title: Coronary arterial hyperreactivity and mesenteric arterial hyporeactivity after myocardial infarction in the rat.
abstract: After myocardial infarction, several neurohumoral systems become activated to maintain systemic perfusion pressure. We evaluated whether this 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 MI or sham operation, vessel segments were isolated, chemically sympathectomized, 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 contractile 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 to vasoconstrictors was observed, whereas vessel wall structure and sensitivity to stimuli were not modified. On the other hand, coronary septal arteries displayed hyperreactivity to all strong contractile stimuli. These observations demonstrate a heterogeneity of arterial reactivity changes at 5 weeks after MI in the rat: (a) no alterations in thoracic aorta, (b) hyporeactivity of mesenteric resistance arteries despite maintenance of media mass, and (c) hyperreactivity of coronary vessels obtained from the hypertrophic remnant myocardium. This could result from the complex regional hemodynamic and neurohumoral changes associated with heart failure and may contribute to the further deterioration of cardiovascular function in this setting.
authors.affiliation: Department of Pharmacology, Cardiovascular Research Institute Maastricht, Universiteit Maastricht, The Netherlands.
authors.forename: F R
authors.initials: FR
authors.lastname: Stassen
authors.forename: G E
authors.initials: GE
authors.lastname: Fazzi
authors.forename: P J
authors.initials: PJ
authors.lastname: Leenders
authors.forename: J F
authors.initials: JF
authors.lastname: Smits
authors.forename: J G
authors.initials: JG
authors.lastname: De Mey
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000503:physiopathology; D001835:Body Weight; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology / Q000502:physiology / Q000503:physiopathology*; D008026:Ligation; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009203:Myocardial Infarction / Q000503:physiopathology*; D009929:Organ Size; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents