title: Differential impairment of vascular reactivity of small pulmonary and systemic arteries in hyperdynamic sepsis.
abstract: We postulated that the redistribution of organ blood flow that occurs in hyperdynamic sepsis is secondary to organ-specific alterations in vascular reactivity. Chronically instrumented rats were randomized to cecal ligation and perforation (CLP) (n = 12) or to a control procedure (n = 11). Cardiac output increased from 107 +/- 23 ml/min at baseline to 152 +/- 32 ml/min at 24 h after CLP (p = 0.037 versus control values). Mean blood pressure did not change in either group. Small arterial ring segment (100- to 200-microns effective lumen radius) from the pulmonary, renal, celiac, and femora arteries were obtained for determination of in vitro responsiveness. Maximal contractile responses to three receptor-operated contractile agonists were significantly depressed in the pulmonary (p = 0.001) and the celiac (p = 0.001) arteries from CLP versus control rats. The renal artery showed a trend toward decreased responsiveness (p = 0.049), but not difference was seen in the femoral artery (p = 0.172). EC50 values were unchanged. A similar, but less marked, pattern was observed for KCI-induced contractions in that depressed responses were noted in the pulmonary (p = 0.045) and celiac (p = 0.064) arteries. Vasodilator responses to acetylcholine were normal in all vessels. Nitroprusside relaxant responses were enhanced in the pulmonary artery (p = 0.022), but they were normal in the other vessels. We conclude that hyperdynamic, normotensive sepsis is associated with an organ-specific alteration of vascular smooth muscle function that particularly affects receptor-operated contractile responses. The differential expression of this altered vascular responsiveness between organs may contribute to the observed variance in regional blood flows in sepsis.
authors.affiliation: A. C. Burton Vascular Biology Laboratories, Victoria Hospital Research Institute, University of Western Ontario, London, Canada.
authors.forename: C M
authors.initials: CM
authors.lastname: Martin
authors.forename: A
authors.initials: A
authors.lastname: Yaghi
authors.forename: W J
authors.initials: WJ
authors.lastname: Sibbald
authors.forename: D
authors.initials: D
authors.lastname: McCormack
authors.forename: N A
authors.initials: NA
authors.lastname: Paterson
mesh_terms: D000818:Animals; D002406:Catheterization, Peripheral / Q000295:instrumentation / Q000379:methods; D002432:Cecum / Q000293:injuries / Q000502:physiology; D002445:Celiac Artery / Q000187:drug effects / Q000503:physiopathology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005263:Femoral Artery / Q000187:drug effects / Q000503:physiopathology*; D006439:Hemodynamics / Q000187:drug effects; D007416:Intestinal Perforation / Q000503:physiopathology; D008026:Ligation; D008297:Male; D011651:Pulmonary Artery / Q000187:drug effects / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012077:Renal Artery / Q000187:drug effects / Q000503:physiopathology*; D012772:Shock, Septic / Q000503:physiopathology*; D014655:Vascular Resistance / Q000187:drug effects*