Thematische Bibliographien / Cardioprotective

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Auswahl der wissenschaftlichen Literatur zum Thema „Cardioprotective“

Autor: Grafiati

Veröffentlicht am 18. Mai 2024

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Zeitschriftenartikel zum Thema "Cardioprotective"

Atwal, Kamail S., und Gary J. Grover. „Treatment of Myocardial Ischemia with ATP-Sensitive Potassium Channel (KATP) Openers“. Current Pharmaceutical Design 2, Nr. 5 (Oktober 1996): 585–95. http://dx.doi.org/10.2174/1381612802666221004183709.

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ATP-sensitive potassium channel (KATP) openers are potent antihypertensive agents due to their peripheral vasodilating properties. Although KATP openers have been shown to be direct cardioprotective agents, they carry a certain degree of liability for their use as cardioprotective agents. Their potent coronary and peripheral vasodilating properties can cause complications such as coronary artery steal and hypotension resulting in underperfusion of the tissue already at risk. Also, cardioprotection is not related to action potential shortening and the development of agents devoid of this activity would be desirable. Recent studies indicate that the beneficial effects of myocardial preconditioning might be mediated via opening of the KATP· Therefore, the opening of KATP might constitute an endogenous protective mechanism used by the heart under ischemic stress. Development of therapeutics to mimic this powerful protective mechanism is an attractive approach for the discovery of myocardial protecting agents. In this review, we describe the progress made towards understanding the cardioprotective properties of KATP openers including the discovery of agents that might offer a higher margin of safety for the treatment of myocardial ischemia with this class of agents. We found distinct structure-activity relationships for the cardioprotective and vasorelaxant potencies of KATP openers. Based on the structure-activity relationship studies, we were able to find cardioprotective KATP openers (BMS- 180448) which, despite being equipotent to the first generation agents (e.g., cromakalim) as cardioprotectants, had lower vasorelaxant potencies. The cardioprotecti ve effects of these selective KA TP openers in animal models of myocardial ischemia-reperfusion are also discussed in this review.

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Gupta, I., A. Goyal, NK Singh, HN Yadav und PL Sharma. „Hemin, a heme oxygenase-1 inducer, restores the attenuated cardioprotective effect of ischemic preconditioning in isolated diabetic rat heart“. Human & Experimental Toxicology 36, Nr. 8 (12.10.2016): 867–75. http://dx.doi.org/10.1177/0960327116673169.

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Background: Attenuated cardioprotective effect of ischemic preconditioning (IPC) by reduced nitric oxide (NO) is a hallmark during diabetes mellitus (DM). Recently, we reported that the formation of caveolin–endothelial nitric oxide synthase (eNOS) complex decreases the release of NO, which is responsible for attenuation of IPC-induced cardioprotection in DM rat heart. Heme oxygenase-1 (HO-1) facilitates release of NO by disrupting caveolin–eNOS complex. The activity of HO-1 is decreased during DM. This study was designed to investigate the role of hemin (HO-1 inducer) in attenuated cardioprotective effect of IPC in isolated diabetic rat heart. Methods: DM was induced in male Wistar rat by single dose of streptozotocin. Cardioprotective effect was assessed in terms of myocardial infarct size and release of lactate dehydrogenase and creatine kinase in coronary effluent. The release of NO was estimated indirectly by measuring the release of nitrite in coronary effluent. Perfusion of sodium nitrite, a precursor of NO, was used as a positive control. Result: IPC-induced cardioprotection and increased release of nitrite were significantly attenuated in a diabetic rat as compared to a normal rat. Pretreatment with hemin and daidzein, a caveolin inhibitor, alone or in combination significantly restored the attenuated cardioprotection and increased the release of nitrite in diabetic rat heart. Zinc protoporphyrin, a HO-1 inhibitor, significantly abolished the observed cardioprotection and decreased the release of nitrite in hemin pretreated DM rat heart. Conclusion: Thus, it is suggested that hemin restores the attenuated cardioprotective effect in diabetic rat heart by increasing the activity of HO-1 and subsequently release of NO.

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Huh, Joon, Garrett J. Gross, Hiroshi Nagase und Bruce T. Liang. „Protection of cardiac myocytes via δ1-opioid receptors, protein kinase C, and mitochondrial KATP channels“. American Journal of Physiology-Heart and Circulatory Physiology 280, Nr. 1 (01.01.2001): H377—H383. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h377.

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The objective of the present study was to investigate the role of δ1-opioid receptors in mediating cardioprotection in isolated chick cardiac myocytes and to investigate whether protein kinase C and mitochondrial ATP-sensitive K+(KATP) channels act downstream of the δ1-opioid receptor in mediating this beneficial effect. A 5-min preexposure to the selective δ1-opioid receptor agonist (−)-TAN-67 (1 μM) resulted in less myocyte injury during the subsequent prolonged ischemia compared with untreated myocytes. 7-Benzylidenenaltrexone, a selective δ1-opioid receptor antagonist, completely blocked the cardioprotective effect of (−)-TAN-67. Naltriben methanesulfonate, a selective δ2-opioid receptor antagonist, had only a slight inhibitory effect on (−)-TAN-67-mediated cardioprotection. Nor-binaltorphimine dihydrochloride, a κ-opioid receptor antagonist, did not affect (−)-TAN-67-mediated cardioprotection. The protein kinase C inhibitor chelerythrine and the KATP channel inhibitors glibenclamide, a nonselective KATP antagonist, and 5-hydroxydecanoic acid, a mitochondrial selective KATPantagonist, reversed the cardioprotective effect of (−)-TAN-67. These results suggest that the δ1-opioid receptor is present on cardiac myocytes and mediates a potent cardioprotective effect via protein kinase C and the mitochondrial KATP channel.

