Effects of Isoflurane on Brain Stem Blood Flow and Renal Sympathetic Nerve Activity during Induced Hypotension

Abstract

Effects of isoflurane on arterial blood pressure, regional blood flow in the brain stem, and renal sympathetic nerve activity were compared with those during vasodilator-induced hypotension using decerebrate unanesthetized cats. Either prostaglandin E₁ (PGE₁) or trinitroglycerin (TNG) was used to decrease the mean arterial pressure 30% below the control level. The effects of isoflurane (0.5 MAC for 15 min) were examined in the following three conditions: (1) during PGE₁-induced hypotension; (2) during TNG-induced hypotension, and (3) without either vasodilator. Isoflurane decreased the brain stem blood flow in parallel with a systemic blood pressure fall. Electrical activity of the renal sympathetic nerve consisted of a high-amplitude phasic and a low-amplitude tonic discharge. Isoflurane decreased the phasic activity and increased the tonic activity. Although the two vasodilators had a similar effect on systemic blood pressure and renal sympathetic discharge, TNG decreased the brain stem blood flow to a lesser extent than PGE₁. However, the effects of isoflurane on all parameters were statistically identical in the three conditions not treated and pretreated with either vasodilator. Also, the blood concentrations of isoflurane did not differ among the three conditions. The present study demonstrates that isoflurane produces similar effects on systemic blood pressure, regional cerebral blood flow and sympathetic efferent discharge during vasodilator-induced hypotension and without any vasodilator.

Sevoflurane and nitrous oxide anaesthesia suppresses heart rate variabilities during deliberate hypotension

“…The present result is comparable with that of Kiriyama and his colleagues in which iso¯urane anaesthesia was found to abolish the effects of prostaglandin E1 and nitroglycerin on renal sympathetic nerve activity [23]. The potent suppressive effect of volatile anaesthetics on the autonomic nervous system may eliminate the unique actions of hypotensive drugs used for deliberate hypotension.…”

Reduction of cerebral hyperemia with anti-hypertensive medication after electroconvulsive therapy

“…22 NTG and PGE1 have minimal effects on cerebral blood flow. 13 However, the results of the present study could not be explained by the known action of the drug on cerebral circulation under stable condition. Since the cerebral circulation after electrically induced seizure is thought to be different from that in normal subjects, the action of each drug can be modified by multiple factors.…”

“…[13][14] Nitroglycerin is a NO donor, which relaxes smooth muscle through a cyclic GMP-dependent cascade. 6,13 Several reports describe adrenergic blocking agents as the best choice for blood pressure control during ECT, 1 8 because activation of the adrenergic system is considered a major cause of this phenomenon. However, other anti-hypertensive medicines were also tested and reported to effectively control blood pressure.…”

Elastin insufficiency causes hypertension, structural defects and abnormal remodeling of renal vascular signaling

“…However, the use of anesthetics often confounds the determination of blood pressure phenotypes because of their effects on autonomic function and other vasoactive hormone systems that directly affect vascular resistance, including angiotensin II. [35][36][37] To characterize the type of hypertension in Eln þ/À mice, we modified the standard radiotelemetry implantation surgical protocol enabling the diurnal monitoring of blood pressure and heart rate in conscious mice. As shown in Figure 9, nighttime SBP of Eln þ/À mice on normal salt diet at baseline was markedly elevated relative to WT control mice in both sexes (Eln þ/À 136 AE 2 vs. WT 112 AE 6 mm Hg; P < 0.01).…”