title: Does isoflurane alter mesenteric venous capacitance in the intact rabbit?
abstract: Volatile anesthetics act at a number of sites to alter cardiovascular function and the response of the cardiovascular system to barostatic reflexes. We examined the effects of isoflurane on reflex regulation of mesenteric venous capacitance vessels. To determine whether isoflurane alters mesenteric venous capacitance, continuous direct observations of mesenteric vein diameter, intravenous pressure, and mesenteric sympathetic efferent nerve activity (SENA) were made in 31 chloralose-anesthetized New Zealand white rabbits. Simultaneous measurements were obtained for aortic pressure and heart rate. The responses to changes in baroreceptor activation by means of either bilateral carotid occlusion (BCO) or aortic nerve stimulation (ANS) were studied in one group of 18 rabbits, while the response to direct electric activation by means of celiac ganglion stimulation (CGS) was studied in another group of 13 rabbits. In both groups, isoflurane vapor was administered at levels of 0.75% or 1.5%, and superfused isoflurane was administered directly to the vessel in doses of either 3% or 5% equilibrated with physiologic salt solution. Anesthetic levels were verified by mass spectrometry for expired gas and by gas chromatography for blood and superfusate levels. Inhaled isoflurane reduced hemodynamic variables and SENA in a dose-dependent fashion, but these same variables were unaffected by superfused isoflurane. One and one-half percent inhaled isoflurane abolished all reflex responses to baroreceptor stimulation in mesenteric capacitance veins and in SENA, but superfused isoflurane produced no corresponding attenuation of reflex responses to baroreceptor stimulation. Neither inhaled nor superfused isoflurane suppressed the reflex venoconstriction in response to CGS. Both inhaled and superfused isoflurane dilated the baseline vein diameter before stimulation. These results indicate that isoflurane dose increase the diameter of mesenteric venous capacitance vessels and inhibits reflex-induced constriction of mesenteric veins, whereas mesenteric sympathetic efferent nerve activity decreases and the reflex responses to activation of the carotid sinus and aortic baroreceptors are attenuated by inhaled isoflurane. The mechanism of this action appears to be primarily through the inhibition of central or peripheral sympathetic ganglionic transmission of barostatic control.
authors: Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
authors: J B
authors: JB
authors: McCallum
authors: T A
authors: TA
authors: Stekiel
authors: Z J
authors: ZJ
authors: Bosnjak
authors: J P
authors: JP
authors: Kampine
mesh_terms: D000818:Animals; D006439:Hemodynamics / Q000502:physiology; D006706:Homeostasis; D007530:Isoflurane / Q000494:pharmacology*; D008297:Male; D008642:Mesenteric Veins / Q000187:drug effects* / Q000294:innervation / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology
chemical_list: D007530:Isoflurane