ANESTHETIC AGENT CHOICE INFLUENCES OUTCOME FROM EXPERIMENTAL PERIOPERATIVE STROKE
It is unclear if damage during perioperative stroke is linked to the anesthetic agent employed during prior surgical procedure. We examined 2 representative agents, propofol and halothane, to test the hypothesis that anesthetic “preconditioning” improves outcome from middle cerebral artery occlusion (MCAO) induced on emergence from short or prolonged anesthesia. Male Wistar rats (200–300 g) were anesthetized briefly (<1 h) with halothane (1–2%) for placement of a femoral arterial and venous catheter and of a retaining sleeve for chronic laser Doppler perfusion (LDP) probe on the cranium. Twenty fours hours following instrumentation, spontaneously ventilated rats were reanesthetized with either halothane (1–2%) or intravenous propofol (10 mg/kg bolus and 30 mg/kg/hr infusion). Rats were subjected to 2 h of MCAO following exposure to either short (< 1 hr;n=8, Short-Hal; n=8, Short-Prop) or long (8 hr) (n=8, Long-Hal; n=8, Long-Prop) anesthetic. Anesthesia was discontinued after the first 15 min of cerebral ischemia, which was documented by abrupt fall in LDF-signal during suture placement. Pericranial temperature, PaO2, PaCO2 and blood pressure were maintained in a normal range, without differences between groups. LDP-signal between groups was silmiar during MCAO and reperfusion. At 22 h of reperfusion, brain infarction volume was determined by TTC-staining. Preconditioning with short duration of halothane resulted in smaller infarction in cortex (87.5 ± 16.6 mm3, 23.5 ± 4.4% of ipsilateral cortex) and caudoputamen complex (CP) (38.3 ± 13.7 mm3, 46.0 ± 5.2% of ipsilateral CP) than in rats preconditioned with equivalent propofol (cortex 177.5 ± 16.9 mm3; 46.6 ± 4.4%; CP 47.8 ± 2.9 mm3, 60.8 ± 3.7%). There was no difference in rats preconditioned with Long-Hal or Long-Prop. Halothane but not propofol preconditioning of <1 hour decreases brain vulnerability to subsequent ischemic insults initiated during emergence from anesthesia. Exposure to longer durations of halothane may activate secondary pathways which negate the protective effects of short-term halothane preischemic conditioning.