[Captopril potentiation of the hypotension induced by halothane]

In a double-blind study, twenty-four ASA 1 and II patients scheduled for otosclerosis surgery were randomized in two groups according to the premedication given orally 1 h before anaesthesia: placebo (group P; n = 12) or 25 mg captopril (group C; n = 12). Anaesthesia was induced with thiopentone, fentanyl and vecuronium and was maintained, after oral tracheal intubation, with N2O/O2 (50/50); 5 min after intubation, the inspired halothane concentration (FIH) was set at 1.8-2% in order to obtain a mean arterial pressure (Pa) of 45-55 mmHg; thereafter, FIH was increased or decreased (+/- 0.5% every 3 min) in order to maintain this Pa value. Ventilation was controlled in order to assure normocapnia (35-40 mmHg). Inspired and expired (FEH) halothane concentrations were monitored by an halothane analyser. The plasma renin (ARP) and conversion enzyme activities (AEC) were measured before anaesthesia (ARP1, AEC1), 5 min (ARP2) and 55 min (ARP3, AEC2) after the start of anaesthesia. In group C, AEC1 and AEC2 were reduced by half, confirming the efficiency of captopril in inhibiting the conversion enzyme. ARP1 and ARP2 were increased in group C (5.42 +/- 4.2 and 9.92 +/- 7.35 micrograms.l-1.h-1. ARP3 increased in both groups (20.75 +/- 8.42 micrograms.l-1.h-1 in group C, and 24.60 +/- 15.40 in group P). Pa decreased to 55 mmHg more rapidly in group C (9 min in group C; 18 min in group P; p less than 0.05) and FEH could be reduced by a third (1.38 +/- 0.29% in group P; 0.90 +/- 0.17% in group C; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)