CORONARY ARTERIAL HYPERREACTIVITY AND MESENTERIC ARTERIAL HYPOREACTIVITY AFTER MYOCARDIAL-INFARCTION IN THE RAT

After myocardial infarction, several neurohumoral systems become activ ated to maintain systemic perfusion pressure. We evaluated whether thi s leads to alterations of wall structure and contractile reactivity in the thoracic aorta, coronary septal artery, and mesenteric resistance arteries. In male Wistar rats, myocardial infarction (MI) was induced by permanent ligation of the left coronary artery. At 5 weeks after M I or sham operation, vessel segments were isolated, chemically sympath ectomized, and mounted in a myograph for recording of isometric force development. Contractile reactivity to high potassium, norepinephrine, phenylephrine, serotonin, and Arg-vasopressin was determined. At the end of the experiments, vessels were fixed for morphometric analysis ( cross-sectional area, media thickness, radius, and wall-to-lumen ratio ). At 5 weeks after myocardial infarction, no alterations of contracti le reactivity or wall structure were observed in the thoracic aorta of MI rats. In mesenteric resistance arteries, a nonselective reduction of maximal active wall tension and of active wall stress in response t o vasoconstrictors was observed, whereas vessel wall structure and sen sitivity to stimuli were not modified. On the Ether hand, coronary sep tal arteries displayed hyperreactivity to all strong contractile stimu li. These observations demonstrate a heterogeneity of arterial reactiv ity changes at 5 weeks after MI in the rat: (a) no alterations in thor acic aorta, (b) hyporeactivity of mesenteric resistance arteries despi te maintenance of media mass, and (c) hyperreactivity of coronary vess els obtained from the hypertrophic remnant myocardium. This could resu lt from the complex regional hemodynamic and neurohumoral changes asso ciated with heart failure and may contribute to the further deteriorat ion of cardiovascular function in this setting.