Key result
Inhalation of 0.5 to 1% halothane prior to 5-min global cerebral ischemia prevented post-ischemic dysfunction of the vagal component of reflex bradycardia in dogs, unlike thiopental.
Why the study?
Does halothane prevent post-ischemic dysfunction of the vagal baroreflex system in a canine model of global cerebral ischemia?
Does halothane prevent post-ischemic dysfunction of the vagal baroreflex system in a canine model of global cerebral ischemia?
Halothane, but not barbiturates, may actively protect the vagal baroreflex system from transient global cerebral ischemia in a canine model.
Answers are grounded in this paper and cite their sources.
Should not guide anesthetic choice in cerebral ischemia; leaves open clinical translation of halothane's vagal effects.
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 influence of ischemia in the absence of anesthetics was similar to that under barbiturate anesthesia. The results suggest that halothane, but not barbiturate, may actively protect the vagal baroreflex system from ischemia.
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Kurihara et al. (1992) studied Transient global cerebral ischemia. Halothane vs. Thiopental or absence of anesthetics was evaluated on Post-ischemic dysfunction of the vagal component of reflex bradycardia. Inhalation of 0.5 to 1% halothane prior to 5-min global cerebral ischemia prevented post-ischemic dysfunction of the vagal component of reflex bradycardia in dogs, unlike thiopental.
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