P671Sex-specific response to ischemia and reperfusion in hearts with different predisposition to hypertension exposed to social stress

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Genetic predisposition and social stress may represent important risk factors in etiology of hypertension associated with impaired myocardial response to ischemia and reperfusion (I/R) in male and female heart. Sex is an important determinant of cardiovascular morbidity and mortality in human population, where men are at higher risk than age-matched premenopausal women. The capability for activation of intrinsic tolerance to I/R injury observed in females as well as in males may persist even in the hearts of animals with genetic predisposition to hypertension and may be modified by long-lasting cardiac adaptation to stressful conditions. For this reason, we aimed to test the impact of chronic stress on the response to sustained I/R in borderline/spontaneously hypertensive rats (BHR/SHR) in comparison with its effects in normotensive Wistar Kyoto (WKY) counterparts.

Male and female 5-week-old BHR (offspring of Wistar mothers and SHR fathers), SHR (offspring of SHR mothers and fathers) and age-matched WKY rats were exposed to 2-week crowding stress (CS), which was induced by caging five rats per cage in a cage for two (200 cm2/rat), while controls (C) were kept four rats per cage in cages for six animals (480 cm2/rat). Langendorff-perfused hearts of stressed and non-stressed WKY, BHR and SHR animals were exposed to 30-min global ischemia and 2-h reperfusion for the evaluation of reperfusion-induced ventricular arrhythmias and size of myocardial infarction (IS, TTC staining).

Female WKY hearts exhibited greater tolerance to reperfusion arrhythmias as compared to males. CS impaired postischemic recovery of contractile function with stronger effect in males. On the other hand, CS decreased the total duration of a more severe form of ventricular arrhythmias - ventricular tachycardia (VT) only in females. BHR animals of both sexes were markedly more prone to VT, while SHR hearts exhibited increased resistance to VT when compared to normotensives and BHRs. We observed dramatically decreased of VT duration in BHR-CS but not in SHR-CS males and females. Interestingly, IS was not affected by CS in normotensives as well as in BHR and SHR hearts.

Social stress modifies parameters of I/R injury in a distinct way. Inherited predisposition to hypertension may be responsible for changes in cardiac ischemic tolerance of animals exposed to social stress, which appears to be sex-dependent.

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