Anesthetic Effects on Blood—Brain Barrier Function during Acute Arterial Hypertension

Abstract

The effects of induced arterial hypertension on penetration of the blood-brain barrier by a protein-bound dye under anesthetic conditions causing cerebral vasoconstriction (sodium thiopental) and vasodilatation (halothane) was studied. Adult New Zealand white rabbits (48) were anesthetized with N2O, 70% O2, 30% and pancuronium bromide, 0.8 mg/kg. Ventilation was regulated to maintain PaCO2 (arterial pressure of CO2) 35 .+-. 2 torr in 32 animals and 22 .+-. 2 torr in 16 animals. Either thiopental in repetitive doses (30-60 mg/kg) or halothane was added to decrease mean arterial blood pressure to 40 torr in 3 min. Evans'' blue dye (3%, 4 ml/kg) was infused i.v., after which various doses of norepinephrine were administered to obtain increases in mean blood pressure of 100-140 torr in 5-40 s. After sacrifice of the rabbits, standardized serial coronal sections were examined under incident light for evidence of Evan''s blue dye extravasation. Dye passage across the blood-brain barrier was significantly greater (P < .05) in rabbits anesthetized with halothane than in those anesthetized with thiopental at normo- and hypocarbia. Mean dye penetration indices (.+-. SE) for halothane-normocarbia, halothane-hypocarbia and thiopental-normocarbia were 21.4 .+-. 7.9, 9.9 .+-. 3.8 and 1.5 .+-. 0.9, respectively. Dye penetration was greatest in grey matter, concentrated around the lateral sagittal fissure and tended to spread in the anastomotic zones between major cerebral arteries. In contrast to thiopental, halothane anesthesia appears to enhance the extravasation of plasma proteins into normal brain during acute arterial hypertension, which may contribute to the development of cerebral edema.