Normalization of Cerebral Blood Flow during Prolonged Halothane Anesthesia

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Abstract
The effects of 150 min halothane (1% inspired in 100% O2) anesthesia on cerebral blood flow (CBF), cerebral metabolic rate for O2 (CMRO2), cerebral vascular resistance (CVR), cardiac output (CO) and cerebral autoregulation of blood flow (CA) were determined in normal goats and in goats following .alpha.- and .beta.-receptor blockade. In normal goats, CBF increased significantly from an awake value of 65 .+-. 5 ml .cntdot. min-1 .cntdot. 100 g-1 to 135 .+-. 12 ml .cntdot. min-1 .cntdot. 100 g-1 following 30 min of halothane anesthesia. After .apprx. 30 min, CBF began to decrease and approached pre-inhalation levels at 150 min. Cerebral vascular resistance and CMRO2 decreased during the first 30 min of inhalation, but significantly increased over the next 120 min of anesthesia. Cardiac output decreased significantly with induction of anesthesia, remained below awake values throughout the 150 min of halothane inhalation, and returned to pre-inhalation levels following anesthesia. Mean arterial blood pressure (MABP) increased slightly, but not significantly after halothane was terminated. Alpha- and .beta.-receptor blockade with phentolamine and propranolol failed to alter the course of CBF, CVR and CMRO2 throughout the entire experimental period as compared with control values. CO failed to return to pre-inhalation levels upon emergence from anesthesia. MABP was significantly lower than the nontreated goats upon emergence from anesthesia. Arterial injections of angiotensin (1 .mu.g) were administered periodically during the 150 min of anesthesia in order to challenge CA. Cerebral blood flow increased significantly in both normal and receptor-blocked animals with each angiotensin injection indicating a loss of CA to rapid increases in MABP. The initial rise in CBF usually associated with halothane inhalation is a transient phenomenon after which CBF gradually returns to control levels over a protracted period of time. The return of CBF to control values is unrelated to CA and is not influenced by .alpha.- and .beta.-adrenergic receptor blockade.