BACKGROUND: Halothane and isoflurane are known to attenuate neurally mediated regulation of mesenteric vein diameter. The current study evaluated the effects of enflurane on baroreflex control of small mesenteric veins. METHODS: Changes in mesenteric vein diameter, intravenous pressure, mean arterial pressure, and heart rate in response to bilateral carotid occlusion, aortic nerve stimulation, and celiac ganglion stimulation were measured in 23 chloralose-anesthetized rabbits before, during, and after 1% and 2% inhaled enflurane administration. In six other rabbits, sympathetic efferent nerve activity was recorded directly from a postganglionic splanchnic nerve, also during bilateral carotid occlusion and aortic nerve stimulation, before, during, and after inhalation of 1% and 2% enflurane. RESULTS: Baseline mean arterial pressure and heart rate decreased, and mesenteric vein diameter increased, in response to inhaled enflurane. Reflex venoconstriction and the increases in mean arterial pressure, intravenous pressure, and heart rate, in response to bilateral carotid occlusion, were significantly inhibited at both levels of inhaled enflurane. Decreases in mean arterial pressure and heart rate, and reflex venodilation in response to aortic nerve stimulation, were attenuated by 2%, but not 1%, enflurane. Mesenteric venoconstriction, blood pressure increase, and bradycardia in response to celiac ganglion stimulation were unaffected by 2% inhaled and 5% superfused enflurane. Both 1% and 2% inhaled enflurane attenuated resting and carotid sinus-mediated increases in sympathetic efferent nerve activity. CONCLUSIONS: These results indicate that enflurane alters splanchnic venous reflexes in large part via the inhibition of sympathetic efferent activity.
BACKGROUND:Halothane and isoflurane are known to attenuate neurally mediated regulation of mesenteric vein diameter. The current study evaluated the effects of enflurane on baroreflex control of small mesenteric veins. METHODS: Changes in mesenteric vein diameter, intravenous pressure, mean arterial pressure, and heart rate in response to bilateral carotid occlusion, aortic nerve stimulation, and celiac ganglion stimulation were measured in 23 chloralose-anesthetized rabbits before, during, and after 1% and 2% inhaled enflurane administration. In six other rabbits, sympathetic efferent nerve activity was recorded directly from a postganglionic splanchnic nerve, also during bilateral carotid occlusion and aortic nerve stimulation, before, during, and after inhalation of 1% and 2% enflurane. RESULTS: Baseline mean arterial pressure and heart rate decreased, and mesenteric vein diameter increased, in response to inhaled enflurane. Reflex venoconstriction and the increases in mean arterial pressure, intravenous pressure, and heart rate, in response to bilateral carotid occlusion, were significantly inhibited at both levels of inhaled enflurane. Decreases in mean arterial pressure and heart rate, and reflex venodilation in response to aortic nerve stimulation, were attenuated by 2%, but not 1%, enflurane. Mesenteric venoconstriction, blood pressure increase, and bradycardia in response to celiac ganglion stimulation were unaffected by 2% inhaled and 5% superfused enflurane. Both 1% and 2% inhaled enflurane attenuated resting and carotid sinus-mediated increases in sympathetic efferent nerve activity. CONCLUSIONS: These results indicate that enflurane alters splanchnic venous reflexes in large part via the inhibition of sympathetic efferent activity.