The influence of a cryogenic brain injury on the cerebrovascular response to isoflurane in the rabbit.

To determine if an acute neurologic injury alters the cerebrovascular response to isoflurane, rabbits were anesthetized with morphine/N2O, mechanically ventilated, surgically instrumented, and assigned to one of three groups. Group 1 animals (n = 8) served as controls and received no injury. In Groups 2 (n = 9) and 3 (n = 8), a 30-s cryogenic injury was produced in the left parietal region using liquid N2 poured into a funnel affixed to the surface of the skull. Regional CBF was measured using microspheres. In Groups 2 and 3, flow was determined before and then 30 and 90 min after injury or at equivalent times in Group 1. After the 90-min data were collected, 1% [approximately 0.5 minimal alveolar concentration (MAC)] and then 2% (approximately 1.0 MAC) isoflurane was administered to uninjured rabbits in Groups 1 and to lesioned rabbits in Group 3. A mean arterial pressure of greater than or equal to 80 mm Hg was maintained during isoflurane administration by an infusion of angiotensin II. In uninjured rabbits (Group 1), 2% isoflurane produced bilaterally symmetrical increases in hemispheric CBF, from 76 +/- 21 (mean +/- SD) to 150 +/- 48 ml 100 g-1 min-1. CBF in the hindbrain increased from 91 +/- 25 to 248 +/- 102 ml 100 g-1 min-1. By contrast, in the lesioned rabbits of Group 3, 2% isoflurane resulted in CBF in the lesioned hemisphere changing from 56 to only 77 ml 100 g-1 min-1 (NS), while in the contralateral hemisphere, CBF rose from 68 to 97 ml 100 g-1 min-1 (also NS). These results indicate that a cryogenic injury attenuates the normal CBF response to a volatile anesthetic, both in the damaged hemisphere as well as in apparently uninjured regions distant from the injury focus. In a separate group of animals, a similar cryogenic injury abolished the CBF response to changing PaCO2 in the injured hemisphere, but not in either the contralateral hemisphere or the cerebellum. It is possible that the CBF effects of isoflurane may be mediated via some intermediary neurogenic and/or biochemical process.