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Gross, Eric R., Jason N. Peart, Anna K. Hsu, John A. Auchampach und Garrett J. Gross. „Extending the cardioprotective window using a novel δ-opioid agonist fentanyl isothiocyanate via the PI3-kinase pathway“. American Journal of Physiology-Heart and Circulatory Physiology 288, Nr. 6 (Juni 2005): H2744—H2749. http://dx.doi.org/10.1152/ajpheart.00918.2004.

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Selective δ-opioid agonists produce delayed cardioprotection that lasts for 24–48 h in rats; however, the maximum length of the cardioprotective window is unclear. In this study, we attempted to prolong the cardioprotective window using a unique δ-opioid agonist, fentanyl isothiocyanate (FIT), which binds irreversibly to the δ-receptor, and determined the role of the phosphatidylinositol 3-kinase (PI3K) pathway as a trigger or end effector of FIT-induced cardioprotection. Initially, male rats were administered FIT (10 μg/kg) 10 min before hearts were subjected to 30 min of ischemia and 2 h of reperfusion followed by infarct size (IS) assessment. Acute FIT administration reduced IS when given before ischemia, 5 min before reperfusion, or 10 s after reperfusion compared with control. IS reduction also occurred following a single dose of FIT at 48, 72, 96, and 120 h after administration vs. control, with the maximum effect observed at 96 h. FIT-induced IS reduction at 96 h was completely abolished when the irreversible PI3K inhibitor wortmannin (15 μg/kg) was given before FIT during the trigger phase; however, the effect was only partially abrogated when wortmannin was given 96 h later. These data suggest that FIT has a prolonged cardioprotective window greater than that of any previously described cardioprotective agent that requires PI3K primarily in the trigger phase but also partially, as a mediator or end effector.

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Schultz, Jo El J., Anna K. Hsu, Hiroshi Nagase und Garrett J. Gross. „TAN-67, a δ1-opioid receptor agonist, reduces infarct size via activation of Gi/oproteins and KATPchannels“. American Journal of Physiology-Heart and Circulatory Physiology 274, Nr. 3 (01.03.1998): H909—H914. http://dx.doi.org/10.1152/ajpheart.1998.274.3.h909.

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We have previously shown that delta (δ)-opioid receptors, most notably δ1, are involved in the cardioprotective effect of ischemic preconditioning (PC) in rats; however, the mechanism by which δ-opioid receptor-induced cardioprotection is mediated remains unknown. Therefore, we hypothesized that several of the known mediators of ischemic PC such as the ATP-sensitive potassium (KATP) channel and Gi/oproteins are involved in the cardioprotective effect produced by δ1-opioid receptor activation. To address these possibilities, anesthetized, open-chest Wistar rats were randomly assigned to five groups. Control animals were subjected to 30 min of coronary artery occlusion and 2 h of reperfusion. To demonstrate that stimulating δ1-opioid receptors produces cardioprotection, TAN-67, a new selective δ1-agonist, was infused for 15 min before the long occlusion and reperfusion periods. In addition, one group received 7-benzylidenenaltrexone (BNTX), a selective δ1-antagonist, before TAN-67. To study the involvement of KATPchannels or Gi/oproteins in δ1-opioid receptor-induced cardioprotection, glibenclamide (Glib), a KATPchannel antagonist, or pertussis toxin (PTX), an inhibitor of Gi/oproteins, was administered before TAN-67. Infarct size (IS) as a percentage of the area at risk (IS/AAR) was determined by tetrazolium stain. TAN-67 significantly reduced IS/AAR as compared with control (56 ± 2 to 27 ± 5%, n = 5, P < 0.05). The cardioprotective effect of TAN-67 was completely abolished by BNTX, Glib, and PTX (51 ± 3, 53 ± 5, and 61 ± 4%, n = 6 for each group, respectively). These results are the first to suggest that stimulating the δ1-opioid receptor elicits a cardioprotective effect that is mediated via Gi/oproteins and KATPchannels in the intact rat heart.

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Intachai, Kannaporn, Siriporn C. Chattipakorn, Nipon Chattipakorn und Krekwit Shinlapawittayatorn. „Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury“. International Journal of Molecular Sciences 19, Nr. 9 (21.08.2018): 2466. http://dx.doi.org/10.3390/ijms19092466.

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Acute myocardial infarction (AMI) is the most common cause of acute myocardial injury and its most clinically significant form. The most effective treatment for AMI is to restore an adequate coronary blood flow to the ischemic myocardium as quickly as possible. However, reperfusion of an ischemic region can induce cardiomyocyte death, a phenomenon termed “myocardial ischemia/reperfusion (I/R) injury”. Disruption of cardiac parasympathetic (vagal) activity is a common hallmark of a variety of cardiovascular diseases including AMI. Experimental studies have shown that increased vagal activity exerts cardioprotective effects against myocardial I/R injury. In addition, acetylcholine (ACh), the principle cardiac vagal neurotransmitter, has been shown to replicate the cardioprotective effects of cardiac ischemic conditioning. Moreover, studies have shown that cardiomyocytes can synthesize and secrete ACh, which gives further evidence concerning the importance of the non-neuronal cholinergic signaling cascades. This suggests that the activation of ACh receptors is involved in cardioprotection against myocardial I/R injury. There are two types of ACh receptors (AChRs), namely muscarinic and nicotinic receptors (mAChRs and nAChRs, respectively). However, the effects of AChRs activation in cardioprotection during myocardial I/R are still not fully understood. In this review, we summarize the evidence suggesting the association between AChRs activation with both electrical and pharmacological interventions and the cardioprotection during myocardial I/R, as well as outline potential mechanisms underlying these cardioprotective effects.

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Pyle, W. Glen, Yi Chen und Polly A. Hofmann. „Cardioprotection through a PKC-dependent decrease in myofilament ATPase“. American Journal of Physiology-Heart and Circulatory Physiology 285, Nr. 3 (September 2003): H1220—H1228. http://dx.doi.org/10.1152/ajpheart.00076.2003.

