scholarly journals Peripheral M-choline-reactive systems in the infarct-limited effect implementation of remote ischemic postconditioning during ischemia-reperfusion of myocardium in experiment

2019 ◽  
Vol 16 (4) ◽  
pp. 424-433 ◽  
Author(s):  
F. I. Vismont ◽  
S. N. Chepelev ◽  
P. F. Jushkevich
Keyword(s):  
Clinical Medicine ◽  
Ischemia Reperfusion ◽  
Reactive Systems ◽  
Myocardial Damage ◽  
Ischemic Postconditioning ◽  
Limited Effect ◽  
Systemic Action ◽  
Remote Ischemic Postconditioning ◽  
Old Rats ◽  
Cardioprotective Effects

The search for new effective methods to prevent or mitigate ischemic myocardial damage and the mechanisms for their realization is an important task of modern experimental and clinical medicine. The aim of the study was to elucidate the significance of peripheral M-choline-reactive systems in the realization of the cardioprotective effects of remote ischemic postconditioning (RIPostC) during ischemia-reperfusion of myocardium in experiment. The study revealed that RIPostC has an infarct-limiting effect during ischemia-reperfusion of myocardium in young and old rats, but under the conditions of systemic action of atropine (2 mg/kg), the infarct-limiting effect of RIPostC remained only in old rats. It seems that the activity of peripheral M-choline-reactive systems is important in the mechanisms of realization of the cardioprotective effects of RIPost in young, but not in old rats.

scholarly journals On the significance of hyperlactatemia in the implementation of the infarct-limiting effect of remote ischemic postconditioning in myocardial ischemia-reperfusion in the experiment

2020 ◽  
Vol 64 (3) ◽  
pp. 332-340
Author(s):  
S. N. Chepelev ◽  
F. I. Vismont ◽  
S. V. Goubkin
Keyword(s):  
Myocardial Ischemia ◽  
Clinical Medicine ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Modern Medicine ◽  
Ischemic Postconditioning ◽  
Social Significance ◽  
Remote Ischemic Postconditioning ◽  
Urgent Task ◽  
Myocardial Ischemia Reperfusion

Modern medicine faces the problem of the growth of cardiovascular pathology. Given the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods to prevent or weaken ischemic myocardial damage and mechanisms for their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to determine the significance of hyperlactatemia in the realization of the infarct-limiting effect of remote ischemic postconditioning (RIPostC) in rat myocardial ischemia-reperfusion in the experiment. The study revealed that after 15-minute RIPostC, which was performed 10 minutes after 30-minute acute myocardial ischemia followed by 120-minute reperfusion, the plasma lactate level in rats increased 1.87 times (87.7 %, p < 0.05) compared with intact animals. It was established that the introduction of L-lactate into the left common jugular vein at a dose of 10 μg/kg, which was carried out 25 minutes after the onset of reperfusion under the conditions of myocardial ischemia (30 minutes) and next reperfusion (120 minutes) and RIPostC (10 minutes after the onset of reperfusion), which was reproduced by ischemia of these limbs, have a heart attack-limiting effect. The increase of the level of blood lactate (hyperlactatemia) after RIPostC in myocardial ischemia-reperfusion is of significance in the implementation of its infarct-limiting effect.

scholarly journals Significance of nitrogen monoxide in the implementation of the infarctlimiting effect of remote ischemic postconditioning in myocardial ischemia-reperfusion in young and old rats

2020 ◽  
Vol 17 (3) ◽  
pp. 353-363
Author(s):  
S. N. Chepelev ◽  
F. I. Vismont
Keyword(s):  
Myocardial Ischemia ◽  
Clinical Medicine ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Social Significance ◽  
Young Rats ◽  
Remote Ischemic Postconditioning ◽  
Old Rats ◽  
Myocardial Ischemia Reperfusion ◽  
Nitric Monoxide

Modern medicine faces the problem of a steady growth of cardiovascular pathology. Given the high medical and social significance of the problem of treating patients with coronary heart disease and acute myocardial infarction, the search for new effective methods to prevent or mitigate ischemic myocardial damage and mechanisms for their implementation is an urgent task of modern experimental and clinical medicine. The aim of the study was to determine the significance of nitric monoxide in realizing the infarction-limiting effect of remote ischemic postconditioning (RIPostC) in myocardial ischemia-reperfusion in young and old rats. The study revealed that RIPostC has a heart attack-limiting effect in myocardial ischemia-reperfusion in both young and old rats; however, under the conditions of the systemic action of the NG-nitro-L-arginine methyl ester inhibitor at a dose of 25 mg/kg (intravenous administration 5 min before the start of reperfusion and 15 min before RIPostC), the effect remains, although not completely, in old rats but not in young rats. Apparently, the NO synthase activity and the blood level of nitric monoxide play a more significant role in the mechanisms of the cardioprotective effects of RIPostC in young rats than in old rats.

