• Toshiharu Kasaba, Masahiko Taniguchi, and Mayumi Takasaki.
• Department of Anesthesiology, Miyazaki Medical College, 5200 Kiyotake-cho, 889-16, Miyazaki, Japan.
• J Anesth. 1997 Sep 1; 11 (3): 208-212.

PurposeTo clarify the sudden onset of profound bradycardia or hypotension during spinal anesthesia, we stimulated vagal nerves (VN) or vagosympathetic trunks (VST) to examine the effects on the autonomic nervous system during spinal anesthesia with different degrees of cardiac sympathetic nerve block.MethodsCats were anesthetized and mechanically ventilated. The left stellate ganglion was exposed to record cardiac sympathetic nerve activity (CSNA). Systolic and diastolic blood pressures (BP), heart rate (HR), and CSNA were measured before and after intrathecal injections of 0.2, 0.5 and 1.0 ml of 1% lidocaine. After each intrathecal injection of lidocaine, bilateral VST (n=5, group A) or VN (n=5, group B) were stimulated and measurements were repeated. ]RESULTS: After 1.0 ml intrathecal injection of 1% lidocaine, CSNA was blocked completely, and BP and HR were decreased. In group A, BP were unchanged following VST stimulation while in group B, BP decreased approximately 30% by VN stimulation from the pre-stimulation levels after 0.2, 0.5, and 1.0 ml injection of 1% lidocaine, respectively. HR decreased further, approximately 35% in group A and 50% in group B, by each stimulation from the prestimulation levels after 0.2, 0.5, and 1.0 ml injection of 1% lidocaine.ConclusionThese results suggest that hypotension and bradycardia during a high level of spinal anesthesia are due to the block of CSNA, and vagal reflex may produce profound hypotension and bradycardia especially in high spinal anesthesia.

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