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Activation of myocardial κ-opioid receptor-protein kinase C (PKC) pathways may improve postischemic contractile function through a myofilament reduction in ATP utilization. To test this, we first examined the effects of PKC inhibitors on κ-opioid receptor-dependent cardioprotection. The κ-opioid receptor agonist U50,488H (U50) increased postischemic left ventricular developed pressure and reduced postischemic end-diastolic pressure compared with controls. PKC inhibitors abolished the cardioprotective effects of U50. To determine whether κ-opioid-PKC-dependent decreases in Ca2+-dependent actomyosin Mg2+-ATPase could account for cardioprotection, we subjected hearts to three separate actomyosin ATPase-lowering protocols. We observed that moderate decreases in myofibrillar ATPase were equally cardioprotective as κ-opioid receptor stimulation. Immunoblot analysis and confocal microscopy revealed a κ-opioid-induced increase in myofilament-associated PKC-ϵ, and myofibrillar Ca2+-independent PKC activity was increased after κ-opioid stimulation. This PKC-myofilament association led to an increase in troponin I and C-protein phosphorylation. Thus we propose PKC-ϵ activation and translocation to the myofilaments causes a decrease in actomyosin ATPase, which contributes to the κ-opioid receptor-dependent cardioprotective mechanism.

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Tonkovic-Capin, Marija, Garrett J. Gross, Zeljko J. Bosnjak, James S. Tweddell, Colleen M. Fitzpatrick und John E. Baker. „Delayed cardioprotection by isoflurane: role of KATP channels“. American Journal of Physiology-Heart and Circulatory Physiology 283, Nr. 1 (01.07.2002): H61—H68. http://dx.doi.org/10.1152/ajpheart.01040.2001.

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Isoflurane mimics the cardioprotective effect of acute ischemic preconditioning with an acute memory phase. We determined whether isoflurane can induce delayed cardioprotection, the involvement of ATP-sensitive potassium (KATP) channels, and cellular location of the channels. Neonatal New Zealand White rabbits at 7–10 days of age ( n = 5–16/group) were exposed to 1% isoflurane-100% oxygen for 2 h. Hearts exposed 2 h to 100% oxygen served as untreated controls. Twenty-four hours later resistance to myocardial ischemia was determined using an isolated perfused heart model. Isoflurane significantly reduced infarct size/area at risk (means ± SD) by 50% (10 ± 5%) versus untreated controls (20 ± 6%). Isoflurane increased recovery of preischemic left ventricular developed pressure by 28% (69 ± 4%) versus untreated controls (54 ± 6%). The mitochondrial KATP channel blocker 5-hydroxydecanoate (5-HD) completely (55 ± 3%) and the sarcolemmal KATPchannel blocker HMR 1098 partially (62 ± 3%) attenuated the cardioprotective effects of isoflurane. The combination of 5-HD and HMR-1098 completely abolished the cardioprotective effect of isoflurane (56 ± 5%). We conclude that both mitochondrial and sarcolemmal KATP channels contribute to isoflurane-induced delayed cardioprotection.

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Zhang, Jimmy, Sergiy M. Nadtochiy, William R. Urciuoli und Paul S. Brookes. „The cardioprotective compound cloxyquin uncouples mitochondria and induces autophagy“. American Journal of Physiology-Heart and Circulatory Physiology 310, Nr. 1 (01.01.2016): H29—H38. http://dx.doi.org/10.1152/ajpheart.00926.2014.

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Mitochondrial quality control mechanisms have been implicated in protection against cardiac ischemia-reperfusion (IR) injury. Previously, cloxyquin (5-chloroquinolin-8-ol) was identified via phenotypic screening as a cardioprotective compound. Herein, cloxyquin was identified as a mitochondrial uncoupler in both isolated heart mitochondria and adult cardiomyocytes. Additionally, cardiomyocytes isolated from transgenic mice expressing green fluorescent protein-tagged microtubule-associated protein light chain 3 showed increased autophagosome formation with cloxyquin treatment. The autophagy inhibitor chloroquine abolished cloxyquin-induced cardioprotection in both cellular and perfused heart (Langendorff) models of IR injury. Finally, in an in vivo murine left anterior descending coronary artery occlusion model of IR injury, cloxyquin significantly reduced infarct size from 31.4 ± 3.4% to 16.1 ± 2.2%. In conclusion, the cardioprotective compound cloxyquin simultaneously uncoupled mitochondria and induced autophagy. Importantly, autophagy appears to be required for cloxyquin-induced cardioprotection.

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Liu, Shu Q., Brandon J. Tefft, Derek T. Roberts, Li-Qun Zhang, Yupeng Ren, Yan Chun Li, Yong Huang, Di Zhang, Harry R. Phillips und Yu H. Wu. „Cardioprotective proteins upregulated in the liver in response to experimental myocardial ischemia“. American Journal of Physiology-Heart and Circulatory Physiology 303, Nr. 12 (15.12.2012): H1446—H1458. http://dx.doi.org/10.1152/ajpheart.00362.2012.

