CARDIAC AND REGIONAL HEMODYNAMIC INTERACTIONS BETWEEN HALOTHANE AND NITRIC-OXIDE SYNTHASE ACTIVITY IN DOGS

Citation
Je. Chelly et al., CARDIAC AND REGIONAL HEMODYNAMIC INTERACTIONS BETWEEN HALOTHANE AND NITRIC-OXIDE SYNTHASE ACTIVITY IN DOGS, Anesthesiology, 85(1), 1996, pp. 142-149
Citations number
18
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
85
Issue
1
Year of publication
1996
Pages
142 - 149
Database
ISI
SICI code
0003-3022(1996)85:1<142:CARHIB>2.0.ZU;2-R
Abstract
Background: In vitro, halothane appears to affect the role played by n itric oxide in the regulation of vascular tone and cardiac function. I n vivo the results of the interactions between halothane and the nitri c oxide pathway remain controversial. The authors investigated the eff ects of halothane on the cardiac and regional hemodynamic properties o f N-methyl-L-arginine (NMA), a specific nitric oxide synthase inhibito r, in dogs. Methods: Twenty-five dogs were chronically instrumented. A ortic pressure, the first derivative of left ventricular pressure, car diac output, heart rate, and carotid, coronary, mesenteric, hepatic, p ortal and renal blood flows were continuously recorded. N-methyl-L-arg inine was infused intravenously at 20 mg/kg over 1 min in awake dogs ( n = 11) and in 1.2% halothane-anesthetized dogs (n = 10). As a control group, the remaining four dogs were studied awake and during 1.2% hal othane for 2 h in the absence of NMA. Results: In awake dogs, NMA prod uced a sustained presser response (34%) and systemic vasoconstriction (40%) associated with a decrease In cardiac output (16%). Regional cir culation changes included an immediate and transient increase in carot id (43%) and coronary (237%) blood flows and a subsequent decrease in carotid blood flow (25%). Hepatic and mesenteric blood flows also decr eased, by 43% and 16%, respectively. Except for the coronary circulati on, regional vascular resistance increased significantly. Halothane di d not affect the presser response to NMA but did blunt the cardiac out put changes. Consequently, the systemic vasoconstriction after nitric oxide synthase inhibition was of shorter duration and of lesser magnit ude during halothane anesthesia. Halothane also blunted the carotid, m esenteric, and renal vasoconstriction induced by NMA. Finally, in 1.2% halothane-anesthetized dogs, NMA induced a coronary vasoconstriction. Conclusions: Halothane minimally interferes with the systemic and reg ional hemodynamic consequences of nitric oxide synthase blockade. The nature and magnitude of the interaction depend on the territory in whi ch they occur.