potential therapeutic target for ischemic stroke. In this review, we examine the evidence that angiogenesis can contribute to beneficial outcomes following focal ischemia in model systems. Several studies have shown that, following cerebral ischemia, endothelial proliferation and subsequent angiogenesis can be detected beginning four days after cerebral ischemia in the border of the ischemic core, or in the ischemic periphery, in rodent and non-human primate models, although initial signals appear within hours of ischemia onset. Components of the neurovascular unit, its participation in new vessel formation, and the nature of the core and penumbra responses to experimental focal cerebral ischemia, are considered here. The potential co-localization of vascular remodeling and axonal outgrowth following focal cerebral ischemia based on the definition of tissue remodeling and the processes that follow ischemic stroke are also considered. The region of angiogenesis in the ischemic core and its surrounding tissue (ischemic periphery) may be a novel target for treatment. We summarize issues that are relevant to model studies of focal cerebral ischemia looking ahead to potential treatments.
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Zhao, Ling, Qiwei Liao, Yueting Zhang, Shufen Tan, Shuqing Li, and Tingyu Ke. "Ischemic Postconditioning Mitigates Retinopathy in Tree Shrews with Diabetic Cerebral Ischemia." Journal of Diabetes Research 2020 (February 12, 2020): 1–10. http://dx.doi.org/10.1155/2020/6286571.
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Ischemic postconditioning (PC) is proved to efficiently protect diabetic patients with acute myocardial infarction from ischemia-reperfusion injury. We aimed to explore the protective roles of ischemic PC on diabetic retinopathy in tree shrews with diabetic cerebral ischemia. A diabetic tree shrew model was established through high-fat diet feeding combined with streptozotocin (STZ) injection, while cortical thrombotic cerebral ischemia was induced photochemically. Tree shrews were divided into the normal control group, sham operation group, diabetes mellitus group, diabetes mellitus+cerebral ischemia group, and diabetes mellitus+cerebral ischemia+PC group (in which the tree shrews with diabetic cerebral ischemia were treated with ischemic PC). H&E staining was used to examine the pathological changes in the retina, and immunohistochemistry was performed to determine the retinal expression of VEGF (vascular endothelial growth factor). The modeling resulted in 77% tree shrews with diabetes. Ischemic PC reduced the blood glucose levels in the tree shrews with diabetic cerebral ischemia. Tree shrews with diabetes had thinned retina with disordered structures, and these pathological changes were aggravated after cerebral ischemia. The retinopathy was alleviated after ischemic PC. Retina expression of VEGF was mainly distributed in the ganglion cell layer in tree shrews. Diabetes and cerebral ischemia increased retinal VEGF expression in a step-wise manner, while additional ischemic PC reduced retinal VEGF expression. Therefore, ischemic PC effectively alleviates retinopathy in tree shrews with diabetic cerebral ischemia, and this effect is associated with reduced retinal VEGF expression.
6
Li, Chuanfu, Race L. Kao, Tuanzhu Ha, Jim Kelley, I. William Browder, and David L. Williams. "Early activation of IKKβ during in vivo myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 3 (March 1, 2001): H1264—H1271. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1264.
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We have demonstrated that in vitro brief ischemia activates nuclear factor (NF)-κB in rat myocardium. We report in vivo ischemia-reperfusion (I/R)-induced NF-κB activation, IκB kinase -β (IKKβ) activity, and IκBα phosphorylation and degradation in rat myocardium. Rat hearts were subjected to occlusion of the coronary artery for up to 45 min or occlusion for 15 min followed by reperfusion for up to 3 h. Cytoplasmic and nuclear proteins were isolated from ischemic and nonischemic areas of each heart. NF-κB activation was increased in the ischemic area (680%) after 10 min of ischemia and in the nonischemic area (350%) after 15 min of ischemia and remained elevated during prolonged ischemia and reperfusion. IKKβ activity was markedly increased in ischemic (1,800%) and nonischemic (860%) areas, and phosphorylated IκBα levels were significantly elevated in ischemic (180%) and nonischemic (280%) areas at 5 min of ischemia and further increased after reperfusion. IκBα levels were decreased in the ischemic (45%) and nonischemic (36%) areas after 10 min of ischemia and remained low in the ischemic area during prolonged ischemia and reperfusion. The results suggest that in vivo I/R rapidly induces IKKβ activity and increases IκBα phosphorylation and degradation, resulting in NF-κB activation in the myocardium.
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Zhan, Xinhua, Bradley P. Ander, Glen Jickling, Renée Turner, Boryana Stamova, Huichun Xu, Dazhi Liu, Ryan R. Davis, and Frank R. Sharp. "Brief Focal Cerebral Ischemia That Simulates Transient Ischemic Attacks in Humans Regulates Gene Expression in Rat Peripheral Blood." Journal of Cerebral Blood Flow & Metabolism 30, no. 1 (September 9, 2009): 110–18. http://dx.doi.org/10.1038/jcbfm.2009.189.
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Blood gene expression profiles of very brief (5 and 10 mins) focal ischemia that simulates transient ischemic attacks in humans were compared with ischemic stroke (120 mins focal ischemia), sham, and naïve controls. The number of significantly regulated genes after 5 and 10 mins of cerebral ischemia was 39 and 160, respectively (fold change ⩾∣1.5∣ and P<0.05). There were 103 genes common to brief focal ischemia and ischemic stroke. Ingenuity pathway analysis showed that genes regulated in the 5 mins group were mainly involved in small molecule biochemistry. Genes regulated in the 10 mins group were involved in cell death, development, growth, and proliferation. Such genes were also regulated in the ischemic stroke group. Genes common to ischemia were involved in the inflammatory response, immune response, and cell death—indicating that these pathways are a feature of focal ischemia, regardless of the duration. These results provide evidence that brief focal ischemia differentially regulates gene expression in the peripheral blood in a manner that could distinguish brief focal ischemia from ischemic stroke and controls in rats. We postulate that this will also occur in humans.
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KAKOKI, MASAO, YASUNOBU HIRATA, HIROSHI HAYAKAWA, ETSU SUZUKI, DAISUKE NAGATA, AKIHIRO TOJO, HIROAKI NISHIMATSU, et al. "Effects of Tetrahydrobiopterin on Endothelial Dysfunction in Rats with Ischemic Acute Renal Failure." Journal of the American Society of Nephrology 11, no. 2 (February 2000): 301–9. http://dx.doi.org/10.1681/asn.v112301.
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The role of nitric oxide (NO) in ischemic renal injury is still controversial. NO release was measured in rat kidneys subjected to ischemia and reperfusion to determine whether (6R)-5,6,7,8-tetrahydro-L-biopterin (BH4), a cofactor of NO synthase (NOS), reduces ischemic injury. Twenty-four hours after bilateral renal arterial clamp for 45 min, acetylcholine-induced vasorelaxation and NO release were reduced and renal excretory function was impaired in Wistar rats. Administration of BH4 (20 mg/kg, by mouth) before clamping resulted in a marked improvement of those parameters (10-8 M acetylcholine, Δrenal perfusion pressure: sham-operated control -45 ± 5, ischemia -30 ± 2, ischemia + BH4 -43 ± 4%; ΔNO: control +30 ± 6, ischemia +10 ± 2, ischemia + BH4 +23 ± 4 fmol/min per g kidney; serum creatinine: control 23 ± 2, ischemia 150 ± 27, ischemia + BH4 48 ± 6 μM; mean ± SEM). Most of renal NOS activity was calcium-dependent, and its activity decreased in the ischemic kidney. However, it was restored by BH4 (control 5.0 ± 0.9, ischemia 2.2 ± 0.4, ischemia + BH4 4.3 ± 1.2 pmol/min per mg protein). Immunoblot after low-temperature sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed that the dimeric form of endothelial NOS decreased in the ischemic kidney and that it was restored by BH4. These results suggest that the decreased activity of endothelium-derived NO may worsen the ischemic tissue injury, in which depletion of BH4 may be involved.
9
Kim, Gyung W., Taku Sugawara, and Pak H. Chan. "Involvement of Oxidative Stress and Caspase-3 in Cortical Infarction after Photothrombotic Ischemia in Mice." Journal of Cerebral Blood Flow & Metabolism 20, no. 12 (December 2000): 1690–701. http://dx.doi.org/10.1097/00004647-200012000-00008.
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Apoptosis-related cell death is linked to oxidative stress and caspases in experimental cerebral ischemia, However, the role of oxidative stress in caspase activation and subsequent apoptotic cell death after cerebral ischemia is unknown, The authors evaluated the role of oxidative stress in ischemic cerebral infarction after photothrombosis and the relation between oxidative stress and caspase-related cell death 6 and 24 hours after ischemia with and without U-74389G, a potent free radical scavenger (10 mg/kg, 30 minutes before and after ischemia induction). Reactive oxygen species, detected by hydroethidine oxidation, and cytosolic cytochrome c were detected in early ischemic lesions. Western blot analysis showed the cleaved form and the level of the proform of caspase-3 in the ischemic lesion 24 hours after ischemia. Decreased caspase-3 immunoreactivity was detected in the antioxidant-treated group after ischemia. Decreased DNA fragmentation and laddering were detected and the lesion was smaller in the treated group after ischemia compared with the untreated group. Oxidative stress and cytochrome c release occur in the ischemic lesion after photothrombotic ischemia. The free radical scavenger attenuated caspase-3 up-regulation, DNA fragmentation, and the final lesion. The authors concluded that oxidative stress may mediate caspase-related apoptotic cell death and subsequent cortical infarction after photothrombotic ischemia.