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Myocardial ischemia (MI) activates innate cardioprotective mechanisms, enhancing cardiomyocyte tolerance to ischemia. Here, we report a MI-activated liver-dependent mechanism for myocardial protection. In response to MI in the mouse, hepatocytes exhibited 6- to 19-fold upregulation of genes encoding secretory proteins, including α-1-acid glycoprotein (AGP)2, bone morphogenetic protein-binding endothelial regulator (BMPER), chemokine (C-X-C motif) ligand 13, fibroblast growth factor (FGF)21, neuregulin (NRG)4, proteoglycan 4, and trefoil factor (TFF)3. Five of these proteins, including AGP2, BMPER, FGF21, NRG4, and TFF3, were identified as cardioprotective proteins since administration of each protein significantly reduced the fraction of myocardial infarcts (37 ± 9%, 34 ± 7%, 32 ± 8%, 39 ± 6%, and 31 ± 7%, respectively, vs. 48 ± 7% for PBS at 24 h post-MI). The serum level of the five proteins elevated significantly in association with protein upregulation in hepatocytes post-MI. Suppression of a cardioprotective protein by small interfering (si)RNA-mediated gene silencing resulted in a significant increase in the fraction of myocardial infarcts, and suppression of all five cardioprotective proteins with siRNAs further intensified myocardial infarction. While administration of a single cardioprotective protein mitigated myocardial infarction, administration of all five proteins furthered the beneficial effect, reducing myocardial infarct fractions from PBS control values from 46 ± 6% (5 days), 41 ± 5% (10 days), and 34 ± 4% (30 days) to 35 ± 5%, 28 ± 5%, and 24 ± 4%, respectively. These observations suggest that the liver contributes to cardioprotection in MI by upregulating and releasing protective secretory proteins. These proteins may be used for the development of cardioprotective agents.

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Dissertationen zum Thema "Cardioprotective"

Simpkin, J. C. „Apelin : a cardioprotective adipocytokine“. Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1445937/.

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The epidemic of obesity has led to increased interest in its role in the pathogenesis of cardiometabolic disease. Adipose tissue, formerly regarded as purely an energy storage site, is now regarded as an important endocrine organ. It produces various peptide hormones, including the adipocytokines which are implicated in metabolic control and disease. Whilst some adipocytokines may contribute to the development of cardiovascular disease, others e.g. adiponectin, may protect against it. The recently identified ligand for the G protein coupled receptor APJ, apelin, is a unique vasoactive adipocytokine. Both apelin and APJ mRNA are highly expressed in the cardiovascular system. Apelin has been found to modulate cardiovascular function, fluid homeostasis and inflammation. To date, however, apelin has not been investigated in the context of ischemia-reperfusion and its benefits in this clinical setting are not yet established. APJ/apelin activates the cell survival cascades Akt/PKB and ERK-1/2 which are associated with the pro-survival Reperfusion Injury Salvage Kinase (RISK) pathway. Apelin also promotes mitogenesis, a feature commonly exhibited by cardioprotective agents. We, therefore, hypothesised that apelin may protect the heart via the RISK pathway in an ischemia/reperfusion (MR) model. We investigated if apelin has potential as a cardioprotective agent employing murine models of ischemia-reperfusion injury and rat cardiomyocytes, in which mitochondrial permeability transition pore (mPTP) opening was examined. Apelin- 13 was found to produce a concentration-dependent decrease in infarct size with a maximal effect being observed at 1000nM. The physiologically less active peptide, apelin-36, also reduced infarct size but to lesser extents than seen with the shorter isoform. LY294002 and U0126, inhibitors of the PI3K-Akt, p44/42, abolished the effects of apelin-13. Further evidence for the involvement of these pathways in the cardioprotective actions of apelin was obtained on Western blot analysis. Apelin-13 delayed mPTP opening which was blocked by LY294002 and MEK inhibitor 1, an alternative inhibitor of p44/42. This is the first study to demonstrate that apelin has a direct cardioprotective action involving the PI3K- Akt, and p44/42 signalling pathways.

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Daubney, J. „The cardioprotective mechanisms of dietary flavonoids“. Thesis, Nottingham Trent University, 2015. http://irep.ntu.ac.uk/id/eprint/27927/.

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Mitotic rat embryonic cardiomyoblast-derived H9c2 cells are widely used as a model cardiomyocyte to study the protective mechanisms of dietary flavonoids, but they lack features of fully differentiated cardiomyocytes. Therefore, this present study aimed to investigate the cytoprotective and cytotoxic effects of the dietary flavonoids quercetin, kaempferol, myricetin and two major quercetin metabolites, quercetin-3-glucoronide and 3’-O-methylquercetin, on fully differentiated H9c2 cells for the first time. The cardiomyocyte-like phenotype of the differentiated H9c2 cells was confirmed by monitoring the expression of cardiac specific troponin T, as well as through the identification of other cardiac specific cytoskeletal markers using MALDI-TOF MS/MS. The cytoprotective effect of quercetin, kaempferol, myricetin, quercetin-3-glucoronide and 3’-O-methylquercetin against hypoxia and H2O2-induced cell death was assessed by monitoring MTT reduction and LDH release. Furthermore the effect of quercetin pre-treatment on ERK1/2, PKB, JNK and p38 MAPK phosphorylation was monitored using western blotting. It was shown that quercetin was the most potent flavonoid at inducing a protective effect, and 3’-O-methylquercetin the most potent metabolite. Using western blotting it was shown that this protective effect is most likely due to quercetin-mediated inhibition of ERK1/2, PKB, JNK and p38 MAPK. Specific inhibitors of these protein kinases did not modulate the observed cytoprotective effect, or cause significant protection alone. The cytotoxic effects of dietary flavonoids, particularly quercetin, was monitored with MTT reduction, LDH release, western blotting to monitor phosphorylation of ERK1/2, PKB, JNK and p38 MAPK and activation of caspase-3, and monitoring intracellular ROS generation with DCFDA assay. The cytotoxic effect of quercetin was shown to be linked to intracellular ROS generation, caspase-3 activation and phosphorylation of ERK1/2, PKB, JNK and p38 MAPK. MALDI-TOF MS for the first time identified several proteins associated with the flavonoid-mediated cytoprotective effect and flavonoid pre-treatment in differentiated H9c2 cells. Most were shown to be linked to the regulation of MAPK and PI3K cell signalling pathways. This present study for the first time demonstrates the cytoprotective and cytotoxic effects of flavonoids on differentiated H9c2 cells, and has identified novel proteins associated with the cytoprotective effect.

