Modulation of cardiac response to ischemia/reperfusion in hypertensive rats exposed to chronic social stress

Abstract

Chronic psychosocial stress (S) impairs vascular regulation leading to hypertension (H). However, modulation of cardiac response to ischemia/reperfusion injury (I/R) by S is not fully characterized, in particular, in hypertensive animals. We explored tolerance to I/R in WKY and SHR rats exposed to 8 w of crowding S induced by caging 5 rats/cage (200 cm2/rat), while controls (C) were kept 4 rats/cage (480 cm2/rat). S did not affect left ventricular (LV) weight in any group, however, it amplified increased BP and reduced elevation of cardiac NOS activity in SHR rats. Neither did S modified myocardial function in hearts of both groups under baseline conditions. Ischemic challenge (25_min I/40_min R) revealed markedly impaired recovery of LV developed pressure (LVDP) in C_SHR (15±6% of baseline value vs. 60±1.5% in the control WKY group; P<0.05) and increased susceptibility to lethal arrhythmias (incidence of SVF 25% and duration of VT 84±22 s vs. SVF 0% and VT 30±12 s in C_WKY; P<0.05). S altered contractile recovery in the WKY group (LVDP 32±5%; P<0.05) and exacerbated arrhythmias (incidence of SVF 40%, duration of VT 70±20 s; P<0.05 vs. unstressed WKY). In contrast, SVF was completely suppressed in stressed SHR hearts, in conjunction with shorter episodes of VT (22±5 s) and better recovery of LVDP (47±12%; P<0.05 vs. unstressed SHR). Conclusion: chronic psychosocial stress represents a higher risk of lethal arrhythmias and contractile failure in normotensive rats exposed to an acute ischaemic challenge indicating a potential development of cross effect of adaptation in hypertensive individuals.