The Inhibitory Action of Halothane on Reflex Constriction in Mesenteric Capacitance Veins
作者:
Thomas Stekiel,
Keizaburo Ozono,
John McCallum,
Zeliko Bosnjak,
William Stekiel,
John Kampine,
期刊:
Anesthesiology
(OVID Available online 1990)
卷期:
Volume 73,
issue 6
页码: 1169-1178
ISSN:0003-3022
年代: 1990
出版商: OVID
关键词: Anesthetics, volatile: halothane;Sympathetic nervous system: baroreflex; reflex venoconstriction; sympathetic efferent nerve activity
数据来源: OVID
摘要:
Potent inhalational anesthetics depress autonomic reflex responses at multiple sites. Most studies emphasize cardiac chronotropk changes and changes in systemic blood pressure. Recently, active reflex venoconstriction of 500–1,000 μm O.D. mesenteric veins has been demonstrated. In the current study, the effects of halothane on the reflex responses of similar mesenteric veins were measured. Mesenteric vein diameter and intravenous pressure were measured in 500–1,000 μm O.D. veins from the mesentery of segments of terminal ileum externalizedin situfrom 27 New Zealand white rabbits anesthetized with alpha-chloralose. Mean arterial pressure was measured with femoral arterial cannulation, and heart rate was determined from the arterial pressure signal. In a separate group of six animals, sympathetic efferent nerve activity was measured from a postganglionic splanchnic nerve. Reflex venoconstriction and increases in mean arterial pressure and mesenteric vein pressure in response to bilateral carotid occlusion were attenuated by 0.5% and 1% inhaled halothane but not by superfusate equilibrated with 3% halothane. Decreases in mesenteric vein diameter and increases in mesenteric vein pressure in response to celiac ganglion stimulation were unaffected by both 0.5% inhaled halothane and superfusate equilibrated with 5% halothane. The bilateral carotid occlusion reflex-mediated increase in sympathetic efferent nerve activity was depressed by both 0.5% and 1% inhaled halothane. The effect of inhaled halothane on prestimulation baseline vein diameter was inconsistent. Superfusate equilibrated with 5% but not 3% halothane caused baseline venodilation. These results suggest a mechanism whereby control of venous tone is inhibited by halothane proximal to the postganglionic neuron. This could involve central or ganglionic inhibition.
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