The role of stressor intensity in influencing the course of heart disease in cardiomyopathic hamsters

• Published in: Proceedings of the Society for Experimental Biology and Medicine Vol. 212; no. 3; p. 248
• Main Authors: Chang, Q, Natelson, B H, Ottenweller, J E, Conway, R S
• Format: Journal Article
• Language: English
• Published: United States 01.07.1996
• Subjects: Analysis of Variance; Animals; Arginine Vasopressin - pharmacology; Blood Pressure - physiology; Cardiomyopathy, Dilated - physiopathology; Coronary Vessels - drug effects; Coronary Vessels - physiopathology; Cricetinae; Disease Models, Animal; Hemodynamics; Immobilization; Stress, Physiological - physiopathology; Time Factors; Vascular Resistance - physiology; Ventricular Function - physiology
• ISSN: 0037-9727
• DOI: 10.3181/00379727-212-44013

Our earlier work showed that stress had progressively more serious consequences in a hamster model of congestive heart failure as the magnitude of heart failure worsened. Based on that study, we hypothesized that the intensity of the stressor used might play an important part in determining this outcome as well as in influencing coronary reactivity to arginine vasopressin (AVP). Cardiomyopathic (2.5, 6.5, and 10 months) hamsters (CMHs) were stressed with a 2-hr period of supine immobilization for five consecutive days. Stressor intensity was increased by exposing the hamsters to progressively longer periods at 4 degrees C: the low stress group was never put in the cold; the moderate stress group was exposed to cold for 1 hr, and the high stress group for 2 hr. CMHs were anesthetized and sacrificed 5 days after stress, and their hearts were perfused using a modified Langendorff system. Maximum +/- dP/dt, developed pressure, ventricular relaxation time, (T), and coronary vascular resistance (CVR) were recorded, and CVR was also measured following coronary infusion of AVP. Stressor intensity had no effect on cardiac mechanics in 2.5-month CMHs. In 6.5-month CMHs, only the high-intensity stressor impaired ventricular mechanics (decreased maximum +/- dP/dt and developed pressure, increased T; P < 0.05), while low and moderate stress produced no effects. In 10-month CMHs, stress at all intensities exacerbated ventricular dysfunction (decreased maximum +/- dP/dt and developed pressure; P < 0.05). These results support our first hypothesis that stressor intensity interacts multiplicatively with severity of the underlying disease to influence the course of heart failure. However, our second hypothesis was not supported, because stress-regardless of intensity-affected reactivity of the coronary vasculature to AVP only in 2.5-month CMHs. A further test of the relation of stressor intensity and coronary vascular reactivity requires study of additional groups of CMHs during the period of their disease characterized by coronary vasospasm.