Journal articles: 'Ischaemia and reperfusion damage'

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Ozkisacik, Sezen, Ali Onur Erdem, Barlas Etensel, Canten Tataroglu, Mukadder Serter, and Mesut Yazici. "Short-interval postconditioning protects the bowel against ischaemia–reperfusion injury in rats." Journal of International Medical Research 45, no. 3 (May 28, 2017): 1036–41. http://dx.doi.org/10.1177/0300060517708921.

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Objective Acute mesenteric ischaemia leads to intestinal damage. Restoration of blood flow results in further damage to tissue, which is called reperfusion injury. This study aimed to investigate the protective effects of short-interval postconditioning and to determine the optimal interval for reperfusion in an experimental rat model of intestinal ischaemia. Methods Forty adult male Wistar rats were grouped as follows: sham (Sh), ischaemia + reperfusion (IR), ischaemia + postconditioning for 5 seconds (PC5), ischaemia + postconditioning for 10 seconds (PC10), and ischaemia + postconditioning for 20 seconds (PC20). For postconditioning, 10 cycles of reperfusion (5, 10, or 20 seconds) interspersed by 10 cycles of 10 seconds of ischaemia were performed. Blood glutathione reductase (GR) and glutathione peroxidase (GPx) levels were measured. Intestinal tissue damage was assessed histopathologically. Results GR levels were significantly higher in the PC5 group than in the IR group (37.7 ± 9.0 vs. 18.5 ± 2.0 min/g Hb). GPx levels were significantly higher in the PC10 group than in the IR group (43.2 ± 9.2 vs. 15.9 ± 4.6 U/g Hb). The histopathological score was significantly lower in the PC5 group (1.1 ± 0.1) than in the IR group (2.1 ± 0.2). Conclusion Short-interval postconditioning reduces reperfusion injury in the ischaemic bowel and the optimal interval for reperfusion is 5 seconds. The long-term effects of short-interval postconditioning and the optimal reperfusion interval in intestinal ischaemia–reperfusion in rats need to be investigated.

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Knight, Kenneth R., Michael F. Angel, Diana A. Lepore, Paul A. Abbey, Laurence I. Arnold, Kathleen A. Gray, Cary G. Mellow, and Bernard McC O'Brien. "Secondary Ischaemia in Rabbit Skin Flaps: The Roles Played by Thromboxane and Free Radicals." Clinical Science 80, no. 3 (March 1, 1991): 235–40. http://dx.doi.org/10.1042/cs0800235.

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1. Biochemical mechanisms of ischaemia were investigated in rabbit skin flaps subjected to 2 h of primary ischaemia then, 24 h later, to 4 h of secondary ischaemia. During secondary ischaemia, flaps underwent either total ischaemia (arterial and venous blood supply occluded) or partial ischaemia (vein only occluded). Some of these flaps were treated at the time of reperfusion with the free-radical scavenger superoxide dismutase (EC 1.15.1.1) and/or the thromboxane synthetase inhibitor UK-38,485. 2. After 30 min of reperfusion, superoxide dismutase treatment significantly reduced blood thromboxane levels, elevated during ischaemia. Superoxide dismutase also reduced tissue levels of malonyldialdehyde and xanthine oxidase, indicators of free-radical damage, and restored the depleted tissue levels of superoxide dismutase. 3. UK-38,485 treatment failed to significantly alter any of these tissue free-radical parameters, although this agent significantly reduced blood thromboxane levels. 4. Combined superoxide dismutase plus UK-38,485 treatment was not significantly better than either treatment alone with respect to any parameter. 5. Partial ischaemia led to consistently higher levels of tissue free radicals and blood thromboxane than did total ischaemia. Thus partial ischaemia appears to result in greater free-radical damage than total ischaemia. 6. These results are consistent with the hypothesis that thromboxane acts as a mediator for free-radical damage in the ischaemic changes within the flap.

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Fabiani, R., C. Ceconi, S. Curello, O. Alfieri, and O. Visioli. "Myocardial damage during ischaemia and reperfusion." European Heart Journal 14, suppl G (November 2, 1993): 25–30. http://dx.doi.org/10.1093/eurheartj/14.suppl_g.25.

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Gariballa, SE, and AJ Sinclair. "Cerebrovascular disease and oxidative stress." Reviews in Clinical Gerontology 9, no. 3 (August 1999): 197–206. http://dx.doi.org/10.1017/s0959259899009314.

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There is strong indirect evidence that free radical production appears to be an important mechanism of brain injury after exposure to ischaemia and reperfusion. Although significant brain damage occurs during an ischaemic episode, new cerebral damage can occur after reperfusion. One proposed mechanism for the brain damage that occurs during reperfusion involves generation of free radicals. Body defences against free radicals depends on the balance between free radical generation and the antioxidant protective defence system. Many of these protective antioxidants are essential nutrients or have essential nutrients as part of their molecule that has to be obtained from diet.

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Picozzi, Piero, Nicholas V. Todd, and H. Alan Crockard. "Regional Blood-Brain Barrier Permeability Changes after Restoration of Blood Flow in Postischemic Gerbil Brains: A Quantitative Study." Journal of Cerebral Blood Flow & Metabolism 5, no. 1 (March 1985): 10–16. http://dx.doi.org/10.1038/jcbfm.1985.2.

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A quantitative technique utilising [14C]α-aminoisobutyric acid as a tracer was used to study cerebrovascular permeability in 22 Mongolian gerbils. Seven other animals were used to measure cerebral blood volumes. Global cerebral ischaemia was produced by temporary bilateral carotid artery occlusion (60 min) in 16 gerbils that were sacrificed at 1, 2, and 3 h following reperfusion. The blood-to-brain transfer constant was significantly increased after 2 h of reperfusion in the ischaemic zones and also in structures, like the cerebellum, not supplied by the carotid artery and not ischaemic during the vessel occlusion. The blood-brain barrier (BBB) alterations were coincident with the onset of ischaemia—induced seizures that were accompanied by sudden “spikes” of systemic blood pressure. Epilepsy may play an important role in the development of BBB damage in this ischaemic model, and this factor must be considered in the interpretation of BBB damage data in gerbils.

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Rőth, Erzsébet. "A szabad gyökös reakciók jelentősége a szívizom ischaemiás-reperfúziós károsodásában és az endogén adaptáció indukálásában." Orvosi Hetilap 156, no. 47 (November 2015): 1908–11. http://dx.doi.org/10.1556/650.2015.30304.

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The reperfusion of acute ischaemic myocardium is essential for myocardial salvage, so called “gold standard” therapy, however it can results serious damage in the myocardium. Functional alterations occur, including depressed contractile function and decreased coronary flow as well as altered vascular reactivity. Over the several decades it has been demonstrated that oxygen radical formation is greatly increased in post-ischaemic heart and serves as a critical central mechanism of ischaemic-reperfusion injury. However it has been demonstrated that free radical play an important role in the endogenous adaptation phenomenon of the heart, too. Ischaemic preconditioning is a cellular adaptive response of the heart to stress, which provides the most potent endogenous protection against reperfusion arrhytmias, stunning and infarction. Postconditioning defined as brief periods of ischaemia and reperfusion during the very early minutes of reperfusion stimulates endogenous adaptation. Postconditioning may also attenuate the damage to endothelial cells and cardiomyocytes from oxidants, cytokines, proteases and inflammatory cells. Orv. Hetil., 2015, 156(47), 1908–1911.

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Solaini, Giancarlo, and David A. Harris. "Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion." Biochemical Journal 390, no. 2 (August 23, 2005): 377–94. http://dx.doi.org/10.1042/bj20042006.

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Heart tissue is remarkably sensitive to oxygen deprivation. Although heart cells, like those of most tissues, rapidly adapt to anoxic conditions, relatively short periods of ischaemia and subsequent reperfusion lead to extensive tissue death during cardiac infarction. Heart tissue is not readily regenerated, and permanent heart damage is the result. Although mitochondria maintain normal heart function by providing virtually all of the heart's ATP, they are also implicated in the development of ischaemic damage. While mitochondria do provide some mechanisms that protect against ischaemic damage (such as an endogenous inhibitor of the F1Fo-ATPase and antioxidant enzymes), they also possess a range of elements that exacerbate it, including ROS (reactive oxygen species) generators, the mitochondrial permeability transition pore, and their ability to release apoptotic factors. This review considers the process of ischaemic damage from a mitochondrial viewpoint. It considers ischaemic changes in the inner membrane complexes I–V, and how this might affect formation of ROS and high-energy phosphate production/degradation. We discuss the contribution of various mitochondrial cation channels to ionic imbalances which seem to be a major cause of reperfusion injury. The different roles of the H+, Ca2+ and the various K+ channel transporters are considered, particularly the K+ATP (ATP-dependent K+) channels. A possible role for the mitochondrial permeability transition pore in ischaemic damage is assessed. Finally, we summarize the metabolic and pharmacological interventions that have been used to alleviate the effects of ischaemic injury, highlighting the value of these or related interventions in possible therapeutics.

