Anesthesiology · 1994
Minimum alveolar concentration for halothane in the rat is resistant to effects of forebrain ischemia and reperfusion.
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McFarlane C, Warner D S, Dexter F, Ludwig P A
Аннотация
BACKGROUND: Because glutamate antagonists can substantially alter the minimum alveolar concentration (MAC) of volatile anesthetics, glutamate has been implicated as an important neurotransmitter in processes contributing to the anesthetic state. Cerebral ischemia profoundly alters glutamatergic neurotransmission and thus may also alter halothane MAC.
METHODS: Fasted rats were surgically prepared for forebrain ischemia. One half of the animals served as operative shams (n = 24). Remaining rats underwent 10 min of bilateral carotid occlusion combined with systemic hypotension (n = 24). In animals in both groups brain circulation was restored for 1 h, 24 h, or 7 days (n = 8). At each of these intervals, MAC for halothane was determined by the tail-clamp method. Histologic damage in the hippocampus, cortex, caudoputamen, and thalamus was measured in animals allowed to survive 7 days.
RESULTS: Blood pressure, arterial blood gas tensions and pH, pericranial temperature, and plasma glucose values measured immediately before ischemia were similar among groups. Neither ischemia nor duration of reperfusion significantly altered halothane MAC as compared with operative shams (sham 1 h = 0.9 +/- 0.1 vol%, 24 h = 1.0 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%; ischemia 1 h = 0.9 +/- 0.1 vol%, 24 h = 0.9 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%). Histologic damage in the hippocampus and caudoputamen was severe in the ischemic group of animals. Mild injury was observed in the motor and cingulate cortex as well as the thalamus. There was no evidence of histologic injury in sham-operated animals.
CONCLUSIONS: The absence of effect of ischemic forebrain injury on halothane MAC is consistent with findings made in other models of supratentorial cerebral injury. These results support the contention that anatomic foci for motor responses elicited during MAC determination are localized at levels caudal to the forebrain.
METHODS: Fasted rats were surgically prepared for forebrain ischemia. One half of the animals served as operative shams (n = 24). Remaining rats underwent 10 min of bilateral carotid occlusion combined with systemic hypotension (n = 24). In animals in both groups brain circulation was restored for 1 h, 24 h, or 7 days (n = 8). At each of these intervals, MAC for halothane was determined by the tail-clamp method. Histologic damage in the hippocampus, cortex, caudoputamen, and thalamus was measured in animals allowed to survive 7 days.
RESULTS: Blood pressure, arterial blood gas tensions and pH, pericranial temperature, and plasma glucose values measured immediately before ischemia were similar among groups. Neither ischemia nor duration of reperfusion significantly altered halothane MAC as compared with operative shams (sham 1 h = 0.9 +/- 0.1 vol%, 24 h = 1.0 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%; ischemia 1 h = 0.9 +/- 0.1 vol%, 24 h = 0.9 +/- 0.1 vol%, 7 days = 1.0 +/- 0.2 vol%). Histologic damage in the hippocampus and caudoputamen was severe in the ischemic group of animals. Mild injury was observed in the motor and cingulate cortex as well as the thalamus. There was no evidence of histologic injury in sham-operated animals.
CONCLUSIONS: The absence of effect of ischemic forebrain injury on halothane MAC is consistent with findings made in other models of supratentorial cerebral injury. These results support the contention that anatomic foci for motor responses elicited during MAC determination are localized at levels caudal to the forebrain.