10
Pan, Hui-Lin, Shao-Rui Chen, Gloria M. Scicli, and Oscar A. Carretero. "Cardiac interstitial bradykinin release during ischemia is enhanced by ischemic preconditioning." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 1 (July 1, 2000): H116—H121. http://dx.doi.org/10.1152/ajpheart.2000.279.1.h116.
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Ischemic preconditioning is known to protect the myocardium from ischemia-reperfusion injury. We examined the transmural release of bradykinin during myocardial ischemia and the influence of ischemic preconditioning on bradykinin release during subsequent myocardial ischemia. Myocardial ischemia was induced by occlusion of the left anterior descending coronary artery in anesthetized cats. Cardiac microdialysis was performed by implantation and perfusion of dialysis probes in the epicardium and endocardium. In eight animals, bradykinin release was greater in the endocardium than in the epicardium (14.4 ± 2.8 vs. 7.3 ± 1.7 ng/ml, P < 0.05) during 30 min of ischemia. In seven animals subjected to preconditioning, myocardial bradykinin release was potentiated significantly from 2.4 ± 0.6 ng/ml during the control period to 23.1 ± 2.5 ng/ml during 30 min of myocardial ischemia compared with the non-preconditioning group (from 2.7 ± 0.6 to 13.4 ± 1.9 ng/ml, P < 0.05, n = 6). Thus this study provides further evidence that transmural gradients of bradykinin are produced during ischemia. The results also suggest that ischemic preconditioning enhances bradykinin release in the myocardial interstitial fluid during subsequent ischemia, which is likely one of the mechanisms of cardioprotection of ischemic preconditioning.
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Nishimura, Masaki, Toshiyuki Sugino, Kazuhiko Nozaki, Yasushi Takagi, Itaro Hattori, Junya Hayashi, Nobuo Hashimoto, Tetsuo Moriguchi, and Eisuke Nishida. "Activation of p38 Kinase in the Gerbil Hippocampus Showing Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 23, no. 9 (September 2003): 1052–59. http://dx.doi.org/10.1097/01.wcb.0000084251.20114.65.
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Ischemic tolerance is a phenomenon in which brief episodes of ischemia protect against the lethal effects of subsequent periods of prolonged ischemia. The authors investigated the activation of p38 mitogen-activated protein kinase (p38) in the gerbil hippocampus by Western blotting and immunohistochemistry to clarify the role of p38 kinase in ischemic tolerance. After the 2-minute global ischemia, immunoreactivity indicating active p38 was enhanced at 6 hours of reperfusion and continuously demonstrated 72 hours after ischemia in CA1 and CA3 neurons. Pretreatment with SB203580, an inhibitor of active p38 (0–30 μmol/L), 30 minutes before the 2-minute ischemia reduced the ischemic tolerance effect in a dose-dependent manner. Immunoblot analysis indicated that alteration of the phosphorylation pattern of p38 kinase in the hippocampus after subsequent lethal ischemia was induced by the preconditioning. These findings suggest that lasting activation of p38 may contribute to ischemic tolerance in CA1 neurons of the hippocampus and that components of the p38 cascade can be target molecules to modify neuronal survival after ischemia.
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Danilova, T. V. "Features of epilepsy in acute and chronic cerebral ischemia." Kazan medical journal 98, no. 6 (December 15, 2017): 877–83. http://dx.doi.org/10.17750/kmj2017-877.
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Aim. To study clinical features, functional and neuroimaging characteristics of the brain of patients with ischemic brain disease and epileptic seizures. Methods. 772 patients with acute and chronic cerebral ischemia (265 stroke patients with epileptic seizures and 174 patients with seizures on the background of chronic cerebral ischemia, and 203 patients with stroke and 130 patients with chronic cerebral ischemia without seizures) were comprehensively examined. The clinical neurological examination, electroencephalography, magnetic resonance imaging, ultrasound duplex scanning of extra- and intracranial arteries with the assessment of the level and degree of stenosis and cerebrovascular reactivity were carried out. Results. Focal seizures prevailed in patients with cerebral ischemia. In patients with epileptic seizures on the background of both ischemic stroke and chronic cerebral ischemia cortical localization of ischemic foci prevailed. Early epileptic seizures in patients with ischemic stroke developed with significantly more frequent localization of ischemic focus in the right hemisphere with the orientation vector of neuroimaging formation of the ischemic lesion in the caudal direction. In patients with chronic cerebral ischemia with epileptic seizures, along with frequent lesion of the cortex, more frequent damage of white matter of the brain was observed. In patients with acute and chronic ischemia of the brain with epileptic seizures, a higher incidence of stenosis of major arteries and predominance of impaired cerebrovascular reactivity in posterior cerebral circulation system were established. Conclusion. Multimodal examination of patients with acute and chronic cerebral ischemia allowed forming risk groups for epileptic seizures.
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Schwartz, Ilsa, Michel Babajanian, Wen X. Zhang, Jonathan E. Aviv, Hubert Weinberg, Hugh F. Biller, and Mark L. Urken. "Prolongation of Secondary Critical Ischemia Time of Experimental Skin Flaps Using UW Solution as a Normothermic Perfusate." Otolaryngology–Head and Neck Surgery 108, no. 2 (February 1993): 149–55. http://dx.doi.org/10.1177/019459989310800207.
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A myriad of investigations have been published on the pharmacologic manipulation of flaps to enhance tolerance to ischemia. We recently reported a threefold increase in ischemic tolerance of the rat abdominal skin flap pedicle after 6 hours of primary ischemia and 12 hours of reperfusion. Flaps underwent normothermic perfusion washout with lactated Ringer's or U.W. solution, a newly developed organ preservation medium. Perfusion washouts were performed at one of three different points in the protocol: (1) onset of primary ischemia; (2) onset of secondary ischemia; or (3) 2 hours after onset of secondary ischemia. The last group was used to simulate the clinical situation in which flaps are discovered and salvage procedures instituted at a delayed time interval. This is the longest normothermic ischemic interval reported. We undertook the present study to determine the utility of the U.W solution in prolonging the tolerance of the flap to a second ischemic insult after a period of reperfusion. Seventy-five unilateral rat abdominal skin flaps were raised. Secondary ischemia was produced by placing a microvascular clamp across the inferior epigastric pedicle. Flap survival was assessed at 1 week postoperatively. While none of the nonperfused flaps survived 8 hours of secondary ischemia, at least 50% of the U.W. perfused flaps survived an average of 14 hours of secondary ischemia. Lactated Ringer's perfusion washout only modestly increased the ischemic tolerance. Perfusion washout in the secondary ischemic phase improved the ischemic tolerance to a significantly greater degree than in the primary ischemic interval. (OTOLARYNGOL HEAD NECK SURG 1993;108:149-55.)
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Zhou, An, Manabu Minami, Xiaoman Zhu, Sylvia Bae, John Minthorne, Jingquan Lan, Zhi-gang Xiong, and Roger P. Simon. "Altered Biosynthesis of Neuropeptide Processing Enzyme Carboxypeptidase E after Brain Ischemia: Molecular Mechanism and Implication." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (June 2004): 612–22. http://dx.doi.org/10.1097/01.wcb.0000118959.03453.17.
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In this study, using both in vivo and in vitro ischemia models, the authors investigated the impact of brain ischemia on the biosynthesis of a key neuropeptide-processing enzyme, carboxypeptidase E (CPE). The response to brain ischemia of animals that lacked an active CPE was also examined. Combined in situ hybridization and immunocytochemical analyses for CPE showed reciprocal changes of CPE mRNA and protein, respectively, in the same cortical cells in rat brains after focal cerebral ischemia. Western blot analysis revealed an accumulation of the precursor protein of CPE in the ischemic cortex in vivo and in ischemic cortical neurons in vitro. Detailed metabolic labeling experiments on ischemic cortical neurons showed that ischemic stress caused a blockade in the proteolytic processing of CPE. When mice lacking an active CPE protease were subjected to a sublethal episode of focal cerebral ischemia, abundant TUNEL-positive cells were seen in the ischemic cortex whereas only a few were seen in the cortex of wild-type animals. These findings suggest that ischemia has an adverse impact on the neuropeptide-processing system in the brain and that the lack of an active neuropeptide-processing enzyme exacerbates ischemic brain injury.
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Zhang, Zheng G., Wayne Tsang, Li Zhang, Cecylia Powers, and Michael Chopp. "Temporal and spatial expression of neuropilin-1 in focal cerebral ischemic brain." Stroke 32, suppl_1 (January 2001): 317. http://dx.doi.org/10.1161/str.32.suppl_1.317-b.