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Denorme, Frederik, and Simon F. De Meyer. "The VWF-GPIb axis in ischaemic stroke: lessons from animal models." Thrombosis and Haemostasis 116, no. 10 (2016): 597–604. http://dx.doi.org/10.1160/th16-01-0036.

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SummaryStroke is a leading cause of death and long-term disability worldwide. Ischaemic stroke is caused by a blood clot that obstructs cerebral blood flow. Current treatment mainly consists of achieving fast reperfusion, either via pharmacological thrombolysis using tissue plasminogen activator or via endovascular thrombectomy. Unfortunately, reperfusion therapy is only available to a limited group of patients and reperfusion injury can further aggravate brain damage. Hence, there is an urgent need for better understanding of ischaemic stroke pathophysiology in order to develop novel therapeutic strategies. In recent years, the pathophysiological importance of von Willebrand factor (VWF) in ischaemic stroke has become clear from both clinical and experimental studies. In particular, binding of VWF to platelet glycoprotein Ib (GPIb) has become an interesting target for ischaemic stroke therapy. Recent insights show that inhibting the VWF-GPIb interaction could result in a pro-thrombolytic activity improving cerebral reperfusion rates and concurrently reducing cerebral ischaemia/reperfusion damage. This review gives an overview of the experimental evidence that illustrates the crucial role of the VWF-GPIb axis in ischaemic stroke.

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Beyersdorf, F., K. Sarai, Z. Mitrev, L. Eckel, K. Ihnken, and P. Satter. "Studies of Reperfusion Injury in Skeletal Muscle: Controlled Limb Reperfusion to Reduce Post-Ischaemic Syndrome." Cardiovascular Surgery 1, no. 4 (August 1993): 330–36. http://dx.doi.org/10.1177/096721099300100404.

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Revascularization after prolonged complete limb ischaemia may result in both severe damage to skeletal muscle and various systemic manifestations of the postischaemic syndrome. Previous experimental studies performed by the authors have shown that these are caused, to a large extent, by normal reperfusion at normal systemic pressure and that this additional injury can be substantially reduced by controlled reperfusion of the revascularized limb before restoration of the normal circulation. This treatment includes control of the conditions of reperfusion and composition of the initial reperfusate. In the present study, this concept of controlled limb reperfusion was applied to patients with prolonged severe lower limb ischaemia. Controlled limb reperfusion was used in 11 patients after prolonged complete unilateral or bilateral ischaemia. The ischaemic interval ranged from 5 to 21 h. Two patients were in cardiogenic shock, ten had a history of associated cardiac disease and seven coexistent peripheral vascular disease. After systemic heparinization, thromboembolectomy was undertaken using a Fogarty catheter. Cannulas were placed in the iliac, profunda and superficial femoral arteries and connected to a reperfusion set. Oxygenated blood was drawn from the iliac artery and mixed with an asanguineous solution (ratio 6:1). This controlled reperfusate was returned to the profunda and superficial femoral arteries using a single roller pump. The system allows control of both the composition of the reperfusate (Ca2+, pH, osmolarity, glucose, substrate, PO2, free radical scavengers) and the conditions of reperfusion (pressure, flow, temperature). After 30 min of controlled limb reperfusion, the cannulas were removed, the arteriotomy closed and normal blood reperfusion started. All nine patients who were haemodynamically stable before operation survived the procedure and were discharged with full functional recovery, including one patient with acute aortic occlusion of several hours' duration. Thus controlled limb reperfusion avoided the need for amputation and the development of systemic complications. Two patients, who were in cardiogenic shock before operation, died from progressive cardiac failure. It is concluded that controlled arterioarterial limb reperfusion may reduce the local manifestation of the postischaemic syndrome after prolonged periods of ischaemia, salvage limbs thought to be irreversibly damaged by prolonged ischaemia and is easily performed in the operating room.

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Gracia-Sancho, Jordi, Araní Casillas-Ramírez, and Carmen Peralta. "Molecular pathways in protecting the liver from ischaemia/reperfusion injury: a 2015 update." Clinical Science 129, no. 4 (May 21, 2015): 345–62. http://dx.doi.org/10.1042/cs20150223.

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Ischaemia/reperfusion injury is an important cause of liver damage during surgical procedures such as hepatic resection and liver transplantation, and represents the main cause of graft dysfunction post-transplantation. Molecular processes occurring during hepatic ischaemia/reperfusion are diverse, and continuously include new and complex mechanisms. The present review aims to summarize the newest concepts and hypotheses regarding the pathophysiology of liver ischaemia/reperfusion, making clear distinction between situations of cold and warm ischaemia. Moreover, the most updated therapeutic strategies including pharmacological, genetic and surgical interventions, as well as some of the scientific controversies in the field are described.

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Ho, Choon-Kiat, Chee-Wei Lee, Jian Lu, Jian Wu, Woon-Puay Koh, Chung-Yip Chan, Shervanthi Homer-Vanniasinkam, and Alexandre KH Chao. "New Hope for an Old Cure: A Pilot Animal Study on Selective Venesection in Attenuating the Systemic Effects of Ischaemic-Reperfusion Injury." Annals of the Academy of Medicine, Singapore 38, no. 7 (July 15, 2009): 569–75. http://dx.doi.org/10.47102/annals-acadmedsg.v38n7p569.

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Introduction: Reperfusion of acutely ischaemic tissue may, paradoxically, lead to systemic complications. This phenomenon is believed to be initiated by humoral factors that have accumulated in the ischaemic tissue. The ancient art of venesection may reduce the load of these mediators at the point of reperfusion. The aim of this study is to test if selective venesection, by removing the initial venous return from the ischaemic tissue, can attenuate the systemic effects of the ischaemic-reperfusion injury using a porcine model of acute limb ischaemia. Materials and Methods: The right femoral arteries of anaesthetised female pigs were clamped. Twelve pigs were divided into 2 groups (n = 6 per group). In the treatment group, 5% of blood volume was venesected from the ipsilateral femoral vein upon reperfusion; the other arm served as control. The animals were sacrificed after 4 days for histological examination. A pathologist, blinded to the experimental groups, graded the degree of microscopic injury. Results: For the control group, the kidneys showed glomeruli and tubular damage. The livers demonstrated architectural distortion with cellular oedema. There was pulmonary oedema as well as extensive capillary congestion and neutrophil infiltration. Such findings were absent or reduced in the venesected animals. Consequently, the injury scores for the kidney, lung, liver and heart were significantly less for the venesected animals. Conclusion: Selective venesection reduces the remote organ injuries of the ischaemic-reperfusion phenomenon. Key words: Acute ischaemia, Humoral factors, MODS, Pulmonary oedema

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Budas, G. R., and D. Mochly-Rosen. "Mitochondrial protein kinase Cϵ (PKCϵ): emerging role in cardiac protection from ischaemic damage." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 1052–54. http://dx.doi.org/10.1042/bst0351052.

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Mitochondria mediate diverse cellular functions including energy generation and ROS (reactive oxygen species) production and contribute to signal transduction. Mitochondria are also key regulators of cell viability and play a central role in necrotic and apoptotic cell death pathways induced by cardiac ischaemia/reperfusion injury. PKC (protein kinase C) ϵ plays a critical role in cardioprotective signalling pathways that protect the heart from ischaemia/reperfusion. Emerging evidence suggests that the cardioprotective target of PKCϵ resides at the mitochondria. Proposed mitochondrial targets of PKCϵ include mitoKATP (mitochondrial ATP-sensitive K+ channel), components of the MPTP (mitochondrial permeability transition pore) and components of the electron transport chain. This review highlights mitochondrial targets of PKCϵ and their possible role in cardioprotective signalling in the setting of ischaemia/reperfusion injury.

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Veitch, K., A. Hombroeckx, D. Caucheteux, H. Pouleur, and L. Hue. "Global ischaemia induces a biphasic response of the mitochondrial respiratory chain. Anoxic pre-perfusion protects against ischaemic damage." Biochemical Journal 281, no. 3 (February 1, 1992): 709–15. http://dx.doi.org/10.1042/bj2810709.

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Studies of Langendorff-perfused rat hearts have revealed a biphasic response of the mitochondrial respiratory chain to global ischaemia. The initial effect is a 30-40% increase in the rate of glutamate/malate oxidation after 10 min of ischaemia, owing to an increase in the capacity for NADH oxidation. This effect is followed by a progressive decrease in these oxidative activities as the ischaemia is prolonged, apparently owing to damage to Complex I at a site subsequent to the NADH dehydrogenase component. This damage is exacerbated by reperfusion, which causes a further decrease in Complex I activity and also decreases the activities of the other complexes, most notably of Complex III. Perfusion for up to 1 h with anoxic buffer produced only the increase in NADH oxidase activity, and neither anoxia alone, nor anoxia and reperfusion, caused loss of Complex I activity. Perfusing for 3-10 min with anoxic buffer before 1 h of global ischaemia had a significant protective effect against the ischaemia-induced damage to Complex I.

