Comparative effects of nitric oxide inhibition on the coronary vasomotor responses to etomidate, propofol, and thiopental in anesthetized dogs

Peter G Moore, N. D. Kien, R. M. Boldy, J. A. Reitan

Research output: Contribution to journalArticle

7 Scopus citations

Abstract

We examined the hypothesis that the coronary vasomotor responses to etomidate (ETO), propofol (PRO), and sodium thiopental (STP) are mediated through contrasting effects on the resting nitric oxide (NO)-dependent vasodilator tone that opposes adrenergic vasoconstrictor activity in the intact dog. Circumflex flow (CxF) responses to randomized intracoronary microinjections (0.3 mL) of normal saline (NS), alkalinized saline (AS), intralipid (IL), adenosine (ADE, 17 μg), acetylcholine (ACh, 1.25 μg), ETO (6, 12, 60 μg), PRO (30, 60, 300 μg), and STP (75, 150, 750 μg) were quantified in eight isoflurane-anesthetized dogs with fixed ventricular rates (100 bpm). Injections were repeated during intravenous (IV) infusion (50 mg/kg + 1 mg · kg-1 · min-1) of N(G)-nitro-L-arginine methyl ester (L- NAME). ADE and ACh transiently increased CxF to 305% ± 20% (P < 0.001) and 310% ± 29% (P < 0.001) of resting values, respectively. ETO had no effect, whereas PRO (300 μg) provoked small transient increases in CxF to 135% ± 4% (P < 0.05) of control. Responses to STP (750 μg) were characterized by momentary decreases to 74% ± 4% (P < 0.001), followed immediately by increases to 183% ± 11% (P < 0.001) of resting values; NS AS, and IL had no effect. The momentary decreases with STP (750 μg) were significantly augmented during NO inhibition with CxF declining to 49% ± 7% (P < 0.001) of resting values, whereas the secondary increase was unchanged. With L-NAME, CxF responses to ACh were attenuated to 32% ± 3% (P < 0.001) of control, whereas responses to ADE, ETO, and PRO were unchanged. PRO caused small but significant increases in CxF that appear to be NO-independent, whereas NO inhibition accentuated the initial vasoconstrictor response to STP but had no effect on the secondary phase vasodilation. The data suggest that STP may evoke reductions in coronary flow that are profoundly exaggerated under conditions of coronary endothelial dysfunction.

Original languageEnglish (US)
Pages (from-to)439-446
Number of pages8
JournalAnesthesia and Analgesia
Volume79
Issue number3
StatePublished - 1994

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine

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