ROLE OF PROSTAGLANDINS AND NITRIC-OXIDE ON HALOTHANE-INDUCED ARTERIOLAR DILATATION IN RAT DIAPHRAGM

The effects of anaesthetics on the microcirculation of the diaphragm a re incompletely understood. Therefore, we assessed by in vivo intravit al microscopy in rats the action of halothane on diaphragmatic arterio lar diameter and the role of nitric oxide and prostaglandins on haloth ane-induced diaphragmatic arteriolar diameter. We studied 54 rats anae sthetized with thiopentone. Dose-response curves to topically applied Krebs' solution saturated with halothane at increasing concentrations of 0%, 1%, 3% and 5% were carried out in the presence of an inhibitor of nitric oxide synthesis (N omega-nitro-L-arginine (LNA), 300 mu mol litre(-1)) or inhibitors of prostaglandin synthesis (mefenamic acid 20 mu mol litre(-1) or indomethacin 20 mot litre(-1)) or in the absence of any inhibitor. We found dose-dependent arteriolar dilatation which was abolished by mefenamic acid and indomethacin. In contrast, the eff ect of halothane was not modified by LNA. These data demonstrated that halothane-induced arteriolar dilatation in the diaphragm of the rat w as mediated by prostaglandins but nor by nitric oxide.