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Failure of clinical concentrations of halothane to block adenosine diphosphate-induced platelet aggregation in vitro
A dose-related inhibition by halothane of adenosine diphosphate-induced platelet aggregation was measured for human platelets in plasma anticoagulated with sodium citrate 6.8 mmol litre-1 or 13.6 mmol litre-1, or heparin 2 u. ml-1 and for platelets separated from plasma by albumin density gradient centrifugation and requiring no anticoagulant. By maintaining exposure and assay temperature at 37 degrees C, maintaining physiological pH, avoiding age-related deterioration and using an atraumatic equilibration method, no inhibition was found at clinical concentrations of halothane and 50% inhibition required greater than halothane 10%. Sodium citrate, a calcium chelating anticoagulant, was found to enhance halothane inhibition.
A dose-related inhibition by halothane of adenosine diphosphate-induced platelet aggregation was measured for human platelets in plasma anticoagulated with sodium citrate 6.8 mmol litre-1 or 13.6 mmol litre-1, or heparin 2 u. ml-1 and for platelets separated from plasma by albumin density gradient centrifugation and requiring no anticoagulant. By maintaining exposure and assay temperature at 37 degrees C, maintaining physiological pH, avoiding age-related deterioration and using an atraumatic equilibration method, no inhibition was found at clinical concentrations of halothane and 50% inhibition required greater than halothane 10%. Sodium citrate, a calcium chelating anticoagulant, was found to enhance halothane inhibition.