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KNIGHT, Kenneth R., Trixie A. SHINKEL, Peter J. COWAN, Rosalind ROMEO-MEEUW, Anthony J. F. d'APICE, and Wayne A. MORRISON. "Transgenic expression of human complement regulators reduces skeletal muscle ischaemia/reperfusion injury in mice." Clinical Science 108, no. 1 (December 15, 2004): 47–53. http://dx.doi.org/10.1042/cs20040236.

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This study aimed to explore the hypothesis that activated complement components contribute significantly to I/R (ischaemia/reperfusion) injury in skeletal muscle. After 50, 70 and 90 min of tourniquet ischaemia and 24 h of reperfusion, viability of the medial gastrocnemius muscle in CBA-C57BL/6 wild-type mice, assessed histochemically by reduction of NBT (Nitro Blue Tetrazolium) dye, was 60, 21 and 8% respectively. Skeletal muscle viability after 70 min of ischaemia and 24 h of reperfusion in transgenic mice expressing a combination of human CD46, CD55 and CD59, all inhibitors of complement activation, was 45% compared with 24% in ischaemic reperfused wild-type mice (P=0.008; n=6 per group). Muscle from sham-treated transgenic mice and wild-type littermates had no significant loss of viability relative to normal contralateral gastrocnemius muscle. A significant reduction in myeloperoxidase activity (a measure of neutrophil infiltration), xanthine oxidase activity (a source of free radicals) and water content (a measure of oedema) was observed in ischaemic reperfused muscle from transgenic mice compared with ischaemic reperfused wild-type muscle (P<0.05). Haematoxylin and eosin-stained histological sections also showed less damage and less apparent leucocyte infiltration in muscles from ischaemic reperfused transgenic mice than those from wild-type animals given the same degree of injury. Muscles from sham-treated transgenic and wild-type controls were almost identical with normal muscle. It is concluded that complement activation contributes to the pathogenesis of I/R injury in murine skeletal muscle, resulting in increased neutrophil infiltration into the injured muscle, increased free radical production and vascular permeability during reperfusion, and a net detrimental effect on muscle viability.

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Woodman, Owen L. "Approaches to the Prevention of Coronary Vascular Dysfunction Caused by Myocardial Ischaemia and Reperfusion." Current Pharmaceutical Design 5, no. 12 (December 1999): 1077–87. http://dx.doi.org/10.2174/1381612805666230112214526.

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The endothelium is an important regulator of coronary vascular tone due to its ability to release potent vasoactive substances such as the vasodilators nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), prostacyclin (PGl2) and the potent vasoconstrictor endothelin. Endothelial dysfunction has been associated with a number of pathological states such as atherosclerosis, hypertension, diabetes and congestive heart failure. A disturbance of endothelial function may also contribute to the adverse effects that ischaemia and reperfusion exerts on the coronary vasculature. After ischaemia and reperfusion there is usually a selective impairment of endothelium-dependent relaxation in isolated coronary arteries. However, in the intact coronary circulation, there is a general loss of vasodilator reserve as responses to both endothelium-dependent and endothelium-independent agonists are attenuated. The release of vasoconstrictor(s) and plugging of capillaries with leukocytes may contribute to that impairment of the capacity of the coronary circulation to dilate together with the reduction in basal blood flow (no-reflow phenomenon). Ischaemic preconditioning is able to prevent ischaemic damage to the myocardium but the vasculature is less well protected as reperfusion is enhanced but the vasodilator reserve continues to be limited. Pharmacological preservation of vascular function has proved more successful with inhibitors of leukocyte adhesion, calcium channel blockers, endothelin receptor antagonists and inhibitors of oxygen radical generation all offering protection. Further refinement of protocols to preserve endothelial and vascular function after ischaemia will aid reperfusion, enhance vasodilator reserve and maximise recovery of myocardial function.

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Rudolf, R. "Avoiding long-term muscle damage upon ischaemia-reperfusion." Acta Physiologica 219, no. 2 (August 31, 2016): 343–45. http://dx.doi.org/10.1111/apha.12769.

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Lochner, Amanda. "Cardioprotective effect of melatonin against ischaemia reperfusion damage." Frontiers in Bioscience E5, no. 1 (2013): 305–15. http://dx.doi.org/10.2741/e617.

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Burggraf, Dorothe, Milan Vosko, Marion Schubert, Jean-Marie Stassen, and Gerhard Hamann. "Different therapy options protecting microvasculature after experimental cerebral ischaemia and reperfusion." Thrombosis and Haemostasis 103, no. 05 (2010): 891–900. http://dx.doi.org/10.1160/th09-07-0500.

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SummaryRecombinant tissue plasminogen activator (rt-PA) is successfully used in human stroke, but often shows serious drawbacks. To find an alternative, we hypothesised that the novel thrombolytic microplasmin would have fewer adverse effects on haemoglobin extravasation and microvascular damage compared with the effects of rt-PA and tenecteplase (TNK). A constant period of ischaemia (3 hours) was induced in a rat suture model followed by reperfusion (24 hours). Mikroplasmin (10 mg/kg), TNK (5 mg/kg), rt-PA (9 mg/kg) and saline (control), were administered. The volume of the ischaemic lesion was calculated, the loss of collagen type IV and the extravasation of haemoglobin were quantified by Western blotting. The matrix-metalloproteinases 2 and 9 (MMP-2/-9) were quantified by zymography and their endogenous tissue inhibitors (TIMPs) were analysed by reverse zymography. Microplasmin treatment caused the lowest volume of the ischaemic lesion (51.0 ± 22.6 mm3) compared with control (167.3 ± 13.1 mm3; p<0.05). The content of col-lagen type IV was significantly increased and haemoglobin extravasation reduced (154 ± 24%; p<0.05) compared with control (442 ± 124%); MMP-2/-9 and the corresponding TIMPs remained unchanged. In comparison, TNK did not significantly reduce basal lamina damage and caused the highest extravasation. MMP-2/-9 were severely increased after TNK treatment (p<0.05). Thus, the balance between MMPs and TIMPs was shifted toward the inhibitory side with TNK. Microplasmin had a protective effect on the microvascular basal lamina and blood-brain barrier, whereas TNK was significantly disadvantageous from the viewpoint of ischaemic damage. Microplasmin also appears to be safer than other PAs in terms of damage to the microvasculature associated with thrombolytic therapy of ischaemic stroke.

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McKean, T., and W. Mendenhall. "Comparison of the responses to hypoxia, ischaemia and ischaemic preconditioning in wild marmot and laboratory rabbit hearts." Journal of Experimental Biology 199, no. 3 (March 1, 1996): 693–97. http://dx.doi.org/10.1242/jeb.199.3.693.

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Marmots (Marmota flaviventris) are burrowing mammals that may be subjected to low levels of oxygen and high levels of carbon dioxide in their underground environment. Since marmots successfully deal with this physiological challenge, we hypothesized that the isolated perfused marmot heart would be damaged less and recover better from a bout of induced hypoxia or ischaemia than would the heart of a comparison animal, the New Zealand laboratory rabbit (Oryctolagus cuniculus). Isolated marmot and rabbit hearts were made hypoxic by a 30 min perfusion with an oxygen-deficient buffer. The hearts were then perfused with an oxygen-replete buffer and measurements of heart rate, left ventricular pressure and lactate dehydrogenase (LDH) release (an indicator of cell damage) were made over 5 or 10 min intervals for 30 min of hypoxia and 30 min of recovery. There were no species differences in the responses, except that the heart rate in marmots was about 50% of the rate in rabbits during the hypoxia part of the experiment. There was no evidence that the marmot hearts were damaged less or recovered better from hypoxia and reoxgenation than the rabbit hearts. Marmot and rabbit hearts were also subjected to 30 min of total ischaemia; measurements of heart rate, left ventricular pressure and LDH release were obtained during 30 min of reperfusion and compared with the pre-ischaemia values for these variables. There were no significant species differences. When the 30 min ischaemic period was preceded by a 5 min period of ischaemia and a 10 min reperfusion period (preconditioning), the rabbit hearts were protected by this brief ischaemic insult and recovered better than the hearts that had not been subjected to the preconditioning ischaemia. This was not true in the marmot hearts, however, as the preconditioning ischaemia did not promote a greater recovery over that in its absence. When preconditioned marmots hearts were compared with preconditioned rabbit hearts, there were no statistical differences in the responses. The hypothesis that marmot hearts would be damaged less and recover better from hypoxia and ischaemia was not supported by the experimental data.