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6 Neuropilin-1 is a receptor for vascular endothelial grow factor 165 isoform (VEGF 165 ) and plays roles in vasculogenesis and angiogenesis. Neuropilin-1 also binds to semaphorin III which is an inhibitor to axon guidance signal. To seek evidence that neuropilin-1 may play roles in ischemic brain, we examined the temporal and spatial profiles of its expression after focal cerebral ischemia. Male Wistar Rats (n=42) were subjected to 1h to 28 days of embolic middle cerebral artery (MCA) occlusion. Expression of neuropilin-1 was measured by Northern blot, in situ hybridization and immunohistochemistry. Upregulation of neuropilin-1 mRNA was detected in the ischemic hemisphere on Northern blots at 2h and persisted at least 28 days after ischemia. In situ hybridization revealed increased mRNA in the ischemic injury neurons around the boundary of the ischemic lesion at 4h to 48h after ischemia. Seven to twenty-eight days after ischemia, neuropilin-1 mRNA was localized to vessels within the ischemic lesion. Immunostaining for neuropilin-1 showed that some of the ischemic neurons were neuropilin-1 immunoreactive at 2h to 4h after ischemia, and cerebral blood vessels within the ischemic lesion were neuropilin-1 immunoreactive at 2 days to 28 days after ischemia. In addition, hypertrophic astrocytes around the boundary of the ischemic lesion were neuropilin-1 immunoreactive at 1 day to 28 days after ischemia. Double immunofluorescent staining for neuropilin-1 and VEGF showed that neuropilin-1 immunoreactive vessels and astrocytes exhibited VEGF immunoreactivity. Thus our data suggest that upregulation of neuropilin-1 may play a role in angiogenesis in ischemic brain.
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Wang, Jian, and Song-Yuan He. "Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries." Journal of Investigative Medicine 68, no. 7 (August 11, 2020): 1276–81. http://dx.doi.org/10.1136/jim-2020-001328.
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This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and β-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and β-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and β-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.
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Wu, Bin, Akifumi Ootani, Ryuichi Iwakiri, Takehiro Fujise, Seiji Tsunada, Shuji Toda, and Kazuma Fujimoto. "Ischemic preconditioning attenuates ischemia-reperfusion-induced mucosal apoptosis by inhibiting the mitochondria-dependent pathway in rat small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 4 (April 2004): G580—G587. http://dx.doi.org/10.1152/ajpgi.00335.2003.
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Ischemic preconditioning provides a way of protecting organs from damage inflicted with prolonged ischemia-reperfusion. In this study, we investigated the mechanism of ischemic preconditioning involved in inhibition of prolonged ischemia-reperfusion-induced mucosal apoptosis in rat small intestine. Ischemic preconditioning was triggered by a transient occlusion of the superior mesenteric artery followed by reperfusion. Ischemia-reperfusion was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion in the small intestine. Ischemia-reperfusion alone induced mucosal apoptosis and mitochondrial respiratory dysfunction via promoted reactive oxygen species generation, reduced mitochondrial glutathione oxidation, increased mitochondrial lipid peroxidation, reduced mitochondrial membrane potential, and enhanced release of cytochrome c from mitochondria to activate caspase-9 and caspase-6 in the small intestine. Pretreatment with 20-min ischemia followed by 5-min reperfusion significantly inhibited the prolonged ischemia-reperfusion-induced mucosal apoptosis by 30%. Ischemic preconditioning ameliorated mitochondrial respiratory dysfunction by 50%, reduced reactive oxygen species generation by 38%, and suppressed mitochondrial lipid peroxidation by 36%, resulting in improvement of the mitochondrial membrane potential and prevention of cytochrome c release as well as caspase-6 activation. Results suggest that ischemic preconditioning attenuated ischemia-reperfusion-induced mucosal apoptosis partly by inhibiting the reactive oxygen species-mediated mitochondria-dependent pathway in the rat small intestine.
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YAMAKI, IGOR NAGAI, RUY VICTOR SIMÕES PONTES, FELIPE LOBATO DA SILVA COSTA, VITOR NAGAI YAMAKI, RENAN KLEBER COSTA TEIXEIRA, EDSON YUZUR YASOJIMA, and MARCUS VINICIUS HENRIQUES BRITO. "Kidney ischemia and reperfunsion syndrome: effect of lidocaine and local postconditioning." Revista do Colégio Brasileiro de Cirurgiões 43, no. 5 (October 2016): 348–53. http://dx.doi.org/10.1590/0100-69912016005012.
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ABSTRACT Objective: to evaluate the effects of blocking the regulation of vascular tone on the ischemia and reperfusion syndrome in rats through the use of lidocaine in the postconditioning technique. Methods: we randomized 35 rats into seven groups of five animals: Group 1- Control; Group 2- Ischemia and Reperfusion; Group 3- Ischemia, Reperfusion and Saline; Group 4- Ischemic Postconditioning; Group 5- Ischemic Postconditioning and Saline; Group 6- Lidocaine; Group 7- Ischemic Postconditioning and Lidocaine. Except for the control group, all the others were submitted to renal ischemia for 30 minutes. In postconditioning groups, we performed ischemia and reperfusion cycles of five minutes each, applied right after the main ischemia. In saline and lidocaine groups, we instilled the substances at a rate of two drops per minute. To compare the groups, we measured serum levels of urea and creatinine and also held renal histopathology. Results: The postconditioning and postconditioning + lidocaine groups showed a decrease in urea and creatinine values. The lidocaine group showed only a reduction in creatinine values. In histopathology, only the groups submitted to ischemic postconditioning had decreased degree of tubular necrosis. Conclusion: Lidocaine did not block the effects of postconditioning on renal ischemia reperfusion syndrome, and conferred better glomerular protection when applied in conjunction with ischemic postconditioning.
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Duarte, Sinésio Grace, Antônio Dorival Campos, and Benedicto Oscar Colli. "Functional evaluation of temporary focal cerebral ischemia: experimental model." Arquivos de Neuro-Psiquiatria 61, no. 3B (September 2003): 751–56. http://dx.doi.org/10.1590/s0004-282x2003000500009.
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OBJECTIVE: Despite cerebral ischemia being a frequent clinical pathologic state, the tolerance of neural tissue to oxygen absence and to reperfusion is controversial. This study aims to evaluate the effects of focal cerebral ischemia/reperfusion, by analyzing the mitochondrial respiration. METHOD: Sixty-four adult rats underwent focal cerebral ischemia by middle cerebral artery occlusion, during 15, 30 and 60 minutes, followed by 10 minutes or 19 hours of reperfusion. The effects of ischemia were analyzed measuring the O2 consumption by mitochondria in the ischemic and non-ischemic areas. RESULTS: There was compromise of the mitochondrial respiration after 30 and 60 minutes of ischemia, followed by 10 minutes of reperfusion but there was no alteration in this function after 19 hours of reperfusion. CONCLUSION: Compromise of the mitochondrial function occurred after 30 minutes of ischemia but, until one hour of ischemia, if the reperfusion was prolonged there was no evidence of ischemic/reperfusion injuries.
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Sorimachi, Takatoshi, Hiroshi Abe, Shigekazu Takeuchi, and Ryuichi Tanaka. "Neuronal damage in gerbils caused by intermittent forebrain ischemia." Journal of Neurosurgery 91, no. 5 (November 1999): 835–42. http://dx.doi.org/10.3171/jns.1999.91.5.0835.
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Object. The purpose of this study was to investigate the possibility of preventing cumulative neuronal damage after repetitive severe ischemia.Methods. The authors monitored ischemic depolarization in the gerbil hippocampus, which has recently been shown to be a good experimental model of the effects of brief ischemia on the brain, and evaluated neuronal damage in the CA1 subregion 7 days after the ischemic insult. In a single-ischemia paradigm, the results indicate that induction of ischemia-induced neuronal damage depended on the duration of ischemic depolarization. Neuronal damage can be detected in the CA1 subregion after a period of depolarization lasting 210 seconds. Using a double-ischemia paradigm in which the animals were subjected to two periods of ischemia, there was apparently no accumulation of neuronal damage from the first ischemic episode to the second, provided the duration of the first period of ischemic depolarization did not exceed 90 seconds. Neuronal damage accumulated when the duration of the first ischemia episode exceeded 90 seconds, regardless of the duration of the reperfusion interval between the two ischemic insults. Finally, when the ischemic insult was spread over four separate episodes, each lasting 90 seconds (with a reperfusion interval of 5 minutes), neuronal damage was not found when the total depolarization period was less than 420 seconds.Conclusions. The authors conclude that cumulative neuronal damage may be avoided by adopting an intermittent ischemia approach. The implications of these results for human surgery requiring temporary occlusion of the cerebral arteries are discussed.
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Gupta, Sachin, and Deeksha S. Tomar. "Ischemic Gut in Critically Ill (Mesenteric Ischemia and Nonocclusive Mesenteric Ischemia)." Indian Journal of Critical Care Medicine 24, S4 (2020): S157—S161. http://dx.doi.org/10.5005/jp-journals-10071-23611.
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Sapmaz, Ali, A. Tulga Ulus, Nilüfer N. Turan, F. Figen Kaymaz, Hija Yazıcıoğlu, Siyar Ersöz, Erdal Simsek, and Cüneyt Köksoy. "Which type of conditioning method protects the spinal cord from the ischemia–reperfusion injury in 24 hours?" Vascular 23, no. 6 (February 2, 2015): 614–21. http://dx.doi.org/10.1177/1708538114568702.
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Objective This study was designed to test the effects of different types of preconditioning and postconditioning methods on spinal cord protection following aortic clamping. Methods The animals (rabbits) were divided into sham-operated, ischemic preconditioning, remote ischemic preconditioning, simultaneous aortic and ischemic remote preconditioning, and ischemic postconditioning groups. After neurological evaluations, ultrastructural analysis and immunohistochemical staining for caspase-3 were evaluated after 24 h following ischemia. Results The neurological outcomes of the remote ischemic preconditioning (4.2 ± 0.4) and ischemic postconditioning (4.6 ± 0.8) groups were significantly improved when compared with the ischemia group (2.2 ± 04). The immunohistochemical analysis revealed that the lowest percentage of apoptosis was in-group ischemic preconditioning at 12.5 ± 30.6%. In the comparison of intracellular edema in an ultrastructural analysis, the ischemic preconditioning and ischemic postconditioning groups had significantly lower values than the ischemia group. Conclusion The conditioning methods attenuate ischemia–reperfusion injury for spinal cord injury. Ischemic and remote preconditioning and also postconditioning methods are simple to perform and inexpensive.
