Mechanism of Vascular Responsiveness to Barbiturates in Isolated and Perfused Canine Basilar Arteries

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Abstract
We inserted stainless steel cannulae to compare vascular responses to five kinds of barbiturates and to investigate the mechanism of vascular responsiveness to thiopental in isolated and perfused canine basilar arteries. Intraluminal thiopental (10 to 3000 μg) usually caused a distinctly biphasic vascular response, i.e., initial vasoconstriction followed by vasodilatation. The vasoconstriction was always greater than the vasodilatation in percentage of change. Thiamylal (10 to 3000 μg) evoked similar vascular responses. Pentobarbital, phenobarbital, and amobarbital (100 to 3000 μg) induced slight monophasic vasodilatation in lower doses and a weak biphasic response in higher doses. Pretreatment with phentolamine and ketanserin, an α-adrenoceptor antagonist and a 5-hydroxytryptamine2 inhibitor, did not alter vasoconstriction to thiopental. Increasing doses of pretreatment with diltiazem, a potent calcium antagonist, depressed the vasoconstriction induced by potassium chloride in a dose-related manner, but thiopental-induced constriction was only slightly suppressed by diltiazem treatment. Endothelial removal produced by intraluminal saponin treatment significantly enhanced vasoconstriction to potassium chloride, but thiopental-induced constriction was not enhanced significantly after saponin treatment. These findings suggest that thiopental-induced vasoconstriction does not involve adrenergic and serotonergic mechanisms and is due to intracellular movement of calcium ions in canine basilar arteries.