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Muraski, John A. „The cardioprotective effects of Pim-1 kinase“. Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3310011.

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Thesis (Ph. D.)--University of California, San Diego and San Diego State University, 2007.
Title from first page of PDF file (viewed September 4, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (p. 90-103).

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Hassan, Lobna Mohammed Saber Abdel. „Intracellular mechanisms of action of cardioprotective agents“. Thesis, University of Sunderland, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338350.

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McCafferty, Kieran. „Novel cardioprotective strategies for the uraemic heart“. Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8725.

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Cardiovascular disease is the leading cause of death in patients with underlying chronic kidney disease (CKD). Up to one third of patients presenting with an acute coronary syndrome have CKD stage 3-5. Outcomes following acute myocardial infarction in patients with underlying CKD remain poor. CKD patients are routinely excluded from clinical trials in novel cardioprotective strategies resulting in a paucity of prospective data on which to base guidelines for clinical practice. The aims of this work were to: • Establish and characterise two models of chronic uraemia in rodents: the subtotal nephrectomy model and the adenine diet model. • Determine the effects of underlying chronic uraemia on myocardial ischaemia tolerance. • Examine pharmacological cardioprotective strategies in the context of underlying uraemia using a PARP inhibitor • Investigate the cardioprotective effects of ischaemic conditioning in the context of uraemia. Ischaemic preconditioning and postconditioning protocols were used in both uraemic and non-uraemic animals in a model of acute myocardial infarction. • Preliminary work, using standard molecular biological techniques, was carried out in order to confirm the putative survival pathways responsible for the effect of preconditioning. • Investigate the effect of combining early and late remote ischaemic preconditioning to identify whether summation of these strategies could provide additional tissue protection in a model of acute kidney injury. The results demonstrate that both models develop a uraemic phenotype. Subtotal nephrectomy animals exhibit reduced ischaemia tolerance. PARP inhibition as a pharmacological post conditioning agent was shown to be ineffective at conferring tissue protection, whereas both ischaemic preconditioning and postconditioning were effective cytoprotective strategies in both non-uraemic and uraemic animals. Furthermore, additional benefit was seen when early and late remote preconditioning were summated in a rodent model of acute kidney injury. This work provides a basis for future clinical trials in cardioprotection in the context of underlying CKD.

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Poolman, Toryn. „Investigations into the cardioprotective properties of resveratrol“. Thesis, University of Leicester, 2004. http://hdl.handle.net/2381/29695.

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In this study the ability of resveratrol to inhibit the activation of the monocyte respiratory burst was investigated.;Differentiated U937 (dU937) cells were pre-treated with resveratrol before stimulation with f-met-leu-phe (fMLP), phorbol 12-myristate-13-acetate (PMA) or arachidonic acid (AA). The extra-cellular and total production of reactive oxygen species (ROS) were measured by isoluminol and luminol chemiluminescence (CL). Superoxide production was measured using lucigenin. Resveratrol was found to inhibit ROS production induced by all three stimuli. Measurement of ROS production was also confirmed using with two used, 2',7'-dichlorofluorescein (DCF) and dihydrorhodamine (DHR). Again resveratrol inhibited both responses. There were significant between the inhibitory effects of resveratrol on peroxidase-dependent (isoluminol, luminol, DCF and DHR) and independent (lucigenin- ROS measuring principles. Moreover, resveratrol was found to be oxidised by the horseradish peroxidase/hydrogen peroxide system.;The cell signal transduction pathways activated by fMLP, PMA and AA were investigated. Only fMLP was found to activate phosphatidylinositol-3-kinase (PI3K) and Akt, using specific inhibitors of both kinases. Resveratrol inhibited PI3K activity with little direct effect on other kinases shown to regulate the respiratory burst, including Akt, extra-cellular regulated protein kinase (ERK); and protein kinase C (PKC). Akt and ERK were found to be activated by fMLP.;In conclusion, resveratrol was found to be a potent inhibitor of ROS production, particularly if a peroxidase-dependent measuring principle was used. Resveratrol can be oxidised by peroxidases, which inhibit the oxidation of the redox probe. Use of a detection method that did not require peroxidase revealed that resveratrol was still a potent inhibitor of fMLP-induced ROS. Moreover, this inhibitory dose of resveratrol correlated with its ability to inhibit the PI3K-Akt pathway, one of the major regulatory pathways of fMLP-induced ROS production. Modulation of these cell signalling intermediates by resveratrol might represent an important anti-inflammatory pathway and further add to its potential cardioprotective properties.

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Wright, Denis Matthew John, und mikewood@deakin edu au. „Potential antiarrhythmic and cardioprotective agents based on adenosine“. Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20050915.160941.

