Inhibition of sympathetic neural outflow during thiopental anesthesia in humans.

The effects of sodium thiopental on postganglionic muscle sympathetic nerve activity (MSNA) and the reflex augmentation in MSNA produced by hypotension were examined in seven ASA physical status I and II patients, 34-65 yr old. Direct recordings of MSNA were obtained from a 5-micron-tipped, epoxy-coated needle percutaneously placed into the common peroneal nerve. Induction of anesthesia with sodium thiopental (4 mg/kg) significantly decreased R-R interval duration an average of 157 +/- 44 ms (mean +/- SEM) decreased systolic pressure (radial artery) an average of 11 +/- 4 mm Hg, and reduced tonic MSNA from 38 +/- 11 to 18 +/- 5 bursts/100 cardiac cycles (P less than 0.01). Baroreceptor reflex regulation of cardiac intervals and MSNA were determined by sequential boluses of nipride (100 micrograms) and phenylephrine (150 micrograms). Awake baroreceptor slopes relating R-R interval to systolic pressure were 9.5 +/- 2.9 ms/mm Hg and decreased 61% to 2.4 +/- 0.5 ms/mm Hg (P less than 0.01) during sodium thiopental infusions (0.25 mg.kg-1.min-1). Moreover baroreceptor slopes relating MSNA to diastolic pressure in awake patients were -4.0 +/- 0.9 bursts/mm Hg and were reduced by 95% to -0.3 +/- 0.18 bursts/mm Hg (P less than 0.01). Despite the fact that hypotension did not elicit increases in MSNA in anesthetized patients, laryngoscopy and tracheal intubation produced profound augmentations in MSNA. Thus, sodium thiopental reduces tonic levels of MSNA and markedly attenuates baroreceptor reflex control mechanisms. However, profound augmentations in sympathetic activity occurred in response to laryngoscopy and tracheal intubation during thiopental anesthesia.