Metabolic correlates of neurologic and behavioral injury after prolonged hypothermic circulatory arrest  Craig K. Mezrow, MSa, Alejandro Gandsas, MDa, Ali M. Sadeghi, MDa, Peter S. Midulla, MDa, Howard H. Shiang, DVMa, Robert Green, MDb, Ian R. Holzman, MDb, Randall B. Griepp, MDa  The Journal of Thoracic and Cardiovascular Surgery  Volume 109, Issue 5, Pages 959-975 (May 1995) DOI: 10.1016/S0022-5223(95)70322-5 Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 1 Cerebral blood flow in all four experimental groups during recovery from hypothermia. Values for all time points after the start of rewarming (Table VI) are expressed as a percent of baseline cerebral blood flow. Both HCA groups showed significantly higher cerebral blood flows during rewarming when compared to baseline. Cerebral blood flow was significantly below baseline values at 2 and 4 hours after HCA and LFCPB, but not in the control group. *p < 0.05 versus baseline (37° C);a p < 0.05 versus control (18° C); b p < 0.05 versusLFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 2 Cerebral vascular resistance during recovery from hypothermia. Values for all time points after the start of rewarming (Table VI) are expressed as a percent of baseline cerebral vascular resistance. Groups are as previously described. Two and 4 hours after hypothermia, cerebral vascular resistance is significantly increased in all groups. *p < 0.05 versus baseline (37° C); a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 3 Cerebral oxygen metabolism at all time points for all four groups (see Table VII). Cerebral metabolism is significantly lower in all groups at the end of cooling but returns to baseline rates by 2 hours after the start of rewarming and is sustained at baseline levels throughout the recovery period. The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 4 Cerebral oxygen extraction for all groups during recovery from hypothermia. Values for all time points after the start of rewarming (Table VIII) are presented as a percent of baseline values. Oxygen extraction fell significantly at 30° C in the HCA groups but then increased markedly in all groups at 2 hours and in all but the hypothermic control group at 4 hours after the operation. In the 90 min HCA group, extraction of oxygen was still higher than in all other groups as late as 8 hours after the operation. *p < 0.05 versus baseline (37° C);a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 5 Sagittal sinus oxygen saturation. Values for percent saturation are given for all groups, as previously described, for all time points, corresponding to the data in Table VIII. Significant increases in sagittal sinus saturation were seen in all groups at the end of cooling, but sagittal sinus saturations were significantly depressed at 2 and 4 hours after the start of rewarming. *p < 0.05 versus baseline (37° C); a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 6 Cerebral glucose metabolism in all four groups at all time points. There was a significant reduction in the use of glucose by the brain at the end of cooling, but glucose metabolism returned promptly to baseline values after rewarming (see Table IX). *p < 0.05 versus baseline (37° C); a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 7 Cerebral glucose extraction in all four groups during recovery from hypothermia. Values were significantly increased in the 90-minute HCA group at 2, 4, and 8 hours after the operation and in the LFCPB group at 4 hours. *p < 0.05 versus baseline (37° C);a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions

Fig. 8 Ratio of cerebral blood flow (CBF) to cerebral metabolic rate of oxygen (CMRO2 ), giving an estimate of appropriateness of cerebral blood flow. Data are from Table X. A ratio similar to what is seen at baseline, when cerebral autoregulation is intact, seems likely to represent an ideal value. By this standard, all groups had significant "luxury perfusion" by the end of cooling and only the HCA groups showed a marked hyperemia at 30° C. All groups show a lower-than-ideal ratio at 2 hours, which persisted in all but the hypothermic control group at 4 hours. By 8 hours, the ratio CBF/CMRO2 had returned to values not significantly different from baseline in all groups, although the ratio was still significantly lower in the 90 min HCA group than in the other groups. *p < 0.05 versus baseline (37° C); a p < 0.05 versus control (18° C); b p < 0.05 versus LFCPB (18° C); c p < 0.05 versus 30 min HCA (18° C). The Journal of Thoracic and Cardiovascular Surgery 1995 109, 959-975DOI: (10.1016/S0022-5223(95)70322-5) Copyright © 1995 Mosby, Inc. Terms and Conditions