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N-Ethylcarboxamidoadenosine (12) was synthesised from adenosine (1) and the 6-chloro-2,3-O-isopropylidene-AT-ethylcarboxamidoadenosine (25) was synthesised from inosine (19). Employing molecular modelling techniques and the results from previous structure activity relationships it was possible to design and synthesise a N6-substituted N-ethylcarboxamidoadenosines which possessed an oxygen in the N6-substituent either in the form of an epoxide (which was obtained by cpoxidising an alkene with m-CPBA or dimethyldioxirane) or in the form of a cyclic ether as was the case for N6-((tetrahydro-2H--pyran--2-yl)methyl-N-ethylcarboxamidoadenosine (78). These compounds were tested for their biological activity at the A1 adenosine receptor by their ability to inhibit cAMP accumulation in DDT, MF2 cells. The EC50 values obtained indicated that the N6-(norborn-5-en-2-yl)-N-ethylcarboxamidoadenosines were the most potent. Of theseN6-(S-endo-norbrn-5-en-2-yI)-N-ethylcarboxaniidoadenosine (56) was the most potent (0.2 nM). N6-(exo-norborn-5-en-2-yl)-2-iodo-N-ethylcarboxamidoadenosine (79) was synthesised from guanosine (22) and was also evaluated for its potency at the A, receptor (24.8 ± 1.5 nM). At present 79 is being evaluated for its selectivity for the A1 receptor compared to the other three receptor subtypes (A2a, A2b, A3). A series of N6-(benzyl)-N-ethylcarboxamidoadenosines were synthesised with substitutions at the 4-position of the phenyl ring. Another series of compounds were synthesised which replaced the methylene spacer between the N6H and the N6-aromatic or lipophilic substituent The replacement groups -were carbonyl and trans-2- cyclopropyl moieties. The N6-acyl compounds were obtained by reacting 2,3-O- di(tert-butyldimethylsilyl)-AT-ethylcarboxamidoadenosinc (59) with the appropriate acid chloride and then deprotecting with lelrabutylammonium fluoride in tetrahydrofuran. The compound N6-(4-(1,2-dihydroxy)ethyl)benzyl-N- ethylcarboxamidoadenosine (125) was synthesised by the reaction of 4-(1,2-0- isopropylidene-ethyl)benzyl aminc (123) with 6-chloro-2,3-0-isopropylidene-N- ethylcarboxamidoadenosine (25). Compound 123 was synthesised from an epoxidation of vinylbenzyl phthalimide (118) followed by an acidic ring opening to yield the diol which was isopropylidenated to yield 4-(l,2-O-isopropylidene- elhyl)benzyl phlhalimide (122), It was hoped that the presence of the diol functionality in 125 would increase water solubility whilst maintaining potency at the A3 receptor.

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Sopizhenko, Nadia. „Properties of cardioprotective preparations and their antistress effect“. Thesis, Київський національний університет технологій та дизайну, 2019. https://er.knutd.edu.ua/handle/123456789/13167.

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Barbalace, Maria Cristina <1988&gt. „17β-estradiol modulates cardioprotective effects of nutraceutical compounds“. Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2018. http://amsdottorato.unibo.it/8526/1/Barbalace_Maria_Cristina_tesi.pdf.

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Cardiovascular disease rarely manifests in pre-menopausal women meanwhile, the incidence of these pathologies dramatically increases after the menopause suggesting the possibility that sex hormones could have a key role. 17β-estradiol is the main female circulating hormone in the premenopausal period and showed protective effects on the cardiovascular system. Moreover, recent evidences underlie the importance to take into account the gender in clinical studies as it can influence the response to cardiovascular medications. Therefore, we hypothesize that sex hormones can also influence the cardioprotective effects of nutraceutical compounds, such as sulforaphane, isothiocyanate present in Brassica vegetables. This study was designed to investigate the protective effects of sulforaphane in presence of 17β-estradiol against H2O2-induced oxidative damage in cardiomyocytes. 17β-estradiol enhanced sulforaphane cardioprotection against H2O2-induced cell death with respect to 17β-estradiol or sulforaphane alone, as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyl-tetrazolium bromide and lactate dehydrogenase assays. Moreover, 17β-estradiol boosted sulforaphane antioxidant activity, reducing intracellular reactive oxygen species and 8-hydroxy-2′-deoxyguanosine levels and increasing the expression of phase II enzymes. The observed effects seem to be not mediated by estrogen receptor α and β, as we used specific antagonists. Otherwise, ERK1/2 and Akt signaling pathways seem to be involved, as the treatment with specific inhibitors reduced the protective effect of sulforaphane/17β-estradiol co-treatment. Furthermore, estrogen receptor β and G protein-coupled receptor 30 seem to contribute to Akt activation, as using receptor specific agonists sulforaphane-induced Akt phosphorylation was enhanced. The activation of Akt kinase is also involved in the activation of Nrf2 transcription factor elicited by sulforaphane/17β-estradiol co-treatment, as treated cells with Akt-inhibitor, the co-treatment-induced Nrf2 activation was prevented. Our results demonstrated, for the first time, that estrogen could enhance sulforaphane protective effects, suggesting that nutraceutical efficacy might be modulated by sex hormones.

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Maarman, Gerald Jerome. „Melatonin as a novel cardioprotective therapy in pulmonary hypertension“. Doctoral thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/12872.

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Includes bibliographical references.
Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure which leads to right ventricular hypertrophy and failure. The mechanism involved in the pathophysiology of the disease remains unclear but it is suggested that oxidative stress may trigger cardiovascular dysfunction associated with the disease. To date, there is no efficient therapy against PH and novel therapies are urgently needed. Melatonin is a powerful antioxidant that can confer benefit against ischemia-reperfusion injury and hypertension. We therefore hypothesised that melatonin may confer cardiovascular benefits against PH. Methods: Oxidative stress (plasma lipid peroxidation, antioxidant capacity and antioxidant enzyme activity) was assessed in healthy (n=10), in patients with PH (n=10), in Long Evans rats (n≥6) or in a rat model of PH induced 28 days after the injection of monocrotaline (MCT, 80mg/kg, subcutaneous) (n≥6). Melatonin (75ng/L, nutritional concentration), 4mg/kg or 6mg/kg (therapeutic dose) was given daily in the drinking water of rats, with the treatment started 5 days before the injection of MCT, on the day of the injection or 14 days after the injection of MCT. The development of PH was measured by assessing right ventricular hypertrophy, cardiac fibrosis, oxidative stress and cardiac function (via echocardiography and the isolated heart Langendorff perfusion model). Results: Plasma oxidative stress was increased in both patients and rats with PH compared with their respective controls. A chronic treatment with melatonin (75ng/L, 4mg/kg or 6mg/kg) starting on the day of the injection with MCT in rats with PH reduced right ventricular hypertrophy, cardiac dysfunction and plasma oxidative stress compared with control rats. Furthermore, the beneficial effect of melatonin (6mg/kg) could be observed when given as a preventive (5 days prior to the injection of MCT) or as a curative therapy (14 days after the injection of MCT). Conclusions: Our data demonstrate that chronic treatment of melatonin confers cardioprotection in a rat model of PH. As melatonin is inexpensive, safe (no reported side effects) and already available over the counter in many countries, we propose that melatonin should be considered as a novel preventive/curative therapy to limit cardiac dysfunction in patients with PH.