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POP, Lacramioara-Eliza, Dana POP, and Cristina PANTELEMON. "Ambulatory electrocardiographic monitoring as a diagnostic tool for ischemic heart disease in women." Balneo Research Journal 11, Vol.11, no.3 (September 2, 2020): 409–16. http://dx.doi.org/10.12680/balneo.2020.370.
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Introduction. Ischemic heart disease(IHD) is currently the leading cause of mortality in women. In this study we aimed to evaluate ambulatory electrocardiographic monitoring(AECGm) as a diagnostic test for IHD in women. Material and method. The study included 225 female who underwent AECGm divided into 2 groups: 136 previously diagnosed with IHD(IHD+) and 89 controls(IHD-). The IHD+ group was subdivided into AECGm ischemia subgroup(I+) and AECGm non-ischemia subgroup(I-). AECGm was assessed for presence of myocardial ischemia (ST segment depression >5mm), duration and ischemic load (the percentage that episodes of myocardial ischemia accounted throughout the recording). Results and discussions. Patients mean age was 62.31±12.51years. The IHD+ and IHD- groups were similar regarding associated risk factors (hypertension, obesity, dyslipidemia, diabetes mellitus), echocardiographic parameters (left ventricular size, ejection fraction, kinetic disorders), minimum and maximum heart rates(MaxHR) on AECGm. Statistically significant differences were identified regarding presence of atrial fibrillation episodes(AFibE) (IHD+:21.3% vs IHD-:8.9%), myocardial ischemia (IHD+:55.14% vs IHD-:42.69%), ischemic load (IHD+:15.23±30.54% vs IHD-:4.7±15.65%), duration of ischemia (IHD+:174.16±380.75 minutes vs IHD-:59.44 ± 209.02 minutes). In multivariate analysis, ischemia episodes, ischemic load and duration of ischemia were predicted by obesity, MaxHR and AFibE. Statistically significant differences were also identified regarding presence of AFibE (I+:30% vs I-:8.9%), MaxHR (I+:120 vs I-:111beats/minute), obesity (I+:20% vs I-:41%), diabetes mellitus (I+:16% vs I-:69%), hypertension (I+:76% vs I-:90%). Conclusions. Although myocardial ischemia was also present in IHD- group, our study demonstrated that the diagnosis of IHD can be established by AECGm using the threshold values of ischemic load (> 27%) and ischemic duration (> 315minutes).
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Bosnjak, Zeljko J., and Zhi-Dong Ge. "The application of remote ischemic conditioning in cardiac surgery." F1000Research 6 (June 16, 2017): 928. http://dx.doi.org/10.12688/f1000research.11018.1.
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Perioperative myocardial ischemia and infarction are the leading causes of morbidity and mortality following anesthesia and surgery. The discovery of endogenous cardioprotective mechanisms has led to testing of new methods to protect the human heart. These approaches have included ischemic pre-conditioning, per-conditioning, post-conditioning, and remote conditioning of the myocardium. Pre-conditioning and per-conditioning include brief and repetitive periods of sub-lethal ischemia before and during prolonged ischemia, respectively; and post-conditioning is applied at the onset of reperfusion. Remote ischemic conditioning involves transient, repetitive, non-lethal ischemia and reperfusion in one organ or tissue (remote from the heart) that renders myocardium more resistant to lethal ischemia/reperfusion injury. In healthy, young hearts, many conditioning maneuvers can significantly increase the resistance of the heart against ischemia/reperfusion injury. The large multicenter clinical trials with ischemic remote conditioning have not been proven successful in cardiac surgery thus far. The lack of clinical success is due to underlying risk factors that interfere with remote ischemic conditioning and the use of cardioprotective agents that have activated the endogenous cardioprotective mechanisms prior to remote ischemic conditioning. Future preclinical research using remote ischemic conditioning will need to be conducted using comorbid models.
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Lakshmanan, Rajesh, Gopi Ukani, Muhammad Tipu Rishi, and Nilanjana Maulik. "Trimodal rescue of hind limb ischemia with growth factors, cells, and nanocarriers: fundamentals to clinical trials." Canadian Journal of Physiology and Pharmacology 95, no. 10 (October 2017): 1125–40. http://dx.doi.org/10.1139/cjpp-2016-0713.
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Peripheral artery disease is a severe medical condition commonly characterized by critical or acute limb ischemia. Gradual accumulation of thrombotic plaques in peripheral arteries of the lower limb may lead to intermittent claudication or ischemia in muscle tissue. Ischemic muscle tissue with lesions may become infected, resulting in a non-healing wound. Stable progression of the non-healing wound associated with severe ischemia might lead to functional deterioration of the limb, which, depending on the severity, can result in amputation. Immediate rescue of ischemic muscles through revascularization strategies is considered the gold standard to treat critical limb ischemia. Growth factors offer multiple levels of protection in revascularization of ischemic tissue. In this review, the basic mechanism through which growth factors exert their beneficial properties to rescue the ischemic limb is extensively discussed. Moreover, clinical trials based on growth factor and stem cell therapy to treat critical limb ischemia are considered. The clinical utility of stem cell therapy for the treatment of limb ischemia is explained and recent advances in nanocarrier technology for selective growth factor and stem cell supplementation are summarized.
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Kolocassides, K. G., M. Galinanes, and D. J. Hearse. "Preconditioning accelerates contracture and ATP depletion in blood-perfused rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (October 1, 1995): H1415—H1420. http://dx.doi.org/10.1152/ajpheart.1995.269.4.h1415.
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We investigated the effect of preconditioning on the ischemia-induced depletion of ATP in the blood-perfused rat heart. Isolated hearts (n = 5/group) were aerobically perfused with whole blood from a support rat and subjected to zero-flow global ischemia (37 degrees C) for periods up to 35 min. Frozen hearts were taken for metabolic analysis. Ischemic contracture was assessed with an isovolumic intraventricular balloon. The study groups were 1) control (C) with unprotected ischemia, 2) preconditioning (PC; 2 cycles of 3-min ischemia/3-min reperfusion), and 3) cardioplegia (CP; St. Thomas') before ischemia. Preconditioning accelerated, whereas cardioplegia delayed, ischemic contracture (time to peak contracture: PC = 8.1 +/- 0.3 and CP = 25.1 +/- 0.2 min vs. C = 15.6 +/- 0.3 min, P < 0.05). The ischemia-induced decline in ATP was delayed by cardioplegia but accelerated by preconditioning (P < 0.05). In a parallel study, preconditioning and cardioplegia protected postischemic contractile function to a similar extent. Thus, in the blood-perfused rat heart, preconditioning accelerated ischemic contracture and depletion of ATP. In contrast, cardioplegia slowed ischemic contracture and ATP depletion.
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Hoshida, S., T. Kuzuya, H. Fuji, N. Yamashita, H. Oe, M. Hori, K. Suzuki, N. Taniguchi, and M. Tada. "Sublethal ischemia alters myocardial antioxidant activity in canine heart." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 1 (January 1, 1993): H33—H39. http://dx.doi.org/10.1152/ajpheart.1993.264.1.h33.
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We examined antioxidant activity in the pre-conditioned canine myocardium with four 5-min episodes of regional ischemia and reperfusion. Immediately after repetitive brief ischemia, mitochondrial Mn-superoxide dismutase (SOD) activity in the ischemic myocardium significantly increased compared with that in the nonischemic myocardium (18.7 +/- 2.1 vs. 14.9 +/- 1.0 U/mg protein, P < 0.05). Although no difference was seen in the activity between these regions after 3 h of the sublethal ischemia, a significant increase in the activity of the ischemic myocardium reappeared after 24 h compared with that of the nonischemic myocardium (26.7 +/- 0.9 vs. 20.8 +/- 0.9 U/mg protein, P < 0.05). Mn-SOD content increased gradually in the ischemic myocardium after sublethal ischemia, with a peak after 24 h (2.8 +/- 0.1 vs. 2.1 +/- 0.1 microgram/mg protein, P < 0.05). There were no differences in the activity and content of Cu, Zn-SOD between these regions after sublethal ischemia. Activities of glutathione peroxidase and reductase were significantly higher and lower, respectively, in the ischemic myocardium than those of the nonischemic myocardium immediately after repetitive brief ischemia, but no differences between these regions were seen in activities after 3 or 24 h. These results indicate that a brief ischemic insult alters myocardial antioxidant activity not only immediately after but also 24 h after sublethal ischemia.
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Zhan, Ren-Zhi, Hideyoshi Fujihara, Hiroshi Baba, Tomohiro Yamakura, and Koki Shimoji. "Ischemic Preconditioning Is Capable of Inducing Mitochondrial Tolerance in the Rat Brain." Anesthesiology 97, no. 4 (October 1, 2002): 896–901. http://dx.doi.org/10.1097/00000542-200210000-00022.
