去甲肾上腺素对大鼠低温期间基础脑氧代谢率（CMRO2）的激活作用。

Norepinephrine activation of basal cerebral metabolic rate for oxygen (CMRO2) during hypothermia in rats.

作者信息

Nemoto E M, Klementavicius R, Melick J A, Yonas H

机构信息

Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pennsylvania, USA.

出版信息

Anesth Analg. 1996 Dec;83(6):1262-7. doi: 10.1097/00000539-199612000-00023.

DOI:10.1097/00000539-199612000-00023

PMID:8942597

Abstract

In an earlier study on the effect of mild hypothermia (34 degrees C) on the cerebral metabolic rate for oxygen (CMRO2) in rats, we used norepinephrine (NE) to support arterial blood pressure while inducing isoelectricity on the electroencephalogram (EEG) with thiopental (TP). Even with administration of sufficient TP to reduce a fully active EEG to an isoelectric EEG, CMRO2 was often unchanged. Based on this observation, we hypothesized that NE had activated CMRO2 despite thiopental coma. Therefore, we studied the effect of NE compared with donor blood (DB) infusion to maintain arterial blood pressure during TP-induced isoelectric EEG on whole-brain CBF (H2 clearance) and CMRO2 during normothermia (38 degrees C) and mild hypothermia (34 degrees C) in rats during 70% N2O/30% O2 analgesia. Cerebral blood flow (CBF) and CMRO2 were measured in four groups of rats at 38 degrees C followed by measurements at either 38 degrees C (two groups) or 34 degrees C (two groups) and during TP-induced EEG isoelectricity. Within each of the two groups at 38 degrees C and 34 degrees C, arterial pressure was sustained by either DB (n = 10) or NE (n = 9) infusion. At 38 degrees C, CMRO2 in the DB and NE groups was 7.92 +/- 1.05 and 6.4 +/- 0.80 mL x 100 g-1.min-1 and decreased to 50% of normal (3.95 +/- 0.70 and 3.32 +/- 0.40 mL x 100 g-1.min-1, respectively) during TP isoelectricity for a functional:basal CMRO2 distribution of 50% +/- 4% and 50% +/- 4%. At 34 degrees C, CMRO2 values in the DB and NE groups were 6.31 +/- 1.41 and 5.41 +/- 2.02 mL x 100 g-1.min-1, respectively. During TP-induced isoelectricity, CMRO2 values in both groups were reduced to 2.37 +/- 0.43 and 3.55 +/- 1.27 mL x 100g-1.min-1, respectively, resulting in a functional:basal CMRO2 distribution of 61%:38% in the DB group and the reverse, or 27%:73%, in the Ne group. Basal CMRO2 was significantly (P < 0.05) larger in the NE-infused rats. These results suggest that NE infusion, by increasing CMRO2 during mild hypothermia, could nullify its protective effects in the ischemic brain.

摘要

在一项早期关于轻度低温（34摄氏度）对大鼠脑氧代谢率（CMRO2）影响的研究中，我们使用去甲肾上腺素（NE）维持动脉血压，同时用硫喷妥钠（TP）诱导脑电图（EEG）出现等电位。即便给予足够的TP使完全活跃的EEG降至等电位EEG，CMRO2通常仍无变化。基于这一观察结果，我们推测尽管处于硫喷妥钠昏迷状态，NE仍激活了CMRO2。因此，我们研究了在70%氧化亚氮/30%氧气镇痛期间，在大鼠体温正常（38摄氏度）和轻度低温（34摄氏度）时，与输注供血者血液（DB）相比，输注NE以维持TP诱导的EEG等电位期间动脉血压对全脑脑血流量（H2清除率）和CMRO2的影响。在四组大鼠体温38摄氏度时测量脑血流量（CBF）和CMRO2，随后在38摄氏度（两组）或34摄氏度（两组）以及TP诱导的EEG等电位期间进行测量。在38摄氏度和34摄氏度的两组中，每组均通过输注DB（n = 10）或NE（n = 9）来维持动脉血压。在38摄氏度时，DB组和NE组的CMRO2分别为7.92±1.05和6.4±0.80 mL×100 g-1·min-1，在TP等电位期间降至正常的50%（分别为3.95±0.70和3.32±0.40 mL×100 g-1·min-1），功能性CMRO2与基础CMRO2的分布分别为50%±4%和50%±4%。在34摄氏度时，DB组和NE组的CMRO2值分别为6.31±1.41和5.41±2.02 mL×100 g-1·min-1。在TP诱导的等电位期间，两组的CMRO2值分别降至2.37±0.43和3.55±1.27 mL×100g-1·min-1，导致DB组功能性CMRO2与基础CMRO2的分布为61%:当给予去甲肾上腺素(NE)时，其分布为27%:73%。输注NE的大鼠基础CMRO2显著更大（P < 0.05）。这些结果表明，在轻度低温期间输注NE会增加CMRO2，从而可能抵消其对缺血性脑的保护作用。