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Zhang, Ya-Jun, Wen-Jing Guo, Zi-Yuan Tang, Hong-Bin Lin, Pu Hong, Jing-Wei Wang, Xuan-Xuan Huang, Feng-Xian Li, Shi-Yuan Xu, and Hong-Fei Zhang. "Isoflurane Attenuates Cerebral Ischaemia–Reperfusion Injury via the TLR4-NLRP3 Signalling Pathway in Diabetic Mice." Oxidative Medicine and Cellular Longevity 2022 (April 4, 2022): 1–16. http://dx.doi.org/10.1155/2022/2650693.

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Ischaemic stroke is a severe disease worldwide. Restoration of blood flow after ischaemic stroke leads to cerebral ischaemia–reperfusion injury (CIRI). Various operations, such as cardiac surgery with deep hypothermic circulatory arrest, predictably cause cerebral ischaemia. Diabetes is related to the occurrence of perioperative stroke and exacerbates neurological impairment after stroke. Therefore, the choice of anaesthetic drugs has certain clinical significance for patients with diabetes. Isoflurane (ISO) exerts neuroprotective and anti-neuroinflammatory effects in patients without diabetes. However, the role of ISO in cerebral ischaemia in the context of diabetes is still unknown. Toll-like receptor 4 (TLR4) and NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome activation play important roles in microglia-mediated neuroinflammatory injury. In this study, we treated a diabetic middle cerebral artery occlusion mouse model with ISO. We found that diabetes exacerbated cerebral ischaemia damage and that ISO exerted neuroprotective effects in diabetic mice. Then, we found that ISO decreased TLR4-NLRP3 inflammasome activation in microglia and the excessive autophagy induced by CIRI in diabetic mice. The TLR4-specific agonist CRX-527 reversed the neuroprotective effects of ISO. In summary, our study indicated that ISO exerts neuroprotective effects against the neuroinflammation and autophagy observed during diabetic stroke via the TLR4-NLRP3 signalling pathway.

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de Prati, Alessandra, Bruno Podesser, Giuseppe Faggian, Tiziano Scarabelli, Alessandro Mazzucco, Elena Darra, Alessio Rungatscher, Seth Hallström, and Hisanori Suzuki. "Dual modulation of nitric oxide production in the heart during ischaemia/reperfusion injury and inflammation." Thrombosis and Haemostasis 104, no. 08 (2010): 200–206. http://dx.doi.org/10.1160/th09-08-0554.

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SummaryNitric oxide (NO) homeostasis maintained by neuronal/endothelial nitric oxide (NO) synthase (n/eNOS) contributes to regulate cardiac function under physiological conditions. At the early stages of ischaemia, NO homeostasis is disturbed due to Ca2+-dependent e/nNOS activation. In endothelial cells, successive drop in NO concentration may occur due to both uncoupling of eNOS and/or successive inhibition of nNOS catalytic activity mediated by arachidonic acid-induced tyrosine phosphorylation of this enzyme. The reduced NO bioavailability triggers nuclear factor (NF)-κB activation followed by the induction of inducible NOS (iNOS) expression. In cardiomyocytes ischaemia also triggers the induction of iNOS expression during reperfusion. The massive amounts of NO which are subsequently produced following iNOS induction may exert on cardiomyocytes and the other cell types of cells of the heart, such as endothelial and smooth muscle cells, macrophages and neutrophils, opposing effects, either beneficial or toxic. The balance between these two double-faced actions may contribute to the final clinical outcomes, determining the degree of functional adaptation of the heart to ischaemia/reperfusion injury. In the light of this new vision on the critical role played by the cross-talk between n/eNOS and iNOS as well as the non enzymatic NO production by nitrite, we have reason to believe that new pharmacological measurements or experimental interventions, such as ischaemic preconditioning, aimed at counteracting the drop in NO levels beyond the normal range of NO homeostasis during early reperfusion can represent an efficient strategy to reduce the extent of functional impairment and cardiac damage in the heart exposed to ischaemia/reperfusion injury.

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Messent, M., M. J. D. Griffiths, and T. W. Evans. "Pulmonary Vascular Reactivity and Ischaemia-Reperfusion Injury in the Rat." Clinical Science 85, no. 1 (July 1, 1993): 71–75. http://dx.doi.org/10.1042/cs0850071.

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1. The endothelium has been shown to modulate the pulmonary vascular response to hypoxia in the rat. Acute lung injury is associated with loss of hypoxic pulmonary vasoconstriction and increased pulmonary vascular permeability. Similar loss of the vascular response to hypoxia is seen after ischaemia-reperfusion injury of the myocardium. 2. The effects of reperfusion injury on pulmonary endothelial integrity, as shown by the albumin escape index and hypoxic pulmonary vasoconstriction, were investigated in isolated, blood-perfused rat lungs. 3. Ischaemia for 0.5 h, which itself caused no increase in the albumin escape index, was followed by reperfusion for 0.25 h, 0.5 h and 1 h. Controls were subjected to 2 h of perfusion only (n = 5 in all groups). The pulmonary pressor response to hypoxia (fractional inspired oxygen concentration, 3%) was measured before and after ischaemia-reperfusion, and the dilator response to acetylcholine was measured after ischaemia-reperfusion in all cases. 4. Ischaemia-reperfusion significantly increased the albumin escape index after 0.5 h (mean ± SEM, 1.40 ± 0.27) and 1 h (2.0 ± 0.30) compared with controls (0.54 ± 0.30, P <0.05 in both cases). The pulmonary pressor response to hypoxia was augmented significantly after reperfusion when compared with baseline hypoxic pulmonary vasoconstriction (change from baseline: 13.2 ± 4.63 and 22.2 ± 7.1% after 0.5 and 1.0 h of reperfusion, respectively, P <0.05). Vasorelaxation of sustained hypoxic vasoconstriction using acetylcholine was similar in both control lungs and those subjected to ischaemia-reperfusion. 5. These results suggest that the pressor response to hypoxia is augmented after damage to the pulmonary vascular endothelium induced by ischaemia-reperfusion. Although this may be due to diminished release of endothelium-derived relaxing factors, the normal vasodilator response to acetylcholine suggests the phenomenon is not due to a reduction in the release of endothelium-derived relaxing factor/nitric oxide.

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Grages, Anna Marei, Nicole Verhaar, Christiane Pfarrer, Gerhard Breves, Marion Burmester, Stephan Neudeck, and Sabine Kästner. "Low Flow versus No Flow: Ischaemia Reperfusion Injury Following Different Experimental Models in the Equine Small Intestine." Animals 12, no. 16 (August 22, 2022): 2158. http://dx.doi.org/10.3390/ani12162158.

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In experimental studies investigating strangulating intestinal lesions in horses, different ischaemia models have been used with diverging results. Therefore, the aim was to comparatively describe ischaemia reperfusion injury (IRI) in a low flow (LF) and no flow (NF) model. Under general anaesthesia, 120 min of jejunal ischaemia followed by 120 min of reperfusion was induced in 14 warmbloods. During ischaemia, blood flow was reduced by 80% (LF, n = 7) or by 100% (NF, n = 7). Intestinal blood flow and oxygen saturation were measured by Laser Doppler fluxmetry and spectrophotometry. Clinical, histological, immunohistochemical and Ussing chamber analyses were performed on intestinal samples collected hourly. Tissue oxygen saturation was significantly lower in NF ischaemia. The LF group exhibited high variability in oxygen saturation and mucosal damage. Histologically, more haemorrhage was found in the LF group at all time points. Cleaved-caspase-3 and calprotectin-stained cells increased during reperfusion in both groups. After NF ischaemia, the tissue conductance was significantly higher during reperfusion. These results aid in the selection of suitable experimental models for future studies. Although the LF model has been suggested to be more representative for clinical strangulating small intestinal disease, the NF model produced more consistent IRI.

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Pedrini, L., C. Guarnieri, E. Pisano, L. Masetti, I. Vaona, A. Muttini, R. Motta, L. Sardella, A. Saccà, and M. D'Addato. "Prevention of Reperfusion Syndrome in Acute Muscular Ischaemia with Free Radical Scavengers and Membrane-Protecting Compounds: An Experimental Study." Cardiovascular Surgery 1, no. 4 (August 1993): 325–29. http://dx.doi.org/10.1177/096721099300100403.