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Background Preconditioning to ischemia is a phenomenon whereby a brief episode of sublethal ischemia and other nonlethal stressors produce protection against a subsequent detrimental ischemic insult. As mitochondrial dysfunction is related to necrotic and apoptotic neuronal death after cerebral ischemia, the authors examined if ischemic preconditioning is capable of inducing mitochondrial tolerance. Methods Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 8 min in Wistar rats (275-300 g). A 3-min ischemic episode performed 48 h before the 8-min ischemia was used for preconditioning. The extents of hippocampal CA1 neuronal damage were evaluated 7 days after reperfusion by neuro-specific nuclear protein immunostaining. Brain mitochondria were isolated 48 h after animals were subjected to the sham operation or the 3-min conditioning ischemia. Loss of cytochrome c from mitochondria after cerebral ischemia in vivo and after exposure of brain mitochondria to calcium in vitro was used as an indication of mitochondrial dysfunction. Results Results showed that ischemic preconditioning induced by a 3-min ischemic episode dramatically reduced the loss of hippocampal CA1 neurons resulting from a subsequent 8-min ischemia 7 days after reperfusion, and this protection was associated with a preservation of mitochondrial cytochrome c as examined after early reperfusion. Exposure of isolated brain mitochondria to calcium produced a dose-dependent increase in cytochrome c release either at 30 degrees C or at 37 degrees C. Compared with those animals receiving only sham operation, cytochrome c release caused by 100 microm calcium was significantly reduced in conditioned animals. Conclusion Regarding the importance of mitochondrial dysfunction in mediating ischemic neuronal death, the above results indicate that mitochondria may serve as end-effecting organelles to ischemic preconditioning.
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Manabe, Hiroaki, David O. Okonkwo, John L. Gainer, Ryon H. Clarke, and Kevin S. Lee. "Protection against focal ischemic injury to the brain by trans-sodium crocetinate." Journal of Neurosurgery 113, no. 4 (October 2010): 802–9. http://dx.doi.org/10.3171/2009.10.jns09562.
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Object Ischemic injury is a potential complication in a variety of surgical procedures and is a particular impediment to the success of surgeries involving highly vulnerable neural tissue. One approach to limiting this form of injury is to enhance metabolic supply to the affected tissue. Trans-sodium crocetinate (TSC) is a carotenoid compound that has been shown to increase tissue oxygenation by facilitating the diffusivity of small molecules, such as oxygen and glucose. The present study examined the ability of TSC to modify oxygenation in ischemic neural tissue and tested the potential neuroprotective effects of TSC in permanent and temporary models of focal cerebral ischemia. Methods Adult male rats (330–370 g) were subjected to either permanent or temporary focal ischemia by simultaneous occlusion of both common carotid arteries and the left middle cerebral artery (3-vessel occlusion [3-VO]). Using the permanent ischemia paradigm, TSC was administered intravenously beginning 10 minutes after the onset of ischemia at 1 of 8 dosages, ranging from 0.023 to 4.580 mg/kg. Cerebral infarct volume was measured 24 hours after the onset of ischemia. The effect of TSC on infarct volume was also tested after temporary (2-hour) ischemia using a dosage of 0.092 mg/kg. In other animals undergoing temporary ischemia, tissue oxygenation was monitored in the ischemic penumbra using a Licox probe. Results Administration of TSC reduced infarct volume in a dose-dependent manner in the permanent ischemia model, achieving statistical significance at dosages ranging from 0.046 to 0.229 mg/kg. The most effective dosage of TSC in the permanent ischemia experiment (0.092 mg/kg) was further tested using a temporary (2-hour) ischemia paradigm. Infarct volume was reduced significantly by TSC in this ischemia-reperfusion model as well. Recordings of oxygen levels in the ischemic penumbra of the temporary ischemia model showed that TSC increased tissue oxygenation during vascular occlusion, but reduced the oxygen overshoot (hyperoxygenation) that occurs upon reperfusion. Conclusions The novel carotenoid compound TSC exerts a neuroprotective influence against permanent and temporary ischemic injury when administered soon after the onset of ischemia. The protective mechanism of TSC remains to be confirmed; however, the permissive effect of TSC on the diffusivity of small molecules is a plausible mechanism based on the observed increase in tissue oxygenation in the ischemic penumbra. This represents a form of protection based on “metabolic reflow” that can occur under conditions of partial vascular perfusion. It is particularly noteworthy that TSC could conceivably limit the progression of a wide variety of cellular injury mechanisms by blunting the ischemic challenge to the brain.
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Hedayatpour, Azim, Maryam Shiasi, Peyman Modarresi, and Alieh Bashghareh. "Remote ischemic preconditioning combined with atorvastatin improves memory after global cerebral ischemia-reperfusion in male rats." Research Results in Pharmacology 8, no. 2 (June 14, 2022): 27–35. http://dx.doi.org/10.3897/rrpharmacology.8.75753.
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Introduction: Damage to hippocampus can occur through ischemia. Memory problems are among the most significant disabilities after stroke. Therefore, improving memory is of great interest in helping post-stroke patients. This study demonstrated that intraperitoneally injection of atorvastatin with a short cycle of ischemia-reperfusion in the left femoral artery improved hippocampal CA1 neurons injury and memory problems after global cerebral ischemia. Materials and methods: In this article survey, we used 64 animals. Rats were divided into 8 groups, (n=8). Group 1: control; group 2: sham; group 3: global cerebral ischemia (GCI) only; group 4: remote ischemic preconditioning (RIP) + GCI; group 5: GCI + atorvastatin (ATO); group 6: GCI + vehicle; group 7: RIP + GCI + ATO; group 8: RIP + GCI + vehicle. We created global cerebral ischemia (GCI) with 20 min occlusion of the Common carotid artery. Results and discussion: Remote ischemic preconditioning could improve rats performance in water maze tests along with a decrease in neuronal death. Also, atorvastatin combined with remote ischemic preconditioning was more effective for memory improvement and reduction of neuronal death. Inconsistent with our result, the function of the animals in the ischemia group was impaired. CA1 hippocampal neurons have an important role in memory and learning, and they can be damaged after cerebral ischemia. Therefore, ischemia can create memory problems. Remote ischemic preconditioning and atorvastatin had a neuroprotective effect and could improve rat performance in water maze test. Conclusion: This study showed that remote ischemic preconditioning with atorvastatin could improve CA1 neuronal injury and memory. Graphical abstract:
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Sanada, Shoji, Issei Komuro, and Masafumi Kitakaze. "Pathophysiology of myocardial reperfusion injury: preconditioning, postconditioning, and translational aspects of protective measures." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1723—H1741. http://dx.doi.org/10.1152/ajpheart.00553.2011.
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Heart diseases due to myocardial ischemia, such as myocardial infarction or ischemic heart failure, are major causes of death in developed countries, and their number is unfortunately still growing. Preliminary exploration into the pathophysiology of ischemia-reperfusion injury, together with the accumulation of clinical evidence, led to the discovery of ischemic preconditioning, which has been the main hypothesis for over three decades for how ischemia-reperfusion injury can be attenuated. The subcellular pathophysiological mechanism of ischemia-reperfusion injury and preconditioning-induced cardioprotection is not well understood, but extensive research into components, including autacoids, ion channels, receptors, subcellular signaling cascades, and mitochondrial modulators, as well as strategies for modulating these components, has made evolutional progress. Owing to the accumulation of both basic and clinical evidence, the idea of ischemic postconditioning with a cardioprotective potential has been discovered and established, making it possible to apply this knowledge in the clinical setting after ischemia-reperfusion insult. Another a great outcome has been the launch of translational studies that apply basic findings for manipulating ischemia-reperfusion injury into practical clinical treatments against ischemic heart diseases. In this review, we discuss the current findings regarding the fundamental pathophysiological mechanisms of ischemia-reperfusion injury, the associated protective mechanisms of ischemic pre- and postconditioning, and the potential seeds for molecular, pharmacological, or mechanical treatments against ischemia-reperfusion injury, as well as subsequent adverse outcomes by modulation of subcellular signaling mechanisms (especially mitochondrial function). We also review emerging translational clinical trials and the subsistent clinical comorbidities that need to be overcome to make these trials applicable in clinical medicine.
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Hearse, David J., and Fiona J. Sutherland. "Catecholamines and preconditioning: studies of contraction and function in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (July 1, 1999): H136—H143. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h136.
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The aims of this study were to determine whether 1) like ischemic preconditioning, transient exposure to norepinephrine before ischemia exacerbates contracture during ischemia and 2) protection afforded by norepinephrine is stereospecific (receptor mediated). Isolated perfused rat hearts were randomized into five groups ( n = 6/group): 1) ischemic preconditioning (3 min of ischemia + 3 min of reperfusion + 5 min of ischemia + 5 min of reperfusion), 2) untreated control, 3) vehicle control (ascorbic acid), 4) substitution of preconditioning ischemia by perfusion with d-norepinephrine, and 5) substitution of preconditioning ischemia by perfusion with l-norepinephrine. This was followed by 40 min of zero-flow ischemia and 50 min of reperfusion. Ischemic preconditioning and l-norepinephrine exacerbated contracture (time to 50% contracture = 9.2 ± 1.1 and 9.0 ± 1.1 vs. 13.3 ± 0.3, 12.4 ± 0.5, and 13.2 ± 0.4 min for untreated control, vehicle control, and d-norepinephrine, respectively, P < 0.05). Postischemic left ventricular developed pressure was poor in untreated control (23.0 ± 2.2%), vehicle control (26.9 ± 2.3%), and d-norepinephrine (19.8 ± 2.8%) groups but good in preconditioned (52.4 ± 5.1%) and l-norepinephrine (52.5 ± 1.1%) groups ( P < 0.05). Thus norepinephrine preconditioning, like ischemic preconditioning, causes a paradoxical exacerbation of contracture coupled with enhanced postischemic recovery; both effects are stereospecific.
