Changes in catecholamine metabolism in the rostral ventrolateral medulla following halothane and nitroprusside-induced hypotension: an in vivo electrochemical study.

The objective was to observe changes in rostral ventrolateral medulla (RVLM) catecholamine metabolism using in vivo voltammetry following induced hypotension with halothane or nitroprusside (SNP). Rats anesthetized (halothane, metocurine) and ventilated were stereotaxically implanted with carbon microelectrodes in the RVLM. The catechol oxidation current (CA.OC, % baseline) was used as an index of RVLM catecholaminergic metabolism. Groups of rats (n = 5) were given (A) halothane 0.75% for 60 min; (B) halothane 2.75% plus phenylephrine infusion to maintain mean arterial pressure (MAP) for 30 min, then halothane 0.75% for 30 min; (C) halothane (2.5-3.0%) for 30 min (MAP 60 +/- 5 mmHg) then halothane 0.75% for 30 min; (D) halothane 0.75% and sodium nitroprusside (SNP) for 30 min (MAP 60 +/- 5 mmHg), then halothane 0.75% for 30 min. Halothane 0.75% produced no significant change in CA.OC or MAP (A), while halothane 2.5-3.0% produced a significant decrease in MAP and a symmetrical significant increase in CA.OC (ANOVA, P less than 0.5). This increase peaked at 30 min (180 +/- 28%) and reached 110 +/- 9% baseline at 60 min. The halothane and phenylephrine combination produced no significant change in CA.OC or MAP during the 30 min exposure (B). SNP (D) produced a significant increase in CA.OC (peak 48 min, 224 +/- 35%) which remained elevated at 60 min (198 +/- 32%). Thus, the induced hypotension produced activation of RVLM catecholaminergic neurons. SNP induced a prolonged significant increase in RVLM catecholamine metabolism which may relate to rebound hypertension following use of this drug.