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The prevention of oxidant-induced damage following reperfusion was experimentally evaluated. Two pharmacological regimens containing different combinations of antioxidant factors and membrane-stabilizing compounds, such as α-tocopherol (vitamin E), methionine, dexamethasone, mannitol and cysteine, were administered. The reduced/oxidized glutathione (GSH/GSSG) ratio in muscle was used to evaluate oxidative stress. Ischaemia was induced by occluding the aorta and the inferior vena cava with an irrigation-occlusion catheter. After 4h of ischaemia, five sheep were reperfused without any treatment (control group) and five treated with an endoaortic bolus administered at declamping (treatment 1). In five other sheep, treatment started during ischaemia (treatment 2). Ischaemia and, in particular, reperfusion significantly reduced the muscle GSH content, compared with the basal value in the control group; thus the GSH/GSSG ratio decreased significantly in the control group from 10.5(2.2) (mean(s.e.) basal value) to 0.687(0.3) at reperfusion ( P<0.009). Both treatments 1 and 2 significantly prevented a reduction in GSH content induced by reperfusion following ischaemia; the GSH/GSSG ratio (10.5(2.2) basal value) increased to 19.67(4.6) with reperfusion in the treatment group 1, mainly because of a lower decrease of GSH and a lower level of GSSG while it did not change in treatment group 2 (10.7(5.0)). Levels of creatine phosphokinase did not change in the treated groups, although they increased significantly in the control group ( P<0.006). Although oxidative stress is not the only cause of damage in revascularization, this study confirms the protective ability of treatment with free radical scavengers and membrane-stabilizing compounds.

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Akdemir, A., O. Erbaş, M. Ergenoğlu, A. Özgür Yeniel, F. Oltulu, A. Yavaşoğlu, and D. Taskiran. "Montelukast prevents ischaemia/reperfusion-induced ovarian damage in rats." European Journal of Obstetrics & Gynecology and Reproductive Biology 173 (February 2014): 71–76. http://dx.doi.org/10.1016/j.ejogrb.2013.11.021.

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Basalay, Maryna V., Sean M. Davidson, and Derek M. Yellon. "Neuroprotection in Rats Following Ischaemia-Reperfusion Injury by GLP-1 Analogues—Liraglutide and Semaglutide." Cardiovascular Drugs and Therapy 33, no. 6 (November 13, 2019): 661–67. http://dx.doi.org/10.1007/s10557-019-06915-8.

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Abstract Purpose A substantial number of ischaemic stroke patients who receive reperfusion therapy in the acute phase do not ever fully recover. This reveals the urgent need to develop new adjunctive neuroprotective treatment strategies alongside reperfusion therapy. Previous experimental studies demonstrated the potential of glucagon-like peptide-1 (GLP-1) to reduce acute ischaemic damage in the brain. Here, we examined the neuroprotective effects of two GLP-1 analogues, liraglutide and semaglutide. Methods A non-diabetic rat model of acute ischaemic stroke involved 90, 120 or 180 min of middle cerebral artery occlusion (MCAO). Liraglutide or semaglutide was administered either i.v. at the onset of reperfusion or s.c. 5 min before the onset of reperfusion. Infarct size and functional status were evaluated after 24 h or 72 h of reperfusion. Results Liraglutide, administered as a bolus at the onset of reperfusion, reduced infarct size by up to 90% and improved neuroscore at 24 h in a dose-dependent manner, following 90-min, but not 120-min or 180-min ischaemia. Semaglutide and liraglutide administered s.c. reduced infarct size by 63% and 48%, respectively, and improved neuroscore at 72 h following 90-min MCAO. Neuroprotection by semaglutide was abolished by GLP1-R antagonist exendin(9-39). Conclusion Infarct-limiting and functional neuroprotective effects of liraglutide are dose-dependent. Neuroprotection by semaglutide is at least as strong as by liraglutide and is mediated by GLP-1Rs.

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SEIFALIAN, Alexander M., Hamid EL-DESOKY, David T. DELPY, and Brian R. DAVIDSON. "Effects of hepatic ischaemia/reperfusion injury in a rabbit model of Indocyanine Green clearance." Clinical Science 102, no. 5 (April 23, 2002): 579–86. http://dx.doi.org/10.1042/cs1020579.

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Hepatic ischaemia/reperfusion (I/R) injury is a major cause of primary non-function of the graft after liver transplantation. The ability to assess the severity of ischaemic injury would be of prognostic value and allow the possibility of therapeutic interventions. Currently there is no reliable clinical method for assessing the severity of hepatic ischaemic injury. The hepatic handling of Indocyanine Green as a technique for monitoring the severity of I/R injury has been investigated in the present study. A rabbit model of lobar ischaemia was used. At laparotomy, left lobe hepatic ischaemia was produced for 30, 45 or 60min, followed by 60min of reperfusion. Liver function tests, bile excretion and flow in the hepatic microcirculation were measured in animals subjected to I/R injury and in controls. Indocyanine Green was given after reperfusion and its concentration was measured directly in the liver using near-infrared spectroscopy. Indocyanine Green hepatic uptake and excretion rates were calculated. I/R injury produced significant increases in hepatic serum enzymes and decreases in bile excretion and hepatic microcirculation in all I/R groups in comparison with controls. There was a significant reduction in Indocyanine Green uptake and excretion in the I/R groups in comparison with controls, which was correlated with the duration of ischaemia. Indocyanine Green uptake was correlated significantly with flow in the hepatic microcirculation, and its excretion was correlated significantly with the severity of liver damage, as reflected by the changes in serum enzymes and bile excretion. In conclusion, I/R injury affects the hepatic handling of Indocyanine Green, and direct quantification of the uptake and excretion of this dye by near-infrared spectroscopy may be used to objectively assess the degree of I/R injury.

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Steffens, Sabine, Fabrizio Montecucco, and François Mach. "The inflammatory response as a target to reduce myocardial ischaemia and reperfusion injury." Thrombosis and Haemostasis 102, no. 08 (2009): 240–47. http://dx.doi.org/10.1160/th08-12-0837.

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SummaryAcute myocardial infarction is the leading cause of morbidity and mortality in the adult population of developed and developing nations. Although the prompt restoration of antegrade blood flow in the infarct-related coronary artery is the mean therapy for improving survival, reperfusion itself may cause damage to ischaemic myocardial tissue. This event is well known as “reperfusion injury”. Crucial mediators for cardiac damage in the reperfusion phases are oxidative stress, inflammation and leukocyte infiltration. Already approved and novel therapies might directly reduce these inflammatory processes. Treatments modulating chemokine secretion and activity should be considered as very promising approaches to reduce myocardial reperfusion injury.

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Tomečková, Vladimíra, Miroslava Štefanišinová, Miroslava Bilecová-Rabajdová, Eliška Kriššáková, Marián Tomečko, Štefan Tóth, Tímea Pekárová, and Mária Mareková. "A novel method for the detection of liver damage using fluorescence of hepatic mitochondria in a rat model following ischaemia/reperfusion injury of the small intestine." Spectroscopy 26, no. 4-5 (2011): 237–43. http://dx.doi.org/10.1155/2011/453795.

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We present a novel method of assessing damage to the liver using fluorescence analysis of hepatic mitochondria following ischaemia/reperfusion of the small intestine in a rat model. This work is of substantial importance in understanding the syndrome of multiorgan failure after ischemia/transplantation of the small intestine. Mitochondria were isolated from six sample groups that had undergone three different experimental treatments: a control group; a treatment with ischaemia followed by reperfusion of the small intestine (IRx); and, a one hour ischaemia followed by reperfusion after transplant of the small intestine (TRx). The IR treatment was further subdivided into three groups: 1, 24 h and 30 days reperfusion – IR1, IR24, IR720, respectively. Concomitantly, the TR treatment was further subdivided: one group underwent a 1 h reperfusion and another group a 6 h reperfusion following ischaemia and transplant – groups TR1and TR6, respectively. Once treatment had been undergone, mitochondria were isolated and all five experimental groups – IR1, IR24, IR720, Tr1, Tr6– and their emission matrices were analysed compared with that of the control group (C). Comparing fluorescence values in zone A of all experimental groups with those of the control group indicated a reduction in aromatic amino acids in the mitochondria of all experimental groups. Comparison of fluorescent zone B of experimental groups with the control group identified a lack of oxygen in samples IR1, IR24, which was indicated though an increase in the fluorescence of the reduced pyridine nucleotide NADH+H+.

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Rocca, M., G. Giavaresi, P. Caliceti, F. M. Veronese, and R. Giardino. "Pathophysiological and histomorphological evaluation of polyacryloylmorpholine vs polyethylene glycol modified superoxide dismutase in a rat model of ischaemia/reperfusion injury." International Journal of Artificial Organs 19, no. 12 (December 1996): 730–34. http://dx.doi.org/10.1177/039139889601901209.

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Twenty Wistar rats were divided into two groups. Both underwent acute ischaemia followed by reperfusion of the left hind limb. The first group was a control group while the second was treated with PAcM-SOD. The survival percentage of the limb after 10 days was 30% for the first group and 70% for the second. Neither linear regression nor correlation were found between groups as far as the survival percentage of the limb after 10 days and reperfusion pmO2 data were concerned. After ten days the histomorphological analysis was significant regarding the fibre diameter and the percentage of central located nuclei in the specimens of PAcM-SOD treated limbs compared to normal limbs, but not when compared to the muscular fibres of the control group. Comparing these results with others obtained with native SOD and monomethoxypoly (ethylene glycol) modified SOD (mPEG-SOD) used in the same experimental model, we can conclude that the clinical and morphological results were better using mPEG-SOD, and that PAcM-SOD does have a protective effect on ischaemic muscle damage, although it is not as effective as mPEG-SOD in preventing ischaemia/reperfusion injury.

