title: Vasomotor function of pig coronary arteries after chronic coronary occlusion.
abstract: Placement of an ameroid constrictor in large-conduit pig coronary arteries causes progressive stenosis and distal myocardial ischemia. Blood perfusion in the ischemic region is partly dependent on vasomotor responses to neural and humoral factors distal to the occlusion site. To ascertain the degree of impairment of vascular function in pigs, the authors induced myocardial ischemia by placing an ameroid constrictor in the left circumflex coronary artery and examined vascular reactivity and histopathology distal to the constriction site. The sensitivity of the distal left circumflex coronary and nonoccluded control left anterior descending arteries to PGF(2alpha) was similar. After nitric oxide blockade using Nw-nitro-l-arginine methylester (l-NAME), the sensitivity and maximal contraction to PGF(2alpha) were significantly increased in both the left circumflex coronary (EC50: 5.86 +/- 0.74 vs. 3.28 +/- 0.84 microM; C(max): 4.63 +/- 0.28 vs. 6.25 +/- 0.30 g, P < 0.01) and left anterior descending (EC50: 6.57 +/- 0.73 vs. 2.78 +/- 0.16 microM; C(max): 5.09 +/- 0.37 vs. 6.95 +/- 0.39 g, P < 0.01) arteries. Substance P-induced relaxation (100 pM) was blocked to a larger degree in the distal left circumflex coronary artery when compared with the left anterior descending artery (76.9 +/- 4.2% vs. 56.4 +/- 3.1%, P < 0.05). Endothelium-independent relaxation to sodium nitroprusside was similar in the left circumflex coronary and left anterior descending arteries before and after nitric oxide blockade. Histopathologic examination showed no major differences between distal left circumflex coronary artery segments and left anterior descending artery controls. However, scanning electron microscopy showed endothelial hypertrophy and activation in specimens from the left circumflex coronary arteries. In summary, as a result of the major hemodynamic changes induced by a chronic constriction and eventual occlusion of a large coronary artery, distal segments underwent adaptive compensatory changes. Such compensation may be related to an increased nitric oxide production by the hypertrophic endothelium in response to alterations in coronary hemodynamics.
authors.affiliation: The American Cardiovascular Research Institute, Norcross, Georgia 30071, USA.
authors.forename: Jinsheng
authors.initials: J
authors.lastname: Li
authors.forename: Hector
authors.initials: H
authors.lastname: De Leon
authors.forename: Takafumi
authors.initials: T
authors.lastname: Ueno
authors.forename: Jianhua
authors.initials: J
authors.lastname: Cui
authors.forename: Patrick K
authors.initials: PK
authors.lastname: Coussement
authors.forename: Spencer B
authors.initials: SB
authors.lastname: King
authors.forename: Nicolas A F
authors.initials: NA
authors.lastname: Chronos
authors.forename: Keith A
authors.initials: KA
authors.lastname: Robinson
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D011859:Radiography; D013373:Substance P / Q000494:pharmacology; D013552:Swine; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology; D014666:Vasomotor System / Q000000981:diagnostic imaging / Q000187:drug effects / Q000473:pathology / Q000502:physiology*
chemical_list: D013373:Substance P; D019331:NG-Nitroarginine Methyl Ester