Abstract

THAT opiate receptors may mediate the action of inhalation anaesthetics is evident from the fact that intravenous injection of naloxone decreases the pain threshold in rats during inhalation anaesthesia1,2. But inhalation anaesthetics have not only analgesic and hypnotic properties, they also cause undesirable depression of the cardiovascular system. To investigate whether opiate receptors mediate the cardiovascular response to inhalation anaesthesia we perfused continuously the cerebro-ventricular system of both conscious and anaesthetised dogs with naloxone. Effects of anaesthesia with and without naloxone perfusion were compared for blood pressure, heart rate and baroreflex activity. The constant perfusion technique was adopted to avoid the drastic transients of naloxone brain concentrations which occur following intravenous naloxone application3,4 and which might have masked the naloxone effects in recent reports5–7. We show here that (−)naloxone in contrast to (+)naloxone is capable of antagonising the circulatory effects of halothane anaesthesia from the fourth cerebral ventricle.

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