scholarly journals Immediate remote ischemic postconditioning after hypoxia ischemia in piglets protects cerebral white matter but not grey matter

2015 ◽  
Vol 36 (8) ◽  
pp. 1396-1411 ◽  
Author(s):  
Mojgan Ezzati ◽  
Alan Bainbridge ◽  
Kevin D Broad ◽  
Go Kawano ◽  
Aaron Oliver-Taylor ◽  
...  
Keyword(s):  
White Matter ◽  
Corpus Callosum ◽  
Grey Matter ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
White Female ◽  
Resonance Spectroscopy ◽  
Periventricular White Matter ◽  
Remote Ischemic Postconditioning ◽  
Hypoxia Ischemia

Remote ischemic postconditioning (RIPostC) is a promising therapeutic intervention whereby brief episodes of ischemia/reperfusion of one organ (limb) mitigate damage in another organ (brain) that has experienced severe hypoxia-ischemia. Our aim was to assess whether RIPostC is protective following cerebral hypoxia-ischemia in a piglet model of neonatal encephalopathy (NE) using magnetic resonance spectroscopy (MRS) biomarkers and immunohistochemistry. After hypoxia-ischemia (HI), 16 Large White female newborn piglets were randomized to: (i) no intervention ( n = 8); (ii) RIPostC – with four, 10-min cycles of bilateral lower limb ischemia/reperfusion immediately after HI ( n = 8). RIPostC reduced the hypoxic-ischemic-induced increase in white matter proton MRS lactate/N acetyl aspartate ( p = 0.005) and increased whole brain phosphorus-31 MRS ATP ( p = 0.039) over the 48 h after HI. Cell death was reduced with RIPostC in the periventricular white matter ( p = 0.03), internal capsule ( p = 0.002) and corpus callosum ( p = 0.021); there was reduced microglial activation in corpus callosum ( p = 0.001) and more surviving oligodendrocytes in corpus callosum ( p = 0.029) and periventricular white matter ( p = 0.001). Changes in gene expression were detected in the white matter at 48 h, including KATP channel and endothelin A receptor. Immediate RIPostC is a potentially safe and promising brain protective therapy for babies with NE with protection in white but not grey matter.

Cardioprotective effects of nitric oxide-aspirin in myocardial ischemia-reperfused rats

2007 ◽  
Vol 293 (3) ◽  
pp. H1545-H1552 ◽  
Author(s):  
Yilong Fu ◽  
Zhongjing Wang ◽  
Woei Lee Chen ◽  
Philip K. Moore ◽  
Yi Zhun Zhu
Keyword(s):  
Nitric Oxide ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Tween 80 ◽  
Vehicle Group ◽  
Lv Function ◽  
Cardioprotective Effects ◽  
Cox 2

In this study, the cardioprotective effects of nitric oxide (NO)-aspirin, the nitroderivative of aspirin, were compared with those of aspirin in an anesthetized rat model of myocardial ischemia-reperfusion. Rats were given aspirin or NO-aspirin orally for 7 consecutive days preceding 25 min of myocardial ischemia followed by 48 h of reperfusion (MI/R). Treatment groups included vehicle (Tween 80), aspirin (30 mg·kg−1·day−1), and NO-aspirin (56 mg·kg−1·day−1). NO-aspirin, compared with aspirin, displayed remarkable cardioprotection in rats subjected to MI/R as determined by the mortality rate and infarct size. Mortality rates for vehicle ( n = 23), aspirin ( n = 22), and NO-aspirin groups ( n = 22) were 34.8, 27.3, and 18.2%, respectively. Infarct size of the vehicle group was 44.5 ± 2.7% of the left ventricle (LV). In contrast, infarct size of the LV decreased in the aspirin- and NO-aspirin-pretreated groups, 36.7 ± 1.8 and 22.9 ± 4.3%, respectively (both P < 0.05 compared with vehicle group; P < 0.05, NO-aspirin vs. aspirin ). Moreover, NO-aspirin also improved ischemiareperfusion-induced myocardial contractile dysfunction on postischemic LV developed pressure. In addition, NO-aspirin downregulated inducible NO synthase (iNOS; 0.37-fold, P < 0.01) and cyclooxygenase-2 (COX-2; 0.61-fold, P < 0.05) gene expression compared with the vehicle group after 48 h of reperfusion. Treatment with NG-nitro-l-arginine methyl ester (l-NAME; 20 mg/kg), a nonselective NOS inhibitor, aggravated myocardial damage in terms of mortality and infarct size but attenuated effects when coadministered with NO-aspirin. l-NAME administration did not alter the increase in iNOS and COX-2 expression but did reverse the NO-aspirin-induced inhibition of expression of the two genes. The beneficial effects of NO-aspirin appeared to be derived largely from the NO moiety, which attenuated myocardial injury to limit infarct size and better recovery of LV function following ischemia and reperfusion.

