title: The role of stressor intensity and underlying vasculopathy in altering coronary reactivity in cardiomyopathic hamsters.
abstract: OBJECTIVE
  Our previous work showed that stress sensitized the vessels of cardiomyopathic hamsters (CMHs), but only hamsters in the lesion-forming period of their life. We hypothesized that we would find an interaction between stressor intensity and microvascular vulnerability.
  
  
  METHODS
  Male CMHs at ages of 1.5, 2.5, and 3.5 months were stressed with supine immobilization for five consecutive days. Stressor intensity was manipulated by immobilizing groups of CMHs at room temperature for 0 minutes, 15 minutes, 30 minutes, 1 hour, or 2 hours. CMHs were anesthetized and sacrificed 5 days after stress, and their hearts were perfused using a modified Langendorff system. Body weight changes and baseline coronary vascular resistance (CVR) were recorded, and CVR was also measured after coronary artery infusion of arginine vasopressin (AVP).
  
  
  RESULTS
  Stress produced no effect on coronary vasculature in 1.5-month-old CMHs. In 2.5-month-old CMHs, only the two highest-intensity stressors enhanced coronary reactivity to AVP. In 3.5-month-old CMHs, higher-intensity stressors produced a marginal AVP-induced increase in CVR; but this marginal increase was significantly lower than the increases seen with the two highest-stressor intensities in the 2.5-month-old CMHs.
  
  
  CONCLUSIONS
  The stress-induced coronary hyperreactivity to AVP seen in 2.5-month-old CMHs diminished when microvascular vulnerability was lower in 3.5-month-old CMHs. For 1.5-month-old CMHs, the resting CVR was extremely high, so that the addition of stress produced no further increase. Thus, stressor intensity interacted with microvascular vulnerability to alter the consequences of stress.
authors.affiliation: Neurobehavioral Unit, Veterans Administration Medical Center, East Orange, NJ 07018-1095, USA.
authors.forename: Q
authors.initials: Q
authors.lastname: Chang
authors.forename: B H
authors.initials: BH
authors.lastname: Natelson
authors.forename: C D
authors.initials: CD
authors.lastname: Goldstein
authors.forename: J E
authors.initials: JE
authors.lastname: Ottenweller
mesh_terms: D000367:Age Factors; D000704:Analysis of Variance; D000818:Animals; D001127:Arginine Vasopressin / Q000009:adverse effects; D009202:Cardiomyopathies / Q000150:complications / Q000503:physiopathology*; D006224:Cricetinae; D004195:Disease Models, Animal; D018450:Disease Progression; D004198:Disease Susceptibility; D008297:Male; D012149:Restraint, Physical / Q000009:adverse effects; D013312:Stress, Physiological / Q000150:complications / Q000503:physiopathology*; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D001127:Arginine Vasopressin