Summary:The metabolic effects of graded whole body hypothermia on complete global cerebral ischemia and recirculation was investigated in the cat. Hypothermia was induced to one of three levels prior to ischemia; T = 26.8° ± OSC (n = 4), T = 32.1° ± 0.2°C (n = 5), and T = 34.6° ± 0.3°C (n = 6), and maintained constant throughout 16 min of ischemia and 1.5-2 h of recircula tion. Intracellular cerebral pH and relative concentrations of high-energy phosphate metabolites were continuously monitored, using in vivo 31p nuclear magnetic resonance (NMR) spectroscopy. Except for the first 4 min of isch emia, no significant differences were detected in the re sponse of adenylate intensities and intracellular pH to ischemia and recirculation between the hypothermic groups. The three hypothermic groups were then pooledThe effect of whole body hypothermia on cere bral metabolism has a long history (Field et aI., 1944). The possible beneficial effects of hypother mia on cerebral pathophysiological conditions have also been explored (see Siesj6, 1978). Whole body hypothermia, when applied judiciously, can curtail metabolic changes and lessen cerebral edema and neuropathologic damage associated with hypoxia (Carlsson et aI., 1976;Rosomoff 1959), and head injury (Shapiro et aI., 1974
141into one group, and the data compared to previously pub lished data from a normothermic group, T = 38.4° ± 0.6°C (n = 14), and a hyperthermic group, T = 40.6° ± 0.2°C (n = 9), subjected to the identical ischemic and NMR measurement protocols. The hypothermic animals exhibited a statistically significant reduction of cerebral intracellular acidosis, both during ischemia and recircu lation, as well as a more rapid return of adenylate inten sities during recirculation, compared to the normothermic or hyperthermic groups. The data thus suggest that mild hypothermia has an ameliorative affect on brain energy metabolism and intracellular pH under conditions of com plete global cerebral ischemia and recirculation. Key Words: 31p NMR spectroscopy-Cerebral ischemia Hypothermia-Body temperature, and cerebral ischemia. emia, including circulatory arrest, with recircula tion (Marshal et aI., 1956; Kramer et aI., 1968; Ber ing, 1974; Perna et aI., 1973; Wolin et aI., 1973;Hickey, 1985) and without recirculation (Stocker et aI., 1986); the isolated perfused brain (Norwood et aI., 1979); and focal cerebral ischemia (Simeone et aI., 1979;Rosomoff, 1957). These studies, which were performed at temperatures below 30°C, sug gest that hypothermia results in a reduction in the rate of degradation of brain energy metabolism dur ing the onset of hypothermic ischemia as well as a reduced level of brain tissue acidosis compared with normothermic ischemia. However, the clinical application of hypothermia is limited by adverse ef fects associated with level as well as the duration of hypothermia (Popovic, 1960;Michenfelder and Milde, 1977;Bjork and Hultquist, 1960; Brunberg et aI., 1974; Connolly et aI., 1962; Olesen et aI., 1971).