scholarly journals The influence of old age on cardioprotective efficiency of pharmacological postconditioning using lactic acid in ischemia-reperfusion of the myocardium in experiment

2021 ◽  
Vol 65 (2) ◽  
pp. 207-216
Author(s):  
S. N. Chepelev ◽  
F. I. Vismont ◽  
S. V. Goubkin ◽  
L. N. Maslov
Keyword(s):  
Lactic Acid ◽  
Cardiovascular Diseases ◽  
Old Age ◽  
Cardiac Arrhythmias ◽  
Clinical Medicine ◽  
Ischemia Reperfusion ◽  
Total Duration ◽  
Reperfusion Of The Myocardium ◽  
Old Rats ◽  
Pharmacological Postconditioning

Not only the prevalence, but also the death rate from the coronary heart disease, including myocardial infarction, is higher in older people than among young people. A demographic shift towards an aging population will lead to a further increase in the prevalence of cardiovascular diseases among the elderly population. Therefore, one of the urgent aims of modern experimental and clinical medicine is to develop methods aimed at limiting reversible and irreversible damage to the myocardium, including in elderly patients. There are a lot of the data supporting the cardioprotective efficiency of such phenomena as ischemic and pharmacological pre- and postconditioning that reduce ischemic and reperfusion damage in young hearts. However, the information on the effectiveness of these phenomena in experiments on old animals is very scarce, contradictory, and not fully understood. The aim of the study was to experimentally evaluate the influence of old age on the reproducibility of the cardioprotective efficiency of pharmacological postconditioning using lactic acid in ischemia-reperfusion of the myocardium. In the course of the study, it was found that neutral lactate, after being administered into the blood flow of animals at a dose of 10 mg/kg 25 minutes after the onset of reperfusion, leads to a decrease in the infarct size of the left ventricle of the myocardium in old rats. Pharmacological postconditioning using lactate is not effective in reducing the duration of cardiac arrhythmias in ischemia-reperfusion of the myocardium in old rats; however, there is a tendency to reduce the incidence of reperfusion arrhythmias and the total duration of cardiac arrhythmias. The obtained data suggest that the presence of such a risk factor for cardiovascular diseases as old age is not a criterion to exclude the use of pharmacological postconditioning with lactate as a way to reduce ischemia and reperfusion injury of myocardium.

scholarly journals Pharmacological Inhibition of S-Nitrosoglutathione Reductase Reduces Cardiac Damage Induced by Ischemia–Reperfusion

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 555
Author(s):  
Oscar Arriagada Castillo ◽  
Gustavo Herrera ◽  
Carlos Manriquez ◽  
Andrea F. Rojas ◽  
Daniel R. González
Keyword(s):  
Ventricular Function ◽  
Ischemia Reperfusion ◽  
Myocardial Damage ◽  
Protein S ◽  
Isolated Rat Heart ◽  
Cardioprotective Effect ◽  
Mitochondrial Proteins ◽  
Cardiac Damage ◽  
Pharmacological Inhibition ◽  
Cardioprotective Effects

The cardioprotective effects of nitric oxide (NO) have been described through S-nitrosylation of several important proteins in the mitochondria of the cardiomyocyte. S-nitrosoglutathione reductase (GSNOR) is an enzyme involved in the metabolism of S-nitrosothiols by producing denitrosylation, thus limiting the cardioprotective effect of NO. The effect of GSNOR inhibition on the damage by cardiac ischemia–reperfusion is still unclear. We tested the hypothesis that pharmacological inhibition of GSNOR promotes cardioprotection by increasing the levels of protein S-nitrosylation. In a model of ischemia–reperfusion in isolated rat heart, the effect of a GSNOR inhibitor, 5-chloro-3-(2-[4-ethoxyphenyl) (ethyl) amino]-2-oxoethyl)-1H-indole-2-carboxylic acid (C2), was investigated. Ventricular function and hemodynamics were determined, in addition to tissue damage and S-nitrosylation of mitochondrial proteins. Hearts treated with C2 showed a lower release of myocardial damage marker creatine kinase and a reduction in the infarcted area. It also improved post-ischemia ventricular function compared to controls. These results were associated with increasing protein S-nitrosylation, specifically of the mitochondrial complexes III and V. The pharmacological inhibition of GSNOR showed a concentration-dependent cardioprotective effect, being observed in functional parameters and myocardial damage, which was maximal at 1 µmol/L, associated with increased S-nitrosylation of mitochondrial proteins. These data suggest that GSNOR is an interesting pharmacological target for cardiac reperfusion injury.

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