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Rodrigo, Ramón, Juan C. Prieto, and Rodrigo Castillo. "Cardioprotection against ischaemia/reperfusion by vitamins C and E plus n−3 fatty acids: molecular mechanisms and potential clinical applications." Clinical Science 124, no. 1 (September 7, 2012): 1–15. http://dx.doi.org/10.1042/cs20110663.

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The role of oxidative stress in ischaemic heart disease has been thoroughly investigated in humans. Increased levels of ROS (reactive oxygen species) and RNS (reactive nitrogen species) have been demonstrated during ischaemia and post-ischaemic reperfusion in humans. Depending on their concentrations, these reactive species can act either as benevolent molecules that promote cell survival (at low-to-moderate concentrations) or can induce irreversible cellular damage and death (at high concentrations). Although high ROS levels can induce NF-κB (nuclear factor κB) activation, inflammation, apoptosis or necrosis, low-to-moderate levels can enhance the antioxidant response, via Nrf2 (nuclear factor-erythroid 2-related factor 2) activation. However, a clear definition of these concentration thresholds remains to be established. Although a number of experimental studies have demonstrated that oxidative stress plays a major role in heart ischaemia/reperfusion pathophysiology, controlled clinical trials have failed to prove the efficacy of antioxidants in acute or long-term treatments of ischaemic heart disease. Oral doses of vitamin C are not sufficient to promote ROS scavenging and only down-regulate their production via NADPH oxidase, a biological effect shared by vitamin E to abrogate oxidative stress. However, infusion of vitamin C at doses high enough to achieve plasma levels of 10 mmol/l should prevent superoxide production and the pathophysiological cascade of deleterious heart effects. In turn, n−3 PUFA (polyunsaturated fatty acid) exposure leads to enhanced activity of antioxidant enzymes. In the present review, we present evidence to support the molecular basis for a novel pharmacological strategy using these antioxidant vitamins plus n−3 PUFAs for cardioprotection in clinical settings, such as post-operative atrial fibrillation, percutaneous coronary intervention following acute myocardial infarction and other events that are associated with ischaemia/reperfusion.

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Patel, Hemanshu, Sidney G. Shaw, Xu Shi-Wen, David Abraham, Daryll M. Baker, and Janice C. S. Tsui. "Toll-Like Receptors in Ischaemia and Its Potential Role in the Pathophysiology of Muscle Damage in Critical Limb Ischaemia." Cardiology Research and Practice 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/121237.

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Toll-like receptors (TLRs) are key receptors of the innate immune system which are expressed on immune and nonimmune cells. They are activated by both pathogen-associated molecular patterns and endogenous ligands. Activation of TLRs culminates in the release of proinflammatory cytokines, chemokines, and apoptosis. Ischaemia and ischaemia/reperfusion (I/R) injury are associated with significant inflammation and tissue damage. There is emerging evidence to suggest that TLRs are involved in mediating ischaemia-induced damage in several organs. Critical limb ischaemia (CLI) is the most severe form of peripheral arterial disease (PAD) and is associated with skeletal muscle damage and tissue loss; however its pathophysiology is poorly understood. This paper will underline the evidence implicating TLRs in the pathophysiology of cerebral, renal, hepatic, myocardial, and skeletal muscle ischaemia and I/R injury and discuss preliminary data that alludes to the potential role of TLRs in the pathophysiology of skeletal muscle damage in CLI.

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Sun, XF, LL Wang, JK Wang, J. Yang, H. Zhao, BY Wu, YF Wang, and L. Wang. "Effects of Simvastatin on Lung Injury Induced by Ischaemia–Reperfusion of the Hind Limbs in Rats." Journal of International Medical Research 35, no. 4 (July 2007): 523–33. http://dx.doi.org/10.1177/147323000703500412.

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We investigated whether simvastatin reduces lung injury caused by ischaemia–reperfusion of the hind limbs in rats. The control group underwent dissection of bilateral femoral arteries; another group (I/R group) underwent ischaemia of bilateral hind limbs for 2 h followed by 3 h reperfusion; and two other groups were pretreated with 5 or 10 mg/kg per day simvastatin for 3 days and then underwent ischaemia–reperfusion. The control and I/R group rats received placebo (water) instead of simvastatin. The lungs of the I/R rats showed marked histopathological changes compared with the other groups. Lung tissue myeloperoxidase, malondialdehyde, neutrophil count and lung injury scores in both simvastatin groups were significantly lower than in the I/R group; 10 mg/kg per day simvastatin significantly reduced lung water content although 5 mg/kg per day did not. Expression of haem oxygenase-1 (HO-1) protein in lung tissue was significantly greater in the simvastatin groups than in the I/R group. Simvastatin protects against lung injury associated with lower extremity ischaemia–reperfusion by reduction of neutrophil aggregation and oxidative damage, and upregulation of HO-1 expression in the injured lung.

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Ischia, Joseph, Damien M. Bolton, and Oneel Patel. "Why is it worth testing the ability of zinc to protect against ischaemia reperfusion injury for human application." Metallomics 11, no. 8 (2019): 1330–43. http://dx.doi.org/10.1039/c9mt00079h.

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Ischaemia (interruption in the blood/oxygen supply) and subsequent damage induced by reperfusion (restoration of blood/oxygen supply) ultimately leads to cell death, tissue injury and permanent organ dysfunction.

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Nakatake, Richi, Mareike Schulz, Christina Kalvelage, Carina Benstoem, and René H. Tolba. "Effects of iNOS in Hepatic Warm Ischaemia and Reperfusion Models in Mice and Rats: A Systematic Review and Meta-Analysis." International Journal of Molecular Sciences 23, no. 19 (October 7, 2022): 11916. http://dx.doi.org/10.3390/ijms231911916.

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Warm ischaemia is usually induced by the Pringle manoeuver (PM) during hepatectomy. Currently, there is no widely accepted standard protocol to minimise ischaemia-related injury, so reducing ischaemia-reperfusion damage is an active area of research. This systematic review and meta-analysis focused on inducible nitric oxide synthase (iNOS) as an early inflammatory response to hepatic ischaemia reperfusion injury (HIRI) in mouse- and rat-liver models. A systematic search of studies was performed within three databases. Studies meeting the inclusion criteria were subjected to qualitative and quantitative synthesis of results. We performed a meta-analysis of studies grouped by different HIRI models and ischaemia times. Additionally, we investigated a possible correlation of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) regulation with iNOS expression. Of 124 included studies, 49 were eligible for the meta-analysis, revealing that iNOS was upregulated in almost all HIRIs. We were able to show an increase of iNOS regardless of ischemia or reperfusion time. Additionally, we found no direct associations of eNOS or NO with iNOS. A sex gap of primarily male experimental animals used was observed, leading to a higher risk of outcomes not being translatable to humans of all sexes.

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Ravingerová, Táňa, Adriana Adameová, Tara Kelly, Efthymia Antonopoulou, Dezider Pancza, Mária Ondrejčáková, Vinoth Kumar Megraj Khandelwal, Slávka Čarnická, and Antigone Lazou. "Changes in PPAR gene expression and myocardial tolerance to ischaemia: relevance to pleiotropic effects of statinsThis article is one of a selection of papers published in a special issue on Advances in Cardiovascular Research." Canadian Journal of Physiology and Pharmacology 87, no. 12 (December 2009): 1028–36. http://dx.doi.org/10.1139/y09-071.

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Peroxisome proliferator-activated receptors (PPAR), which are key transcriptional regulators of lipid metabolism and energy production, have been suggested to play an important role in myocardial ischaemia–reperfusion (I/R) injury. Their role in cardioprotection, however, is not yet fully elucidated. Statins have shown beneficial effects on I/R damage beyond lipid lowering, and some of their cardioprotective cholesterol-independent effects may be related to the regulation of PPAR. To clarify this issue, we explored a potential link between a response to I/R and changes in cardiac PPARα protein and gene expression in simvastatin-treated normocholesterolaemic rats. After 5 days of treatment with simvastatin (10 mg/kg per day, p.o.), Langendorff-perfused hearts were subjected to 30 min regional ischaemia (occlusion of the left anterior descending coronary artery) or global ischaemia and 2 h reperfusion for the evaluation of the infarct size (triphenyltetrazolium chloride and planimetry; as percentage of risk area), ischaemic arrhythmias, and postischaemic contractile recovery. Baseline PPARα mRNA and protein levels were increased by 3-fold and 2-fold, respectively, in simvastatin-treated hearts compared with the untreated controls. Simvastatin-treated hearts exhibited smaller size of infarction (11.5% ± 0.4% vs. 33.7% ± 4% in controls; p < 0.01), improved postischaemic contractile recovery, and lower severity of arrhythmias during ischaemia and early reperfusion. Enhanced resistance to I/R injury was associated with preservation of mRNA and protein levels of PPARα in contrast to their marked downregulation in controls. In conclusion, statin-induced changes in the expression of PPARα may contribute to attenuation of myocardial I/R injury and thus suggest the involvement of cardioprotective mechanisms independent of inhibition of HMG-CoA reductase.

