title: Mechanisms of renal hemodynamic impairment during infrarenal aortic cross-clamping.
abstract: Infrarenal aortic cross-clamping is associated with impairment of renal hemodynamics due to vasoconstriction, the mechanism of which remains under debate. To assess the renal effect of two potent renal vasodilators (enalapril, a converting enzyme inhibitor, and nicardipine, a calcium antagonist), 24 patients scheduled for reconstructive aortic surgery were randomly allocated to one of three treatment groups (n = 8 each) and received either a placebo, nicardipine, or enalapril. Anesthesia consisted of flunitrazepam, fentanyl, pancuronium, and, occasionally, droperidol. Although aortic cross-clamping was associated with no change in mean arterial blood pressure, decreased cardiac output and increased systemic vascular resistance occurred in control patients (33% and 43%, respectively, both P less than 0.05 versus baseline) and nicardipine-treated patients (51.7% and 67.7%, respectively, both P less than 0.05 versus baseline); however, changes in cardiac output and systemic vascular resistance failed to reach significance in enalapril-treated patients. Glomerular filtration rate (technetium 99-diethylenetriaminepentacetic acid clearance) and effective renal plasma flow (iodo-Hippuran 131 clearance) decreased for the duration of aortic cross-clamping in control patients (42.9% and 18.5%, respectively, both P less than 0.05 versus baseline) and enalapril-treated patients (34.0% and 38.1%, respectively, both P less than 0.05 versus baseline), but no change was observed in nicardipine-treated patients. These results suggest that the reninangiotensin system is not an important determinant of the renal vasoconstriction associated with aortic cross-clamping. In contrast, renal dysfunction may be alleviated by the dihydropyridine derivative nicardipine, which probably acts at the level of the preglomerular resistance vessels.
authors.affiliation: Department of Anesthesiology, Hôpital Saint-Eloi, Montpellier, France.
authors.forename: P
authors.initials: P
authors.lastname: Colson
authors.forename: J
authors.initials: J
authors.lastname: Ribstein
authors.forename: J R
authors.initials: JR
authors.lastname: Séguin
authors.forename: C
authors.initials: C
authors.lastname: Marty-Ane
authors.forename: B
authors.initials: B
authors.lastname: Roquefeuil
mesh_terms: D000328:Adult; D000368:Aged; D001012:Aorta, Abdominal / Q000503:physiopathology*; D001014:Aortic Aneurysm / Q000503:physiopathology / Q000601:surgery*; D001794:Blood Pressure / Q000187:drug effects; D002302:Cardiac Output / Q000187:drug effects; D004311:Double-Blind Method; D004329:Droperidol; D004656:Enalapril / Q000627:therapeutic use*; D005260:Female; D005283:Fentanyl; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular; D009529:Nicardipine / Q000627:therapeutic use*; D012079:Renal Circulation / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D004656:Enalapril; D009529:Nicardipine; D004329:Droperidol; D005283:Fentanyl