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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.
Highlights
The goal of this review is to analyze recent literature utilizing rodent models to examine the impact of psychological stress on sensitivity to myocardial ischemia–reperfusion injury (IRI) in the context of the well-established relationship between stress, myocardial ischemic injury, and cardiovascular disease (CVD)
The disruptive effect of this post-traumatic stress disorder (PTSD) paradigm on the heart is further strengthened by anxiety-like behavior in rats on the elevated plus maze (EPM) prior to myocardial ischemic injury. These data suggest that the psychological stress induced by the PTSD paradigm is having an effect directly on the heart, causing the heart to be more susceptible to damage following a myocardial infarction (MI) [135]
The relationship between stress and CVD continues to receive a substantial amount of attention
Summary
The goal of this review is to analyze recent literature utilizing rodent models to examine the impact of psychological stress on sensitivity to myocardial ischemia–reperfusion injury (IRI) in the context of the well-established relationship between stress, myocardial ischemic injury, and cardiovascular disease (CVD). Stress is a general adaptive response provoked by stimuli that disrupt homeostasis [1, 2]. ACTH, CRH, and GCs provide the negative feedback necessary to dampen the stress response and return the body to homeostasis [4, 6]. Acute stress generally results in an adaptive response to homeostatic changes; the stress response becomes. Physical or psychological stressors can result in the stress response. Stress precipitates psychiatric disease, such as depression and post-traumatic stress disorder (PTSD), and worsens physical health outcomes, such as CVD [12, 13]. Research directed at minimizing the negative impact of stress is important [19, 21,22,23,24,25]
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