Acute Stress Decreases but Chronic Stress Increases Myocardial Sensitivity to Ischemic Injury in Rodents

Abstract

Cardiovascular disease (CVD) is the largest cause of mortality worldwide, and stress is a significant contributor to the development of CVD. The relationship between acute and chronic stress and CVD is well evidenced. Acute stress can lead to arrhythmias and ischemic injury. However, recent evidence in rodent models suggests that acute stress can decrease sensitivity to myocardial ischemia-reperfusion injury (IRI). Conversely, chronic stress is arrhythmogenic and increases sensitivity to myocardial IRI. Few studies have examined the impact of validated animal models of stress-related psychological disorders on the ischemic heart. This review examines the work that has been completed using rat models to study the effects of stress on myocardial sensitivity to ischemic injury. Utilization of animal models of stress-related psychological disorders is critical in the prevention and treatment of cardiovascular disorders in patients experiencing stress-related psychiatric conditions.

Keywords: PTSD; anxiety; cardiovascular; ischemia; rodent; stress.

Figure 1

Effects of a predator-based psychosocial model of PTSD on anxiety-like behavior, growth rate, and myocardial sensitivity to ischemic injury. Rats exposed to the 31-day psychosocial stress paradigm spend less time in the open arms on the EPM (A) and exhibit reduced growth rats (B). Following 20-min ischemia, hearts from psychosocially stressed animals exhibit larger infarcts (C), white regions of representative tissue (samples in the insets) and impaired recovery of contractile function (D). Data are means ± SEM. *p < 0.05 relative to no stress. Adapted from Rorabaugh et al. (135).