title: Peripheral vascular alterations during experimental heart failure in the rat. Do they exist?
abstract: Structural changes of the peripheral vascular component as seen during hypertension and atherosclerosis have been suggested during heart failure but have never been reported. Therefore, we studied possible structural alterations in the peripheral vasculature in an experimental model of heart failure, induced by ligation of the left coronary artery in rats. Large conduit and resistance-type arteries were excised at 1, 3, 5, and 12 weeks after myocardial infarct induction (MI) or sham surgery. Vessel dimensions (medial cross-sectional area [CSA], internal and external diameters, and media-to-lumen ratios) as well as medial collagen and elastin volume fractions were measured by computerized morphometry. The hydroxyproline assay was used to determine collagen and elastin content biochemically. In separate groups of animals, peripheral tissue flows were measured by using radioactive microspheres 5 and 12 weeks after MI. To evaluate the effects of the degree of heart failure, the animals of the 12-week group (n = 10) were subdivided into groups of moderate (< 45% infarct size) and large (> 45% infarct size) infarction. At all time points, body weights of sham-operated and MI rats were comparable. Lung weights of infarcted animals were increased proportionally to infarct size. No major changes in vessel dimensions were seen at the earlier time points. Twelve weeks after coronary artery ligation, significantly smaller CSAs were observed in several large conduit arteries such as the thoracic aorta, carotid artery, and superior mesenteric artery. These changes coincided with reductions in both internal and external diameters. In contrast, internal and external diameters of mesenteric and pulmonary resistance arteries were increased after 12 weeks of coronary artery ligation.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Pathology, Cardiovascular Research Institute Maastricht, University of Limburg, Netherlands.
authors.forename: S
authors.initials: S
authors.lastname: Heeneman
authors.forename: P J
authors.initials: PJ
authors.lastname: Leenders
authors.forename: P J
authors.initials: PJ
authors.lastname: Aarts
authors.forename: J F
authors.initials: JF
authors.lastname: Smits
authors.forename: J W
authors.initials: JW
authors.lastname: Arends
authors.forename: M J
authors.initials: MJ
authors.lastname: Daemen
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000473:pathology; D001013:Aorta, Thoracic / Q000473:pathology; D001783:Blood Flow Velocity; D001808:Blood Vessels / Q000473:pathology*; D002303:Cardiac Output, Low / Q000209:etiology / Q000473:pathology*; D002339:Carotid Arteries / Q000473:pathology; D003331:Coronary Vessels / Q000601:surgery; D004195:Disease Models, Animal; D005109:Extracellular Matrix / Q000737:chemistry; D006909:Hydroxyproline / Q000032:analysis; D008026:Ligation; D008297:Male; D008638:Mesenteric Arteries / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology; D011651:Pulmonary Artery / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D012077:Renal Artery / Q000473:pathology
chemical_list: D006909:Hydroxyproline