Key result
Animal models of acute stress reproduce ventricular arrhythmias and stress cardiomyopathy via elevated sympathetic outflow, but models of chronic stress-induced hypertension remain contentious.
Animal models successfully replicate stress-induced arrhythmias and cardiomyopathy via sympathetic pathways, but are inconsistent in modeling psychogenic hypertension.
May guide acute sympathetic targeting in stress cardiomyopathy; leaves open reliable chronic hypertension models.
Summary 1. Epidemiological and clinical studies from the past 50 years provide unequivocal evidence for a close association and causative links between psychological stresses and cardiovascular dysfunction in humans. Not surprisingly, numerous animal experiments have been undertaken in an attempt to clarify underlying pathophysiological mechanisms. The present review focuses on animal models that provide insight into the mechanisms of stress‐induced cardiovascular dysfunction. 2. Great success was achieved in elucidating the neural pathways and neurotransmitters responsible for the cardiac consequences of acute stressors, such as stress‐induced ventricular arrhythmias and stress cardiomyopathy. These disturbances were reproduced successfully in canine and rodent models. The most important finding from these animal models is that these disturbances are mediated by elevated sympathetic outflow to the ventricular myocardium. 3. In contrast, attempts to induce psychogenic hypertension in rodents produced inconsistent and contentious results. More recent studies using biotelemetry raised serious doubts regarding the validity of earlier results obtained with the tail‐cuff method and it remains unclear whether chronic stress can lead to sustained hypertension in animal models.
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Eugene Nalivaiko (2010) conducted a review in Stress-induced cardiovascular dysfunction. Animal models of psychological stress was evaluated. Animal models of acute stress reproduce ventricular arrhythmias and stress cardiomyopathy via elevated sympathetic outflow, but models of chronic stress-induced hypertension remain contentious.
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