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Ala, Alireza, Jafar Ghobadi, Haleh Yaghubi, and Ali Adib. "The prognostic values of platelet to lymphocyte ratio for predicting mortality in patients with acute mesenteric ischemia: a cross-sectional study." Journal of Research in Clinical Medicine 10 (December 24, 2022): 29. http://dx.doi.org/10.34172/jrcm.2022.029.
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Introduction: Acute mesenteric ischemia (AMI) is a life-threatening disease that can cause multi-organ damage and ultimately lead to death. Early diagnosis and treatment significantly reduce morbidity and mortality rates in high-risk patients. This study aimed to explore the prognostic values of platelet to lymphocyte ratio (PLR) in predicting mortality in patients with mesenteric ischemia. Methods: This prospective study included 126 patients with a complaint of acute abdominal pain, suggesting mesenteric ischemia. Demographic data and measured variables were determined using a pre-designed questionnaire. Statistical analysis was conducted using t test analysis, Spearman correlation analysis, and receiver operating characteristic (ROC) curve. Results: Of 126 studied cases, mesenteric ischemia was confirmed in 47 patients. The mean age in patients with mesenteric ischemia (68 years) was significantly higher than that of non-ischemic patients (65 years). Mean blood bicarbonate level in non-ischemic patients (13.53 mmol/L) was higher than ischemic patients (11.15 mmol/L) (P<0.0001). PLR in patients with mesenteric ischemia and non-ischemic patients was 159 and 151, respectively; this difference was not statistically significant (P=0.14). The overall mortality rate in this study was 61%. Conclusion: Even though the PLR increases in patients with systemic inflammation, it cannot distinguish between patients with mesenteric ischemia and other inflammatory conditions.
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Duszczyk, Malgorzata, Apolonia Ziembowicz, Roman Gadamski, and And Lazarewicz. "Behavioral evaluation of ischemic damage to CA1 hippocampal neurons: Effects of preconditioning." Acta Neurobiologiae Experimentalis 66, no. 4 (December 31, 2006): 311–19. http://dx.doi.org/10.55782/ane-2006-1620.
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In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly reduced neuronal damage in CA1 evoked by injurious ischemia. Behavioral studies demonstrated that preconditioning reduced the locomotor hyperactivity and latency in nest building after test ischemia, in comparison to sham or naive animals. The results indicate that the nest building test and measurement of locomotor activity may be used for an early in vivo prediction of the extent of ischemic brain damage and tolerance induced by ischemic preconditioning. Correspondence should be addressed to J. W. £azarewicz, Email: jerzyl@cmdik.pan.pl
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Packard, Amy E. B., Jason C. Hedges, Frances R. Bahjat, Susan L. Stevens, Michael J. Conlin, Andres M. Salazar, and Mary P. Stenzel-Poore. "Poly-IC Preconditioning Protects against Cerebral and Renal Ischemia-Reperfusion Injury." Journal of Cerebral Blood Flow & Metabolism 32, no. 2 (November 16, 2011): 242–47. http://dx.doi.org/10.1038/jcbfm.2011.160.
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Preconditioning induces ischemic tolerance, which confers robust protection against ischemic damage. We show marked protection with polyinosinic polycytidylic acid (poly-IC) preconditioning in three models of murine ischemia-reperfusion injury. Poly-IC preconditioning induced protection against ischemia modeled in vitro in brain cortical cells and in vivo in models of brain ischemia and renal ischemia. Further, unlike other Toll-like receptor (TLR) ligands, which generally induce significant inflammatory responses, poly-IC elicits only modest systemic inflammation. Results show that poly-IC is a new powerful prophylactic treatment that offers promise as a clinical therapeutic strategy to minimize damage in patient populations at risk of ischemic injury.
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Santos, Carlos Henrique Marques dos, Otoni Moreira Gomes, José Carlos Dorsa Vieira Pontes, Luciana Nakao Odashiro Miiji, and Marco Aurélio Feltrin Bispo. "The ischemic preconditioning and postconditioning effect on the intestinal mucosa of rats undergoing mesenteric ischemia/reperfusion procedure." Acta Cirurgica Brasileira 23, no. 1 (February 2008): 22–28. http://dx.doi.org/10.1590/s0102-86502008000100005.
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PURPOSE: To evaluate the effect of the ischemic preconditioning and the ischemic postconditioning over the tissue injury in the intestinal mucosa of rats undergoing the procedure of mesenteric ischemia and reperfusion. METHODS: Thirty Wistar rats were studied, divided in three groups: group A, undergoing mesenteric ischemia (30 minutes) and reperfusion (60 minutes); group B, mesenteric ischemia and reperfusion preceded by ischemic preconditioning; group C, mesenteric ischemia and reperfusion and, before the beginning of reperfusion, the ischemic postconditioning was performed. At the end, a segment of the small intestine was dissected for histological analysis. The results were evaluated using the CHIU et al.6 classification followed by the statistic treatment. RESULTS: The mean values of the tissue injury levels were: group A, 3.5; group B, 1.2; and group C, 1. The difference between the result of group A with the results of groups B and C was considered statistically significant (p < 0,05). CONCLUSION: The ischemic preconditioning and postconditioning are able to minimize the tissue injury in the intestines of rats that underwent the procedure of mesenteric ischemia and reperfusion.
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Wang, Lei, Xu Zhang, Xiaoxing Xiong, Hua Zhu, Ran Chen, Shudi Zhang, Gang Chen, and Zhihong Jian. "Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke." Antioxidants 11, no. 12 (November 30, 2022): 2377. http://dx.doi.org/10.3390/antiox11122377.
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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.
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Burda, Rastislav, Jozef Burda, and Radoslav Morochovič. "Ischemic Tolerance—A Way to Reduce the Extent of Ischemia–Reperfusion Damage." Cells 12, no. 6 (March 13, 2023): 884. http://dx.doi.org/10.3390/cells12060884.
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Individual tissues have significantly different resistance to ischemia–reperfusion damage. There is still no adequate treatment for the consequences of ischemia–reperfusion damage. By utilizing ischemic tolerance, it is possible to achieve a significant reduction in the extent of the cell damage due to ischemia–reperfusion injury. Since ischemia–reperfusion damage usually occurs unexpectedly, the use of preconditioning is extremely limited. In contrast, postconditioning has wider possibilities for use in practice. In both cases, the activation of ischemic tolerance can also be achieved by the application of sublethal stress on a remote organ. Despite very encouraging and successful results in animal experiments, the clinical results have been disappointing so far. To avoid the factors that prevent the activation of ischemic tolerance, the solution has been to use blood plasma containing tolerance effectors. This plasma is taken from healthy donors in which, after exposure to two sublethal stresses within 48 h, effectors of ischemic tolerance occur in the plasma. Application of this activated plasma to recipient animals after the end of lethal ischemia prevents cell death and significantly reduces the consequences of ischemia–reperfusion damage. Until there is a clear chemical identification of the end products of ischemic tolerance, the simplest way of enhancing ischemic tolerance will be the preparation of activated plasma from young healthy donors with the possibility of its immediate use in recipients during the initial treatment.
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McCully, James D., Yoshiya Toyoda, Masahisa Uematsu, Robert D. Stewart, and Sidney Levitsky. "Adenosine-enhanced ischemic preconditioning: adenosine receptor involvement during ischemia and reperfusion." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (February 1, 2001): H591—H602. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h591.
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Adenosine-enhanced ischemic preconditioning (APC) extends the cardioprotection of ischemic preconditioning (IPC) by both significantly decreasing myocardial infarct size and significantly enhancing postischemic functional recovery. In this study, the role of adenosine receptors during ischemia-reperfusion was determined. Rabbit hearts ( n = 92) were used for Langendorff perfusion. Control hearts were perfused for 180 min, global ischemia hearts received 30-min ischemia and 120-min reperfusion, and IPC hearts received 5-min ischemia and 5-min reperfusion before ischemia. APC hearts received a bolus injection of adenosine coincident with IPC. Adenosine receptor (A1, A2, and A3) antagonists were used with APC before ischemia and/or during reperfusion. GR-69019X (A1/A3) and MRS-1191/MRS-1220 (A3) significantly increased infarct size in APC hearts when administered before ischemia and significantly decreased functional recovery when administered during both ischemia and reperfusion ( P < 0.05 vs. APC). DPCPX (A1) administered either before ischemia and/or during reperfusion had no effect on APC cardioprotection. APC-enhanced infarct size reduction is modulated by adenosine receptors primarily during ischemia, whereas APC-enhanced postischemic functional recovery is modulated by adenosine receptors during both ischemia and reperfusion.
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Omae, Tsuyoshi, Matthew D. Silva, Orna Mayzel-Org, Mark Kazemi, Fihai Li, Christopher H. Sotak, and Marc Fisher. "Temporal evolution of Diffusion / Perfusion Mismatch in a Rat Stroke Model." Stroke 32, suppl_1 (January 2001): 351. http://dx.doi.org/10.1161/str.32.suppl_1.351-c.
