Protection by Halothane of the Vagal Baroreflex System from Transient Global Cerebral Ischemia in Dogs.

Abstract

ABSTRACT-A possible cerebroprotective effect of halothane was investigated in a canine model of 5 min global cerebral ischemia.In pentobarbital-anesthetized dogs, additional inhalation of 0.5 to 1%halothane prior to ischemia prevented the post-ischemic dysfunction of the vagal component of reflex bradycardia. In contrast, pretreatment with thiopental at 10 mg/kg, i.v. failed to prevent it. The influ ence of ischemia in the absence of anesthetics was similar to that under barbiturate anesthesia. The re sults suggest that halothane, but not barbiturate, may actively protect the vagal baroreflex system from ischemia.Keywords: Cerebral ischemia, Halothane, Vagal baroreflexHalothane has been generally considered to be less cerebroprotective than barbiturates against ischemic neuronal injury (1 3). On the contrary, in the previous study (4), we found that the central vagal baroreflex system was more resistant to transient global cerebral ischemia under halothane anesthesia than barbiturates anesthesia. However, it remains to be elucidated whether halothane is actively more protective than bar biturates against the ischemic dysfunction of the baroreflex system or only less harmful for it. Thus, the present study compared the influence of the pretreat ment with halothane and thiopental on the post-ische mic dysfunction of the vagal component of reflex brady cardia in pentobarbital-anesthetized dogs. Additionally, the influence of the withdrawal of anesthesia prior to ischemia was investigated in halothane anesthetized dogs.Mongrel dogs of either sex, weighing about 6 to 17 kg, were anesthetized with sodium pentobarbital (32 mg/kg, i.v., followed by an infusion of 3.2 mg/kg/hr, i.v.) or halothane (2% in room air for induction and 0.75 to 1.0% in room air for maintenance). The ani mals were artificially ventilated (a tidal volume of 20 ml/kg at a rate of 20 breaths/min) and immobilized with suxamethonium chloride (2 mg/kg, i.v., followed by an infusion of 1 mg/kg/hr, i.v.). Arterial Pot and Pco2 were maintained at about 100 and 35 mmHg, re spectively, providing an appropriate volume of 02 and CO2 gasses via a respirator. The rectal temperature was maintained at about 38°C using a heating pad and lamp.Arterial blood pressure was measured from the left femoral artery by means of a pressure transducer (Nihon Kohden, TP-200T), and heart rate was meas ured by a heart rate counter (Nihon Kohden, AT 600G) triggered by the lead II ECG. The cortical EEG was continuously monitored from the parietal skull us ing a frequency analyzer (Nihon Kohden, OEE-7102). Reflex increase in pulse interval by 1-phenylephrine hydrochloride (0.3 to 10 ,u g/kg injected into the left cephalic vein) was correlated with the increase in mean blood pressure by the method of least squares. The slope of the regression line (msec/mmHg) was used as a measure of baroreflex sensitivity (BRS). Incomplete global cerebral ischemia was produced by a 5-min occlusion with clamps of the brachiocephalic artery and the left subclavian artery following ligations of about...

Protection by nicorandil against the dysfunction of the central vagal baroreflex system following transient global cerebral ischaemia in dogs

“…However, such a cytoprotective effect of nicorandil has yet to be established in organs other than the heart. In this context, the present study was conducted to investigate a possible cerebroprotective effect of nicorandil in a canine model of transient global cerebral ischaemia in which we have already confirmed the cerebroprotective effects of some drugs including flunarizine (Kurihara et al, 1989b;1990b), ifenprodil (Kurihara et al, 1990b), beraprost (Kurihara et al, 1990a) and halothane (Kurihara et al, 1992). The results were compared with those obtained with nitroglycerin and nicardipine.…”