To the Editor:-In their recent report entitled “Sevoflurane Inhibits Human Platelet Aggregation and Thromboxane A2Formation, Possibly by Suppression of Cyclooxygenase Activity”(Hirakata H et al., Anesthesiology 1996; 85:1447–53), the authors demonstrate deterioration in platelet functions by a low concentration of sevoflurane, 0.5%. Such a strong inhibitory effect on platelet aggregation is inconsistent with the fact that clinically serious hemorrhagic complications have never been observed in sevoflurane anesthesia. Although their study is well done and informative, we have one concern about their methodology. They used ethanol in the platelet samples to dissolve inhalation anesthetics. Ethanol has been generally recognized to inhibit platelet aggregability.  Moreover, the reporter findings that similar concentration of ethanol did not affect platelets were obtained using rabbits and rats. The platelet reaction to the aggregating agents differs with the spacies.  For example, rabbit and rat platelets show essentially the primary aggregation alone in an adenosine diphosphate (ADP)-induced aggregation study. [2,3] In a human in vitro study using ADP, platelet aggregation was inhibited even with ethanol at less than 100 mM [3,4](they used 0.5% v/v of ethanol, which corresponds to approximately 100 mM). Thus, the inhibitory effect they demonstrated might be attributed to ethanol. We found that platelet aggregation in healthy volunteers (n = 5) is inhibited by ethanol at the same concentration as they used on platelet aggregation. We conclude that the inhibitory effect of sevoflurane on platelet aggregation they reported is attributed to the presence of sevoflurane and ethanol.
Hiroshi Aoki, M.D.
Toshiki Mizobe, M.D., Ph.D.; Department of Anesthesiology; Kyoto Prefectural University of Medicine
Kamigyo-ku; Kyoto, Japan 602