BACKGROUND: Studies in experimental animals show that endogenous Arg-vasopressin (AVP) and the renin-angiotensin system support blood pressure when the sympathetic system is impaired pharmacologically or after epidural anesthesia. However, extrapolation to humans is uncertain. Therefore, we administered an AVP type V1 receptor antagonist and an angiotensin-converting enzyme inhibitor to volunteers and measured the effect on blood pressure after epidural anesthesia. METHODS:Healthy volunteers in whom epidural catheters were placed were randomly assigned to receive 1.25 mg intravenous enalapril or saline placebo followed by 0.5 mg AVP type V1 antagonist beta-mercapto-beta, beta-cyclopentamethylene-propionyl-o-Met-Tyr-Arg-vasopressin (AVPA) or saline placebo. Finally, 2% lidocaine was injected to obtain a T2 level. Controls received intramuscular lidocaine. RESULTS:Blood pressure did not significantly change after T-2 epidural anesthesia in subjects treated with saline placebo, AVPA or enalapril alone (n = 10, for each treatment). In contrast, combined treatment with enalapril and AVPA resulted in a 36 +/- 11% decrease in blood pressure after epidural dosing (n = 6). Controls given intramuscular lidocaine, in place of the epidural did not develop hypotension after AVPA and enalapril treatment (n = 10). CONCLUSIONS: Endogenous AVP and the renin-angiotensin system play important roles in maintaining blood pressure after epidural anesthesia in healthy subjects.
RCT Entities:
BACKGROUND: Studies in experimental animals show that endogenous Arg-vasopressin (AVP) and the renin-angiotensin system support blood pressure when the sympathetic system is impaired pharmacologically or after epidural anesthesia. However, extrapolation to humans is uncertain. Therefore, we administered an AVP type V1 receptor antagonist and an angiotensin-converting enzyme inhibitor to volunteers and measured the effect on blood pressure after epidural anesthesia. METHODS: Healthy volunteers in whom epidural catheters were placed were randomly assigned to receive 1.25 mg intravenous enalapril or saline placebo followed by 0.5 mg AVP type V1 antagonist beta-mercapto-beta, beta-cyclopentamethylene-propionyl-o-Met-Tyr-Arg-vasopressin (AVPA) or saline placebo. Finally, 2% lidocaine was injected to obtain a T2 level. Controls received intramuscular lidocaine. RESULTS: Blood pressure did not significantly change after T-2 epidural anesthesia in subjects treated with saline placebo, AVPA or enalapril alone (n = 10, for each treatment). In contrast, combined treatment with enalapril and AVPA resulted in a 36 +/- 11% decrease in blood pressure after epidural dosing (n = 6). Controls given intramuscular lidocaine, in place of the epidural did not develop hypotension after AVPA and enalapril treatment (n = 10). CONCLUSIONS: Endogenous AVP and the renin-angiotensin system play important roles in maintaining blood pressure after epidural anesthesia in healthy subjects.