Key result
L-lactate postconditioning reduces myocardial infarct size by ~26% in both young and aged models.
Why the study?
The cardioprotective efficacy of L-lactate postconditioning during myocardial ischemia-reperfusion in young and old rats, along with the roles of NO-synthase and M-cholinergic reactive system activity in its implementation, required investigation.
Does postconditioning with L-lactate reduce the size of the myocardial necrotic zone during ischemia-reperfusion in young and old rats, and what is the role of NO-synthase and M-cholinergic systems in mediating this effect?
Does postconditioning with L-lactate reduce the size of the myocardial necrotic zone during ischemia-reperfusion in young and old rats, and what is the role of NO-synthase and M-cholinergic systems in mediating this effect?
Pharmacological postconditioning with L-lactate significantly limits myocardial infarct size in both young and old rats during ischemia-reperfusion, though its mechanism depends on NO-synthase and M-cholinergic system activity only in young animals.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for L-lactate postconditioning in ischemia-reperfusion; leaves open clinical translation and age-specific mechanisms.
Purpose – to study the cardioprotective efficacy of postconditioning with L-lactate (PostL) during myocardial ischemia-reperfusion in young and old rats and to elucidate the role of NOsynthase (NOS) and M-cholinergic reactive system (M-CRS) activity in its implementation. Methods. The study was conducted on young and old anesthetized nonlinear white male rats. The animals were ventilated with room air via a tracheostomy. The right carotid artery and left internal jugular vein were cannulated to measure blood pressure and administer drugs. An electrocardiogram (ECG) was continuously recorded in lead II throughout the experiment. The animals underwent coronary occlusion (30 min) and reperfusion (2 h). The size of the necrotic zone and the risk zone were assessed using computerized planimetry. PostL was modeled 25 min after the start of reperfusion by administering a solution of L-lactate neutralized with NaOH at a dose of 10 mg/kg. The NOS inhibitor N G -nitro-L-arginine methyl ester (L-NAME) was administered to rats at a dose of 25 mg/kg immediately after coronary occlusion, and the 0.2 % M-CRS blocker atropine at a dose of 2 mg/kg was administered 10 min before PostL. Results. PostL exerts a cardioprotective effect and leads to a decrease in the size of the necrotic zone in the left ventricular myocardium in young and old animals by 26.7 and 25.5 % (p < 0.01), respectively. Pretreatment with both the NOS inhibitor L-NAME and the M-CRS blocker atropine abolished the cardioprotective effect of PostL in young but not old rats, indicating the importance of NOS and L-NAME in mediating the cardioprotective effect of PostL in young but not old rats. Conclusion. The activity of M-СRC, like NOS, is important in the implementation of the cardioprotective effect of PostL during myocardial ischemia-reperfusion in rats, depending on their age. Following systemic administration of both the NOS inhibitor L-NAME and the M-CRS blocker atropine, the cardioprotective effect of PostL is maintained in old but not young rats.
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Чепелев et al. (2026) studied Myocardial ischemia-reperfusion injury (n=218). Postconditioning with L-lactate (PostL) vs. Control (0.9% NaCl at 25 min of reperfusion), with or without L-NAME (25 mg/kg) or atropine (2 mg/kg) was evaluated on Necrotic zone size in the left ventricular myocardium (% of area at risk) in young rats (26.7% relative reduction in young rats (25.5% in old rats: 35% vs 47%), p=<0.01). Postconditioning with L-lactate reduced left ventricular necrotic zone size by 26.7% in young rats and 25.5% in old rats (p<0.01), though NOS and M-cholinergic blockade abolished this effect in young rats only.
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