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P69 Background and Purpose: Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) can rapidly detect lesions in acute ischemic stroke. Studies show that lesions by PWI are sometimes larger than those of DWI in patients with acute ischemic stroke, suggests that the mismatch between DWI and PWI is potentially predictive of tissue at high risk for evolving into infarction. The aims of this study were to detect the evolution of the DWI/PWI mismatch in permanent focal experimental ischemia and transient focal experimental ischemia. Methods: Rats were subjected to permanent (n=8) and 60 minutes of temporary ischemia (n=8) using the intraluminal middle cerebral artery occlusion method and then underwent DWI and PWI after occlusion. Rats in the transient ischemic experiments were reperfused 60 minutes after occlusion. An apparent diffusion coefficient map and a cerebral blood flow index map were used to calculate the percent hemispheric lesion volume (%HLV) for each MRI parameter. Results: In permanent ischemia, %HLVs by DWI were 21%, 45%, 60%, 87%, and 101% of %HLV by PWI at 15, 30, 60, 90 and 120 minutes after ischemia, respectively. The ratio did not change after 120 minutes. With 60 minutes of temporary ischemia, the changes were almost the same as those in permanent ischemia before reperfusion. After reperfusion the lesions on PWI were smaller than those on DWI. The DWI lesion did not increase after reperfusion, and was the almost the same size as just before reperfusion. Conclusions: The DWI/PWI mismatch disappears at 2 hours after permanent ischemia, and the region of DWI/PWI mismatch can be saved from ischemic damage if reperfused early, but ischemic lesions seen on DWI can not be reduced by reperfusion after 60 minutes of temporary ischemia in this rat stroke model.
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Daly, Hafedh. "Diagnosis and Management of Acute Limb Ischemia." Angiology & Vascular Surgery 7, no. 2 (June 2, 2022): 1–6. http://dx.doi.org/10.24966/avs-7397/100089.
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Introduction: Acute limb ischemia is considered as a life threatening disease .After twelve hours of ischemia, chances of saving the ischemic limb are lower (78%), with higher mortality (31%) as well. Methods: A total of 54 patients who underwent surgery for acute non traumatic limb ischemia between January 2013 and December 2020 were retrospectively reviewed. Results: We included 30 women and 24 men; median age was 69 years. Twenty patients (37%) were presented with upper limb ischemia, where as 34 patients (63%) with lower limb ischemia. Mean delay between the onset of symptoms and hospital admission of upper limb ischemia was 22 hours, 35% of Patients were diagnosed at the stage IIA of Rutherford classification, while 65% were diagnosed at the stage of II B. Lower limb ischemia patients were admitted after 28.5 hours, 64.8% of patients were diagnosed at the stage of II A of Rutherford, while 32.3% were diagnosed at the stage of II B of Rutherford. Revascularization of all ischemic upper limbs (100%) and the majority of ischemic lower limbs (94.1%) were carried out through endovascular thromboembolectomy with Fogarty ballooncathete. Meanlength of hospitalstaywas 8.3 days for upper limb ischemia cases ; while lower limb ischemia patients required 9.2 days of mean hospitalstay. We report a total of 4 deaths (7.4%). Conclusion: Acute limb ischemia remains a challenging entity for clinicians with significant risk of patient limbloss and mortality. Prompt diagnosis, anticoagulation, and timely revascularization are crucial to minimize the risk of limbloss.
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Zicola, Elisa, Elisa Arrigo, and Daniele Mancardi. "H2S Pretreatment Is Promigratory and Decreases Ischemia/Reperfusion Injury in Human Microvascular Endothelial Cells." Oxidative Medicine and Cellular Longevity 2021 (April 17, 2021): 1–13. http://dx.doi.org/10.1155/2021/8886666.
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Endothelial cell injury and vascular function strongly correlate with cardiac function following ischemia/reperfusion injury. Several studies indicate that endothelial cells are more sensitive to ischemia/reperfusion compared to cardiomyocytes and are critical mediators of cardiac ischemia/reperfusion injury. H2S is involved in the regulation of cardiovascular system homeostasis and can act as a cytoprotectant during ischemia/reperfusion. Activation of ERK1/2 in endothelial cells after H2S stimulation exerts an enhancement of angiogenesis while its inhibition significantly decreases H2S cardioprotective effects. In this work, we investigated how H2S pretreatment for 24 hours prevents the ischemia/reperfusion injury and promotes angiogenesis on microvascular endothelial cells following an ischemia/reperfusion protocol in vitro, using a hypoxic chamber and ischemic buffer to simulate the ischemic event. H2S preconditioning positively affected cell viability and significantly increased endothelial cell migration when treated with 1 μM H2S. Furthermore, mitochondrial function was preserved when cells were preconditioned. Since ERK1/2 phosphorylation was extremely enhanced in ischemia/reperfusion condition, we inhibited ERK both directly and indirectly to verify how H2S triggers this pathway in endothelial cells. Taken together, our data suggest that H2S treatment 24 hours before the ischemic insult protects endothelial cells from ischemia/reperfusion injury and eventually decreases myocardial injury.
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Kato, Hiroyuki, Kyuya Kogure, Tsutomu Araki, Xiao-Hong Liu, Kanefusa Kato, and Yasuto Itoyama. "Immunohistochemical Localization of Superoxide Dismutase in the Hippocampus following Ischemia in a Gerbil Model of Ischemic Tolerance." Journal of Cerebral Blood Flow & Metabolism 15, no. 1 (January 1995): 60–70. http://dx.doi.org/10.1038/jcbfm.1995.7.
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Pretreatment of the gerbil brain with a 2-min period of sublethal ischemia protects against neuronal damage following a subsequent 3-min period of ischemia, which normally destroys pyramidal neurons in the CA1 region of the hippocampus. To clarify the role of superoxide dismutase (SOD) in this ischemic tolerance, we immunohistochemically investigated the alterations in copper-zinc SOD (CuZnSOD) and manganese SOD (MnSOD) in the gerbil hippocampus following 3-min ischemia with or without the first mild ischemia. Normal hippocampus showed an intense CuZnSOD immunostaining in pyramidal neurons but relatively less MnSOD immunostaining. MnSOD, but not CuZnSOD, immunoreactivity increased after the first ischemia. Both CuZnSOD and MnSOD immunoreactivities decreased throughout the hippocampus 4 h after 3 min of ischemia both with and without the first ischemia. The immunostaining recovered in resistant regions (CA3 and dentate gyrus) after 1 day in both groups and in the pretreated CA, after 2 days. Without pretreatment, however, the immunostaining never recovered in the vulnerable CA, region. The results suggest that ischemic tolerance is induced in part by enhanced synthesis of MnSOD in the tolerance-acquired hippocampus. Both CuZnSOD and MnSOD immunoreactivities decreased after the second ischemia even in the pretreated hippocampus in the early reperfusion periods, but ischemic tolerance facilitated the recovery from the postischemic reductions in SOD immunoreactivity.
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Yagita, Yoshiki, Kazuo Kitagawa, Naoki Oyama, Toshiro Yukami, Akihiro Watanabe, Tsutomu Sasaki, and Hideki Mochizuki. "Functional Deterioration of Endothelial Nitric Oxide Synthase after Focal Cerebral Ischemia." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (July 3, 2013): 1532–39. http://dx.doi.org/10.1038/jcbfm.2013.112.
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Endothelial nitric oxide synthase (eNOS) dysfunction is related to secondary injury and lesion expansion after cerebral ischemia. To date, there are few reports about postischemic alterations in the eNOS regulatory system. The purpose of the present study was to clarify eNOS expression, Ser1177 phosphorylation, and monomer formation after cerebral ischemia. Male Wistar rats were subjected to transient focal cerebral ischemia. Endothelial nitric oxide synthase messenger RNA (mRNA) and protein expression increased ~ 8-fold in the ischemic lesion. In the middle cerebral artery core, eNOS-Ser1177 phosphorylation increased 6 hours after ischemia; however, there was an approximately 90% decrease in eNOS-Ser1177 phosphorylation observed 24 hours after ischemia that continued until at least 7 days after ischemia. Endothelial nitric oxide synthase monomer formation also increased 24 and 48 hours after ischemia ( P<0.05), and protein nitration progressed in parallel with monomerization. To assess the effect of a neuroprotective agent on eNOS dysfunction, we evaluated the effect of fasudil, a Rho-kinase inhibitor, on eNOS phosphorylation and dimerization. Postischemic treatment with fasudil suppressed lesion expansion and dephosphorylation and monomer formation of eNOS. In conclusion, functional deterioration of eNOS progressed after cerebral ischemia. Rho-kinase inhibitors can reduce ischemic lesion expansion as well as eNOS dysfunction in the ischemic brain.
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Tian, Guo-Feng, and Andrew J. Baker. "Protective Effect of High Glucose Against Ischemia-Induced Synaptic Transmission Damage in Rat Hippocampal Slices." Journal of Neurophysiology 88, no. 1 (July 1, 2002): 236–48. http://dx.doi.org/10.1152/jn.00572.2001.