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Bücher zum Thema "Cardioprotective"

Kendall, Martin J. Preventing coronary artery disease: Cardioprotective therapeutics in practice. 2. Aufl. London: Martin Dunitz, 1998.

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M, Beale C., Hrsg. The cardioprotective role of HRT: A clinical update. New York: Parthenon Pub. Group, 1996.

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(Germany)), Freiburg Focus on Biomeasurement (9th 1995 Freiburg im Breisgau. Pharmacological evaluation of cardioprotective substances: Experimental induction and indicators of myocardial injury and myocardial protection. Buchenbach, Germany: Gesellschaft für Erfahrungstransfer in der Biomesstechnik e.V., 1996.

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Cardioprotection. Oxford: Oxford University Press, 2009.

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International Symposium, Calcium Antagonists in Cardiovascular Care (1991 : Basle, Switzerland), Hrsg. Verapamil-- a cardioprotective strategy: Highlights from a satellite symposium to the International Symposium, Calcium Antagonists in Cardiovascular Care, Basle, Switzerland, Feb. 13, 1991. New York, NY: Raven Health Care Communications, 1991.

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Minatoguchi, Shinya. Cardioprotection Against Acute Myocardial Infarction. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-15-0167-8.

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Baxter, G. F., und D. M. Yellon, Hrsg. Delayed Preconditioning and Adaptive Cardioprotection. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-5312-6.

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F, Baxter G., und Yellon Derek M, Hrsg. Delayed preconditioning and adaptive cardioprotection. Dordrecht: Kluwer Academic Publishers, 1998.

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Mentzer, Robert M., Masafumi Kitakaze, James M. Downey und Masatsugu Hori, Hrsg. Adenosine, Cardioprotection and Its Clinical Application. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4419-8736-5.

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M, Mentzer Robert, Hrsg. Adenosine, cardioprotection, and its clinical application. Boston: Kluwer Academic Publishers, 1997.

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Buchteile zum Thema "Cardioprotective"

Prasad, Abhiram, und Bernard John Gersh. „Endogenous Cardioprotective Strategies“. In Management of Myocardial Reperfusion Injury, 239–60. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9_11.

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Parratt, J. R. „Cardioprotective Effects of Iloprost“. In Prostacyclin and Its Stable Analogue Iloprost, 301–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71499-3_33.

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McDonald, Fiona M. „Cardioprotective Effects of Prostacyclin Analogues“. In Prostanoids and Drugs, 71–81. New York, NY: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-7938-6_10.

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Hershko, Chaim, Gabriela Link und Abraham M. Konijn. „Cardioprotective Effect of Iron Chelators“. In Iron Chelation Therapy, 77–89. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0593-8_5.

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Mewton, Nathan, François Roubille, Olivier Lairez, Gilles Rioufol, Meyer Elbaz, Christophe Piot und Michel Ovize. „Translating Cardioprotective Strategies into Clinical Settings“. In Management of Myocardial Reperfusion Injury, 87–99. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9_5.

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Khan, Aisha Saleem. „Trees with Hepatoprotective and Cardioprotective Activities“. In Medicinally Important Trees, 133–57. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56777-8_6.

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De Hert, Stefan. „Perioperative Cardioprotective Strategies in Noncardiac Surgery“. In Total Intravenous Anesthesia and Target Controlled Infusions, 749–61. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47609-4_41.

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Alissa, Eman M., und Gordon A. Ferns. „Potential Cardioprotective Effects of Functional Foods“. In Functional Foods and Dietary Supplements, 463–87. Chichester, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118227800.ch17.

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Al-Harrasi, Ahmed, Saurabh Bhatia, Tapan Behl und Deepak Kaushik. „The Cardioprotective Effects of Essential Oils“. In Role of Essential Oils in the Management of COVID-19, 329–58. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003175933-23.

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Lim, Vuanghao, Jun Jie Tan und Yoke Keong Yong. „Kalmegh (Andrographis paniculata) and Cardioprotective Mechanisms“. In Ancient and Traditional Foods, Plants, Herbs and Spices used in Cardiovascular Health and Disease, 193–213. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003220329-15.

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Konferenzberichte zum Thema "Cardioprotective"

Machado, Fernanda, Irene Gómez-Domínguez, Raul Hurtado-Ribeira, Diana Martin, Manuel A. Coimbra, María Dolores del Castillo und Filipe Coreta-Gomes. „Colonic Fermentation of Coffee Melanoidins and Resulting Cardioprotective Metabolites“. In ICC 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/icc2023-14836.

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Нгуен, Т. Х. В., Л. Ю. Лагуткина und А. А. Хамад. „USE OF PLANT-DERIVED CARDIOPROTECTIVE COMPONENTS IN COMPOUND FEED FOR STURGEON FISH“. In DEVELOPMENT AND MODERN PROBLEMS OF AQUACULTURE. ООО "ДГТУ-Принт" Адресс полиграфического предприятия 344003 пл Гагарина, зд. 1, 2023. http://dx.doi.org/10.23947/aquaculture.2023.86-89.

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The article presents the results of an experimental study on the use of cardioprotective components in compound feed for yearling sterlet (Acipenser ruthenus). It was found that feeding fish with a diet containing 3% common barberry increased the absolute and average daily weight gain of the fish. The cardiosomatic index in fish also significantly decreased.