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Ferrari, R., and O. Visioli. "Protective Effects of Calcium Antagonists Against Ischaemia and Reperfusion Damage." Drugs 42, Supplement 1 (1991): 14–27. http://dx.doi.org/10.2165/00003495-199100421-00005.

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Bastounis, E., L. Hadjinikolaou, M. Pikoulis, C. Tsigris, E. Marinos, and P. Toutouzas. "Free radical related myocardial mitochondrial damage following limb ischaemia-reperfusion." Cardiovascular Research 28, no. 12 (December 1, 1994): 1868–71. http://dx.doi.org/10.1093/cvr/28.12.1868.

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Savas, Ç., C. Özogul, E. Karaöz, N. Delibas, and F. Özgüner. "Splenectomy Reduces Remote Organ Damage after Intestinal Ischaemia-Reperfusion Injury." Acta Chirurgica Belgica 103, no. 3 (January 2003): 315–20. http://dx.doi.org/10.1080/00015458.2003.11679431.

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Chaaya, R., C. Alfarano, C. Guilbeau-Frugier, C. Coatrieux, A. S. Kesteman, A. Parini, N. Fares, M. Gue, J. P. Schanstra, and J. L. Bascands. "Pargyline reduces renal damage associated with ischaemia-reperfusion and cyclosporin." Nephrology Dialysis Transplantation 26, no. 2 (July 28, 2010): 489–98. http://dx.doi.org/10.1093/ndt/gfq445.

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Cao, Fang, Sevasti Zervou, and Craig A. Lygate. "The creatine kinase system as a therapeutic target for myocardial ischaemia–reperfusion injury." Biochemical Society Transactions 46, no. 5 (September 21, 2018): 1119–27. http://dx.doi.org/10.1042/bst20170504.

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Restoring blood flow following an acute myocardial infarction saves lives, but results in tissue damage due to ischaemia–reperfusion injury (I/R). Ameliorating this damage is a major research goal to improve recovery and reduce subsequent morbidity due to heart failure. Both the ischaemic and reperfusion phases represent crises of cellular energy provision in which the mitochondria play a central role. This mini-review will explore the rationale and therapeutic potential of augmenting the creatine kinase (CK) energy shuttle, which constitutes the primary short-term energy buffer and transport system in the cardiomyocyte. Proof-of-principle data from several transgenic mouse models have demonstrated robust cardioprotection by either raising myocardial creatine levels or by overexpressing specific CK isoforms. The effect on cardiac function, high-energy phosphates and myocardial injury will be discussed and possible directions for future research highlighted. We conclude that the CK system represents a viable target for therapeutic intervention in I/R injury; however, much needed translational studies will require the development of new pharmacological tools.

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Varga, Ján, Pavel Staško, Štefan Tóth, Zuzana Pristášová, Zuzana Jonecová, Jarmila Veselá, and Mikuláš Pomfy. "Morphological and apoptotic changes in the intestinal mucosa and lung parenchyma after ischaemic/reperfusion injury of the jejunum." Acta Veterinaria Hungarica 58, no. 2 (June 1, 2010): 243–56. http://dx.doi.org/10.1556/avet.58.2010.2.10.

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Ischaemic/reperfusion (IR) injury of the small intestine may lead to the development of multiple organ failure. Little is known about the morphological changes occurring in the organs during the subacute course of this syndrome. The objective of this study was to observe histopathological features and the role of apoptosis in the jejunal mucosa and lung parenchyma after intestinal IR injury in a long-term experiment. Wistar rats (n = 36) were divided into 4 experimental groups (IR 10 , IR 20 , IR 30 , S). Groups IR 10 , IR 20 and IR 30 (each n = 10) were subjected to 1-hour ischaemia of the cranial mesenteric artery followed by 10, 20 or 30 days of reperfusion, respectively. The control group S (n = 6) was not subjected to ischaemia. The jejunal mucosa remained intact after all periods of reperfusion. Apoptotic cells were found particularly in the lamina propria, with the most significant difference observed in the IR 30 group (P < 0.01). The lung parenchyma had lower regenerative capacity, which was confirmed by a high index of histological damage after 30 days of reperfusion (P < 0.01) and by the presence of an increased number of apoptotic cells, especially in the pulmonary interstitium. The number of apoptotic cells was ten times higher than in the control group (P < 0.001).

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Barrett, John A., Claudia K. Derian, Robert S. Swillo, Richard F. Woltmann, and Mark H. Perrone. "The role of the neutrophil and formed elements of the blood in anin vitromodel of reperfusion injury." Mediators of Inflammation 2, no. 1 (1993): 85–92. http://dx.doi.org/10.1155/s0962935193000122.

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Using The globally ischaemic isolated guinea-pig heart we conducted studies to assess the role of activated neutrophils (PMNs) and the role of the endothelium in reperfusion injury. Reperfusion injury was induced by a 20 min period of global ischaemia followed by a 30 min reperfusion with Krebs' buffer supplemented with f-Met–Leu–Phe (fMLP) and heparinized blood. Ischaemia alone or blood alone resulted in a complete recovery in contractile function measured by developed pressure, fMLP (500 μM) and blood, administered to normoxic hearts did not affect contractile function. The combination of 100 μM fMLP and blood beginning at reperfusion and continuing for 30 min decreased the recovery in contractile function (max. 33 ± 6% reovery) while buffer and 100 pM fMLP resulted in a complete recovery in function. In hearts infused with buffer and neutropenic blood incubated with 100 μM fMLP a complete recovery in function was observed. Isolated peritoneal neutrophils, 7–70 × 105PMN/ min, incubated with 100 μM fMLP and Krebs' solution decreased contractile function in a concentration-related manner (max. 44 ± 11% recovery). Platelets, plasma or red blood cells alone incubated with fMLP did not decrease recovery in developed pressure. Platelets and PMN incubated with 100 μM fMLP did not, while red blood cells and PMN did, elicit a reduction in recovery in contractile function (34 ± 4% recovery). A 20 min period of global ischaemia destroys the functional integrity of the endothelium (response to Ach). Pre-treatment of the heart with sufficient H2O2to functionally damage the endothelium, followed by infusion of Krebs' solution supplemented with blood and 100 μM fMLP also elicited a reduction in recovery of contractile function (42 ± 15% recovery). In summary, partially activated neutrophils play a major role in reperfusion injury and there exists a cooperativity between the RBC and PMN in this model.

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Hortmann, Marcus, Samuel Robinson, Moritz Mohr, Maximillian Mauler, Daniela Stallmann, Jochen Reinöhl, Daniel Duerschmied, et al. "The mitochondria-targeting peptide elamipretide diminishes circulating HtrA2 in ST-segment elevation myocardial infarction." European Heart Journal: Acute Cardiovascular Care 8, no. 8 (May 23, 2017): 695–702. http://dx.doi.org/10.1177/2048872617710789.

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Background: The extent of myocardial damage in patients with ST-segment elevation myocardial infarction (STEMI) depends on both the time to reperfusion as well as injury induced by ischaemia–reperfusion resulting in a cascade of cellular and humoral reactions. As a consequence of ischaemia–reperfusion in the heart, the high-temperature requirement serine peptidase 2 (HtrA2) is translocated from the mitochondria to the cytosol, whereupon it induces protease activity-dependent apoptosis mediated via caspases. Myocardial damage induced by reperfusion cannot be monitored due to a current lack in specific biomarkers. We examined the serum level of HtrA2 as a potentially novel biomarker for mitochondrial-induced cardiomyocyte apoptosis. Methods: After informed consent, peripheral blood was obtained from patients ( n=19) with first-time acute anterior STEMI after percutaneous coronary intervention. Within this group, 10 of the patients received the mitochondria-targeting peptide elamipretide (phase 2a clinical study EMBRACE (NCT01572909)). Blood was also obtained from a control group of healthy donors ( n=16). The serum level of HtrA2 was measured by an enzyme-linked immunosorbent assay (ELISA). In a murine model of myocardial ischaemia–reperfusion injury, HtrA2 was determined in plasma by ELISA after left anterior descending artery occlusion. Results: HtrA2 median was significantly increased in patients with STEMI compared to healthy controls 392.4 (240.7–502.8) pg/mL vs. 1805.5 (981.3–2220.1) pg/mL ( P⩽0.05). Elamipretide significantly reduced the HtrA2 median serum level after myocardial infarction 1805.5 (981.3–2220.1) pg/mL vs. 496.5 (379.4–703.8) pg/mL ( P⩽0.05). Left anterior descending artery occlusion in mice significantly increased HtrA2 mean in plasma (117.4 fg/ml±SEM 28.1 vs. 525.2 fg/ml±SEM 96; P⩽0.05). Conclusion: Compared to healthy controls, we found significantly increased serum levels of HtrA2 in patients with STEMI. The result was validated in a murine model of myocardial ischaemia–reperfusion injury. In humans the increased serum level was significantly reduced by the mitochondria-targeting peptide elamipretide. In conclusion, HtrA2 is detectable in serum of patients with STEMI and might present a novel biomarker for mitochondrial-induced cardiomyocyte apoptosis. Consequently, HtrA2 may also show promise as a biomarker for the identification of ischaemia–reperfusion injury. However, this must be validated in a lager clinical trial.