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Cerebral ischemic damage is an important cause of morbidity and mortality. However, there is conflicting evidence regarding the effect of the extracellular glucose concentration in focal and global ischemic injury. This study was designed to investigate this effect in ischemia-induced synaptic transmission damage in rat hippocampal slices. Slices were superfused with artificial cerebrospinal fluid (ACSF) containing various concentrations of glucose before and after ischemia. The evoked somatic postsynaptic population spike (PS) and dendritic field excitatory postsynaptic potential (fEPSP) were extracellularly recorded in the CA1 stratum pyramidal cell layer and s. radiatum after stimulation of the Schaeffer collaterals, respectively. The glucose concentration in ACSF before and after ischemia determined the duration of ischemia tolerated by synaptic transmission as demonstrated by complete recovery of the somatic PS and dendritic fEPSP. Specifically, the somatic PS and dendritic fEPSP completely recovered following 3, 4, and 5 min of ischemia only when slices were superfused with ACSF containing 4, 10, and 20 mM glucose before and after ischemia, respectively. The latencies of the somatic and dendritic ischemic depolarization (ID) occurrence in the CA1 s. pyramidal cell layer and s. radiatum were significantly longer with 10 than 4 mM glucose in ACSF before ischemia and significantly longer with 20 than 10 mM glucose in ACSF before ischemia. Regardless of the glucose concentration in ACSF before and after ischemia, the somatic PS and dendritic fEPSP only partially recovered when ischemia was terminated at the occurrence of ID. These results indicate that high glucose in ACSF during the period before and after ischemia significantly protects CA1 synaptic transmission against in vitro ischemia-induced damage through postponing the occurrence of ID.
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Liu, Shimin, Honglian Shi, Wenlan Liu, Takamitsu Furuichi, Graham S. Timmins, and Ke Jian Liu. "Interstitial pO2 in Ischemic Penumbra and Core are Differentially Affected following Transient Focal Cerebral Ischemia in Rats." Journal of Cerebral Blood Flow & Metabolism 24, no. 3 (March 2004): 343–49. http://dx.doi.org/10.1097/01.wcb.0000110047.43905.01.
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Stroke causes heterogeneous changes in tissue oxygenation, with a region of decreased blood flow, the penumbra, surrounding a severely damaged ischemic core. Treatment of acute ischemic stroke aims to save this penumbra before its irreversible damage by continued ischemia. However, effective treatment remains elusive due to incomplete understanding of processes leading to penumbral death. While oxygenation is central in ischemic neuronal death, it is unclear exactly what actual changes occur in interstitial oxygen tension (pO2) in ischemic regions during stroke, particularly the penumbra. Using the unique capability of in vivo electron paramagnetic resonance (EPR) oximetry to measure localized interstitial pO2, we measured both absolute values, and temporal changes of pO2 in ischemic penumbra and core during ischemia and reperfusion in a rat model. Ischemia rapidly decreased interstitial pO2 to 32% ± 7.6% and 4% ± 0.6% of pre-ischemic values in penumbra and core, respectively 1 hour after ischemia. Importantly, whilst reperfusion restored core pO2 close to its pre-ischemic value, penumbral pO2 only partially recovered. Hyperoxic treatment significantly increased penumbral pO2 during ischemia, but not in the core, and also increased penumbral pO2 during reperfusion. These divergent, important changes in pO2 in penumbra and core were explained by combined differences in cellular oxygen consumption rates and microcirculation conditions. We therefore demonstrate that interstitial pO2 in penumbra and core is differentially affected during ischemia and reperfusion, providing new insights to the pathophysiology of stroke. The results support normobaric hyperoxia as a potential early intervention to save penumbral tissue in acute ischemic stroke.
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Danielisová, Viera, Miroslava Némethová, and Jozef Burda. "Iron Deposition in the Brain Following the Ischemia in a Rat Model of Ischemic Tolerance." Acta Medica (Hradec Kralove, Czech Republic) 47, no. 4 (2004): 285–88. http://dx.doi.org/10.14712/18059694.2018.107.
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Preconditioning of the brain by short-term ischemia increases brain tolerance to the subsequent severer ischemia. In this study, we investigated iron deposition in the cerebral cortex and the ischemic tolerance in a rat model of cerebral ischemia. Forebrain ischemia was induced by four-vessel occlusion for 5 min as ischemic preconditioning. Two days after preconditioning or after the sham-operation, the second ischemia was induced for 20 min. Changes in the cerebral cortex were examined after 1 to 8 weeks of recirculation following 20 min ischemia with or without preconditioning using the iron histochemistry. Granular deposits of the iron were found in the cytoplasm of the pyramidal cells in the layers III and V of the frontal cortex after 1 week of recirculation. When the rats were exposed to 5 min ischemia 2 days before 20 min lasting ischemia, the deposition of iron in the cytoplasm of the pyramidal cells in layers III and V of the frontal cortex was significantly lower during all periods of reperfusion. Preconditioning 5 min ischemia followed by 2 days of reperfusion before 20 min ischemia also prevented degeneration of the pyramidal neurons in layers III and V of the frontal cortex.
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Briones, Tess L., and Barbara Therrien. "Behavioral Effects of Transient Cerebral Ischemia." Biological Research For Nursing 1, no. 4 (April 2000): 276–86. http://dx.doi.org/10.1177/109980040000100404.
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CA1 neurons in the hippocampus, a brain structure involved in learning and memory, are selectively vulnerable to ischemic effects. In this study, the authors examined if duration of ischemia is directly related to extent of CA1 damage and degree of spatial learning deficit. Adult female Wistar rats received either 5-min or 10-min ischemia or sham surgery. Following recovery, rats were tested in the Morris water maze. Histological analysis showed moderate cell loss in CA1 (31%) and CA3 (12%) and minimal cell loss in CA2 (4%) with 5-min ischemia. Increased cell loss was seen in CA1 (68%), CA2 (16%), and CA3 (23%) with 10-min ischemia. Behavioral testing revealed that animals with 10-min ischemia have greater spatial learning deficits and they remain impaired across the test days compared to the 5-min ischemic group. Furthermore, degree of CA1 cell loss accounted for approximately 45% of the variance in spatial learning deficits in the ischemic group. The authors conclude that cell loss is largely confined to CA1 region in rats who received 5 and 10 min of ischemia and that increased ischemic duration results in persistent learning deficits in female rats; also, the degree of behavioral impairment is related to extent of CA1 cell loss.
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Pluta, Ryszard, Janusz Kocki, Jacek Bogucki, Anna Bogucka-Kocka, and Stanisław J. Czuczwar. "LRP1 and RAGE Genes Transporting Amyloid and Tau Protein in the Hippocampal CA3 Area in an Ischemic Model of Alzheimer’s Disease with 2-Year Survival." Cells 12, no. 23 (December 4, 2023): 2763. http://dx.doi.org/10.3390/cells12232763.
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Explaining changes at the gene level that occur during neurodegeneration in the CA3 area is crucial from the point of view of memory impairment and the development of post-ischemic dementia. An ischemic model of Alzheimer’s disease was used to evaluate changes in the expression of genes related to amyloid transport in the CA3 region of the hippocampus after 10 min of brain ischemia with survival of 2, 7 and 30 days and 12, 18 and 24 months. The quantitative reverse transcriptase PCR assay revealed that the expression of the LRP1 and RAGE genes involved in amyloid transport was dysregulated from 2 days to 24 months post-ischemia in the CA3 area of the hippocampus. LRP1 gene expression 2 and 7 days after ischemia was below control values. However, its expression from day 30 to 24 months, survival after an ischemic episode was above control values. RAGE gene expression 2 days after ischemia was below control values, reaching a maximum increase 7 and 30 days post-ischemia. Then, after 12, 18 and 24 months, it was again below the control values. The data indicate that in the CA3 area of the hippocampus, an episode of brain ischemia causes the increased expression of the RAGE gene for 7–30 days during the acute phase and that of LRP1 from 1 to 24 months after ischemia during the chronic stage. In other words, in the early post-ischemic stage, the expression of the gene that transport amyloid to the brain increases (7–30 days). Conversely, in the late post-ischemic stage, amyloid scavenging/cleaning gene activity increases, reducing and/or preventing further neuronal damage or facilitating the healing of damaged sites. This is how the new phenomenon of pyramidal neuronal damage in the CA3 area after ischemia is defined. In summary, post-ischemic modification of the LRP1 and RAGE genes is useful in the study of the ischemic pathways and molecular factors involved in the development of Alzheimer’s disease.
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Mor-Avi, Victor, Keith A. Collins, Claudia E. Korcarz, Milind Shah, Kirk T. Spencer, and Roberto M. Lang. "Detection of regional temporal abnormalities in left ventricular function during acute myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 4 (April 1, 2001): H1770—H1781. http://dx.doi.org/10.1152/ajpheart.2001.280.4.h1770.
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Echocardiographic diagnosis of myocardial ischemia is based on visualizing hypokinesis, which occurs late in the ischemic cascade. We hypothesized that temporal changes in endocardial motion may constitute sensitive early markers of ischemia. Two protocols were performed in 19 anesthetized pigs. Protocol 1 included 54 intracoronary balloon occlusions. Transthoracic images were acquired at baseline and every 15 s during 5 min of occlusion and reperfusion. In protocol 2, ischemia was induced in 12 animals by use of graded dobutamine infusion, after creating significant partial occlusions without a resting wall motion abnormality. Systolic and diastolic endocardial motion was color encoded using color kinesis and analyzed using custom software. All ischemic episodes caused detectable and reversible changes. The earliest sign of ischemia was tardokinesis in 31/54 occlusions, whereas hypokinesis appeared first in 23/54 cases. Dobutamine-induced ischemia caused tardokinesis first in 9/12 and hypokinesis in 3/12 animals. Reversible ischemic changes in regional left ventricular performance can be objectively detected using analysis of echocardiographic images and will likely improve the early noninvasive diagnosis of acute ischemia.