NOREPINEPHRINE ACTIVATION OF BASAL CEREBRAL METABOLIC-RATE FOR OXYGEN(CMRO(2)) DURING HYPOTHERMIA IN RATS

Citation
Em. Nemoto et al., NOREPINEPHRINE ACTIVATION OF BASAL CEREBRAL METABOLIC-RATE FOR OXYGEN(CMRO(2)) DURING HYPOTHERMIA IN RATS, Anesthesia and analgesia, 83(6), 1996, pp. 1262-1267
Citations number
24
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00032999
Volume
83
Issue
6
Year of publication
1996
Pages
1262 - 1267
Database
ISI
SICI code
0003-2999(1996)83:6<1262:NAOBCM>2.0.ZU;2-Z
Abstract
In an earlier study on the effect of mild hypothermia (34 degrees C) o n the cerebral metabolic rate for oxygen (CMRO(2)) in rats, we used no repinephrine (NE) to support arterial blood pressure while inducing is oelectricity on the electroencephalogram (EEG) with thiopental (TP). E ven with administration of sufficient TP to reduce a fully active EEG to an isoelectric EEG, CMRO(2) was often unchanged. Based on this obse rvation, we hypothesized that NE had activated CMRO(2) despite thiopen tal coma. Therefore, we studied the effect of NE compared with donor b lood (DB) infusion to maintain arterial blood pressure during TP-induc ed isoelectric EEG on whole-brain CBF (H-2 clearance) and CMRO(2) duri ng normothermia (38 degrees C) and mild hypothermia (34 degrees C) in rats during 70% N2O/30% O-2 analgesia. Cerebral blood flow (CBF) and C MRO(2) were measured in four groups of rats at 38 degrees C followed b y measurements at either 38 degrees C (two groups) or 34 degrees C (tw o groups) and during TP-induced EEG isoelectricity. Within each of the two groups at 38 degrees C and 34 degrees C, arterial pressure was su stained by either DB (n = 10) or NE (n = 9) infusion. At 38 degrees C, CMRO(2) in the DB and NE groups was 7.92 +/- 1.05 and 6.4 +/- 0.80 mL . 100 g(-1) . min(-1) and decreased to 50% of normal (3.95 +/- 0.70 a nd 3.32 +/- 0.40 mL . 100 g(-1) . min(-1), respectively) during TP iso electricity for a functional:basal CMRO(2) distribution of 50% +/- 4% and 50% +/- 4%. At 34 degrees C, CMRO(2) values in the DB and NE group s were 6.31 +/- 1.41 and 5.41 +/- 2.02 mL . 100 g(-1) min(-1), respect ively. During TP-induced isoelectricity, CMRO(2) values in both groups were reduced to 2.37 +/- 0.43 and 3.55 +/- 1.27 mL . 100 g(-1) . min( -1), respectively, resulting in a functional:basal CMRO(2) distributio n of 61%:38% in the DB group and the reverse, or 27%:73%, in the NE gr oup, Basal CMRO(2) was significantly (P < 0.05) larger in the NE-infus ed rats, These results suggest that NE infusion, by increasing CMRO(2) during mild hypothermia, could nullify its protective effects in the ischemic brain.