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Murphy, Michael P. "Understanding and preventing mitochondrial oxidative damage." Biochemical Society Transactions 44, no. 5 (October 15, 2016): 1219–26. http://dx.doi.org/10.1042/bst20160108.

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Mitochondrial oxidative damage has long been known to contribute to damage in conditions such as ischaemia–reperfusion (IR) injury in heart attack. Over the past years, we have developed a series of mitochondria-targeted compounds designed to ameliorate or determine how this damage occurs. I will outline some of this work, from MitoQ to the mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing reactive oxygen species (ROS) formation in IR injury with therapeutic implications. In addition, the protection by this compound suggested that ROS production in IR injury was mainly coming from complex I. This led us to investigate the mechanism of the ROS production and using a metabolomic approach, we found that the ROS production in IR injury came from the accumulation of succinate during ischaemia that then drove mitochondrial ROS production by reverse electron transport at complex I during reperfusion. This surprising mechanism led us to develop further new therapeutic approaches to have an impact on the damage that mitochondrial ROS do in pathology and also to explore how mitochondrial ROS can act as redox signals. I will discuss how these approaches have led to a better understanding of mitochondrial oxidative damage in pathology and also to the development of new therapeutic strategies.

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Beyersdorf, F. "The use of controlled reperfusion strategies in cardiac surgery to minimize ischaemia/reperfusion damage." Cardiovascular Research 83, no. 2 (April 7, 2009): 262–68. http://dx.doi.org/10.1093/cvr/cvp110.

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Filippenkov, Ivan B., Vasily V. Stavchansky, Alina E. Denisova, Vadim V. Yuzhakov, Larisa E. Sevan’kaeva, Olga Y. Sudarkina, Veronika G. Dmitrieva, et al. "Novel Insights into the Protective Properties of ACTH(4-7)PGP (Semax) Peptide at the Transcriptome Level Following Cerebral Ischaemia–Reperfusion in Rats." Genes 11, no. 6 (June 22, 2020): 681. http://dx.doi.org/10.3390/genes11060681.

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Cerebral ischaemia is the most common cause of impaired brain function. Biologically active peptides represent potential drugs for reducing the damage that occurs after ischaemia. The synthetic melanocortin derivative, ACTH(4-7)PGP (Semax), has been used successfully in the treatment of patients with severe impairment of cerebral blood circulation. However, its molecular mechanisms of action within the brain are not yet fully understood. Previously, we used the transient middle cerebral artery occlusion (tMCAO) model to study the damaging effects of ischaemia–reperfusion on the brain transcriptome in rats. Here, using RNA-Seq analysis, we investigated the protective properties of the Semax peptide at the transcriptome level under tMCAO conditions. We have identified 394 differentially expressed genes (DEGs) (>1.5-fold change) in the brains of rats at 24 h after tMCAO treated with Semax relative to saline. Following tMCAO, we found that Semax suppressed the expression of genes related to inflammatory processes and activated the expression of genes related to neurotransmission. In contrast, ischaemia–reperfusion alone activated the expression of inflammation-related genes and suppressed the expression of neurotransmission-related genes. Therefore, the neuroprotective action of Semax may be associated with a compensation of mRNA expression patterns that are disrupted during ischaemia–reperfusion conditions.

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Liepinsh, Edgars, Marina Makrecka-Kuka, Kristine Volska, Janis Kuka, Elina Makarova, Unigunde Antone, Eduards Sevostjanovs, et al. "Long-chain acylcarnitines determine ischaemia/reperfusion-induced damage in heart mitochondria." Biochemical Journal 473, no. 9 (April 26, 2016): 1191–202. http://dx.doi.org/10.1042/bcj20160164.

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During ischaemia acylcarnitines accumulate in the heart mitochondria, inhibit oxidative phosphorylation and stimulate reactive oxygen species (ROS) production and therefore are harmful to mitochondria. An increase in the acylcarnitine heart content increases the infarct size (IS) whereas a decrease in the mitochondrial acylcarnitine content reduces the IS.

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Peng, Pai-Huei, Mei-Lan Ko, Chau-Fong Chen, and Shu-Hui Juan. "Haem oxygenase-1 gene transfer protects retinal ganglion cells from ischaemia/reperfusion injury." Clinical Science 115, no. 11 (November 3, 2008): 335–42. http://dx.doi.org/10.1042/cs20070384.

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RGC (retinal ganglion cell) death following ischaemic insult is the major cause of a number of vision-threatening diseases, including glaucoma. The aim of the present study was to evaluate the role of HO-1 (haem oxygenase-1) in the retina against IR (ischaemia/reperfusion) injury. Adenovirus-mediated HO-1 gene transfer (Adv-HO-1) was carried out by injection into the vitreous body to induce HO-1 overexpression. At 3 weeks after transfection, levels of HO-1 expression, as measured by Western blot analysis, immunohistochemical staining and activity assay, were drastically up-regulated. Transient retinal ischaemia was induced by raising the intraocular pressure to 150 mmHg for 60 min. Untreated IR caused a significant decrease in RGC numbers at 3 and 7 days after reperfusion (76.1 and 67.2% of control eyes with sham IR respectively; P<0.001). Eyes pretreated with Adv-HO-1 had less RGC loss on day 3 and 7 following reperfusion compared with control eyes injected with Adv-GFP (adenovirus containing a gene for green fluorescent protein; 94.3 and 88.2% respectively; P=0.007 and 0.001). SnP (tin protoporphyrin), an HO-1 inhibitor, counteracted the effects of Adv-HO-1. In conclusion, these findings provide evidence that augmentation of HO-1 enzyme overexpression by intravitreal injection is able to protect RGCs against IR-induced damage.

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Nalamolu, Koteswara Rao, Bharath Chelluboina, Ian B. Magruder, Diane N. Fru, Adithya Mohandass, Ishwarya Venkatesh, Jeffrey D. Klopfenstein, David M. Pinson, Krishna M. Boini, and Krishna Kumar Veeravalli. "Post-stroke mRNA expression profile of MMPs: effect of genetic deletion of MMP-12." Stroke and Vascular Neurology 3, no. 3 (March 9, 2018): 153–59. http://dx.doi.org/10.1136/svn-2018-000142.

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Background and purposeRecent reports from our laboratory demonstrated the post-ischaemic expression profile of various matrix metalloproteinases (MMPs) in rats and the detrimental role of MMP-12 in post-stroke brain damage. We hypothesise that the post-stroke dysregulation of MMPs is similar across species and that genetic deletion of MMP-12 would not affect the post-stroke expression of other MMPs. We tested our hypothesis by determining the pre-ischaemic and post-ischaemic expression profile of MMPs in wild-type and MMP-12 knockout mice.MethodsFocal cerebral ischaemia was induced in wild-type and MMP-12 knockout mice by middle cerebral artery occlusion procedure by insertion of a monofilament suture. One hour after ischaemia, reperfusion was initiated by removing the monofilament. One day after reperfusion, ischaemic brain tissues from various groups of mice were collected, and total RNA was isolated and subjected to cDNA synthesis followed by PCR analysis.ResultsAlthough the post-stroke expression profile of MMPs in the ischaemic brain of mice is different from rats, there is a clear species similarity in the expression of MMP-12, which was found to be predominantly upregulated in both species. Further, the post-stroke induction or inhibition of various MMPs in MMP-12 knockout mice is different from their respective expression profile in wild-type mice. Moreover, the brain mRNA expression profile of various MMPs in MMP-12 knockout mice under normal conditions is also different to their expression in wild-type mice.ConclusionsIn the ischaemic brain, MMP-12 upregulates several fold higher than any other MMP. Mice derived with the genetic deletion of MMP-12 are constitutive and have altered MMP expression profile both under normal and ischaemic conditions.

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Journal articles on the topic 'Ischaemia and reperfusion damage'

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