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 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 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 Remote Ischemic Postconditioning Protects against Myocardial Ischemia-Reperfusion Injury by Inhibition of the RAGE-HMGB1 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xiangming Wang ◽  
Junhong Wang ◽  
Tiantian Tu ◽  
Zakaria Iyan ◽  
Deeraj Mungun ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Control Group ◽  
Mice Model ◽  
Remote Ischemic Postconditioning ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background. The aim of the present study was to observe the effect of RAGE-HMGB1 signal pathway on remote ischemic postconditioning in mice with myocardial ischemia reperfusion injury. Methods. Mice model of MIRI was established and randomly divided into three groups: control group, ischemia reperfusion group, and remote ischemic postconditioning group. Infarction size was detected by Evans blue and TTC staining. Cardiac function was detected by echocardiography measurement. The protein levels of RAGE, HMGB1, P-AKT, and ERK1/2 were detected by Western blot 120 min following reperfusion. Results. RIPostC could decrease the infarct size and increase LVEF and FS compared with I/R group. Two hours after myocardial ischemia reperfusion, the levels of RAGE and HMGB1 were significantly decreased in RIPostC group compared with those in I/R group. The level of p-AKT was significantly higher in the RIPostC group than in the I/R group. LY294002 significantly attenuated RIPostC-increased levels of Akt phosphorylation. Conclusion. RIPostC may inhibit the expression of RAGE and HMGB1 and activate PI3K/Akt signaling pathway to extenuate ischemic reperfusion injury in mice. It could further suppress the oxidative stress, have antiapoptosis effect, and reduce inflammatory reaction, but this effect has certain timeliness.

scholarly journals Ischemic Postconditioning-Mediated DJ-1 Activation Mitigate Intestinal Mucosa Injury Induced by Myocardial Ischemia Reperfusion in Rats Through Keap1/Nrf2 Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Rong Chen ◽  
Wei Li ◽  
Zhen Qiu ◽  
Qin Zhou ◽  
Yuan Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Ischemia Reperfusion ◽  
Intestinal Barrier ◽  
Ischemic Postconditioning ◽  
Nrf2 Pathway ◽  
Myocardial Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal mucosal barrier dysfunction induced by myocardial ischemia reperfusion (IR) injury often leads to adverse cardiovascular outcomes after myocardial infarction. Early detection and prevention of remote intestinal injury following myocardial IR may help to estimate and improve prognosis after acute myocardial infarction (AMI). This study investigated the protective effect of myocardial ischemic postconditioning (IPo) on intestinal barrier injury induced by myocardial IR and the underlying cellular signaling mechanisms with a focus on the DJ-1. Adult SD rats were subjected to unilateral myocardial IR with or without ischemic postconditioning. After 30 min of ischemia and 120 min of reperfusion, heart tissue, intestine, and blood were collected for subsequent examination. The outcome measures were (i) intestinal histopathology, (ii) intestinal barrier function and inflammatory responses, (iii) apoptosis and oxidative stress, and (iv) cellular signaling changes. IPo significantly attenuated intestinal injury induced by myocardial IR. Furthermore, IPo significantly increased DJ-1, nuclear Nrf2, NQO1, and HO-1 expression in the intestine and inhibited IR-induced apoptosis and oxidative stress. The protective effect of IPo was abolished by the knockdown of DJ-1. Conversely, the overexpression of DJ-1 provided a protective effect similar to that of IPo. Our data indicate that IPo protects the intestine against myocardial IR, which is likely mediated by the upregulation of DJ-1/Nrf2 pathway.

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