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Petrović, Anica, Jovana Bradić, Marijana Andjić, Aleksandar Kočović, Jovana Novaković und Vladimir Jakovljević. „CARDIOPROTECTIVE EFFECTS OF LADY’S BEDSTRAW EXTRACT: FOCUS ON OXIDATIVE STRESS“. In 2nd International Symposium on Biotechnology. Faculty of Agronomy in Čačak, University of Kragujevac, 2024. http://dx.doi.org/10.46793/sbt29.75ap.

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Beside the widespread traditional use of Lady’s Bedstraw in the treatment of numerous diseases and conditions, itʼs effects on heart function and redox status has still not been fully clarified. The aim of our study was to examine the effects of methanol extract of Lady’s Bedstraw on oxidative stress parameters during on ischemia-reperfusion (I/R) injury in isolated rat heart. Our results demonstrated that treatment with methanol extract of Lady’s Bedstraw preserved diminished production of many prooxidants. Promising potential of Lady’s Bedstraw in the present study in a model of pharmacological preconditioning may be a starting point for future researches.

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Kammerer, Susanne. „No cardioprotective effect of ACE inhibitors in patients with cancer“. In ACC 2024 Scientific Session, herausgegeben von Marc Bonaca. Baarn, the Netherlands: Medicom Medical Publishers, 2024. http://dx.doi.org/10.55788/74e63393.

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Tabima Martinez, Diana Marcela, Victor Bilan, Stevan P. Tofovic und Mark T. Gladwin. „Is Nitrite Cardioprotective In An Obese And Pulmonary Hypertensive Rat Model?“ In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4768.

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Kisel, J., E. Ballard, S. Eui-Sik, N. Hart, S. Srivastava, P. Murphy, P. Marino, S. Kapetanakis und J. Steier. „Cardioprotective medication in Duchenne muscular dystrophy: a single-centre cohort study“. In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.455.

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Ojha, S., S. Azimullah, H. Al Taee und MFN Meeran. „Cardioprotective effect of (-)-α-Bisabolol in animal model of myocardial infarction“. In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608133.

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Ahmad, Taseer, ‪Taous‬ Khan, Abdul Shah, Tahira Tabassum, Sultan Almedhesh, Hamdan Al shehri Al, Alasmary Yahia, Mater Mahnashi und Mohammed Alqahtani. „Cardioprotective effect of juglone on isoproterenol-induced myocardial injury in SD rats“. In The 1st International E-Conference on Antioxidants in Health and Disease. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/cahd2020-08916.

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Kisel, J., E. Ballard, E. Suh, N. Hart, S. Kapetanakis, S. Srivastava, P. Marino, P. Murphy und J. Steier. „S124 Cardioprotective medication in Duchenne muscular dystrophy: a single-centre cohort study“. In British Thoracic Society Winter Meeting 2022, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 23 to 25 November 2022, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2022. http://dx.doi.org/10.1136/thorax-2022-btsabstracts.130.

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Xuan, Yuan, Fu Wei, Qiusheng Zheng, Ju Bao, Xu Bo und Qiusheng Zheng. „Antioxidative and cardioprotective activities of total flavonoids from Moldavian balm (Dracocephalum moldavica L.)“. In 2010 International Conference on Bioinformatics and Biomedical Technology (ICBBT 2010). IEEE, 2010. http://dx.doi.org/10.1109/icbbt.2010.5478987.

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Berichte der Organisationen zum Thema "Cardioprotective"

Garlid, Anders. Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling? Portland State University Library, Januar 2000. http://dx.doi.org/10.15760/etd.1640.

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Herzinger, Thomas. Effects of the Cardioprotective Drugs Dexrazoxane and ADR-925 on Doxorubicin Induced Ca2+ Release from the Sarcoplasmic Reticulum. Portland State University Library, Januar 2000. http://dx.doi.org/10.15760/etd.6945.

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Li, Peng, und Junjun Liu. Effect of tumor necrosis factor inhibitors on the risk of adverse cardiovascular events in patients with psoriasis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2022. http://dx.doi.org/10.37766/inplasy2022.8.0090.

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Review question / Objective: Previous studies have indicated a cardioprotective effect of tumor necrosis factor inhibitor (TNFi) therapy in adult patients with psoriasis (Pso). However, most were retrospective studies, and the association between cardiometabolic comorbidities and major adverse cardiovascular events (MACE) has not been validated in randomized controlled trials (RCTs). Condition being studied: Because the available evidence has recently increased, we performed the present updated meta-analysis and meta-regression of cohort studies and RCTs to evaluate whether TNFi therapy can decrease the risk of MACE among patients with Pso and to assess the associations between cardiometabolic comorbidities and MACE.

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Takeda, Mamoru. Neurophysiological Mechanisms Underlying the Attenuation of Nociceptive and Pathological Pain by Phytochemicals: Clinical Application as Therapeutic Agents. Progress in Neurobiology, April 2024. http://dx.doi.org/10.60124/j.pneuro.2024.10.02.

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Although phytochemicals are plant-derived toxins that are primarily produced by plants as a form of defense against insects or microbes, several lines of studies have demonstrated that phytochemicals (e.g., polyphenols, carotenoids, and amino acids) have several beneficial biological actions for human health, such as anti-oxidative, anti-inflammatory, and cardioprotective effects. Recent studies have demonstrated that phytochemicals can modulate neuronal excitability in the nervous system, including nociceptive sensory transmission, so it is possible that phytochemicals could be complementary alternative medicine candidates; specifically, therapeutic agents against pain. The focus of this review is to elucidate the mechanisms underlying the modulatory effects of phytochemicals on neuronal electrical signals, such as generator potentials, action potentials, and postsynaptic potentials, in the nociceptive pathway neurons resulting in potential local anesthetic effects, intravenous anesthesia and analgesic effects, and inflammatory pain relief effects. In addition, we discuss the contribution of phytochemicals to the relief of nociceptive and/or pathological pain and their potential clinical application on the basis of our recent studies in vivo.

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