THE ROLE OF STRESSOR INTENSITY IN INFLUENCING THE COURSE OF HEART-DISEASE IN CARDIOMYOPATHIC HAMSTERS

Our earlier work showed that stress had progressively more serious con sequences in a hamster model of congestive heart failure as the magnit ude of heart failure worsened. Based on that study, we hypothesized th at 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 mont hs) hamsters (CMHs) were stressed with a 2-hr period of supine immobil ization 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 g roup 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 +/-d P/ dt, developed pressure, ventricular relaxation time, (T), and coron ary 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 hi gh-intensity stressor impaired ventricular mechanics (decreased maximu m +/-dP/dt and developed pressure, increased T; P < 0.05), while low a nd moderate stress produced no effects. In 10-month CMHs, stress at al l intensities exacerbated ventricular dysfunction (decreased maximum /-dP/dt and developed pressure; P < 0.05). These results support our f irst hypothesis that stressor intensity interacts multiplicatively wit h severity of the underlying disease to influence the course of heart failure. However, our second hypothesis was not supported, because str ess-regardless of intensity-affected reactivity of the coronary vascul ature 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 characte rized by coronary vasospasm.