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低温状态下犬脑温度、代谢与功能之间的关系。

The relationship among canine brain temperature, metabolism, and function during hypothermia.

作者信息

Michenfelder J D, Milde J H

机构信息

Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota 55905.

出版信息

Anesthesiology. 1991 Jul;75(1):130-6. doi: 10.1097/00000542-199107000-00021.

DOI:10.1097/00000542-199107000-00021
PMID:2064037
Abstract

Cerebral protection by hypothermia is commonly attributed to cerebral metabolic suppression. However, at temperatures below 28 degrees C, the relationship of temperature to cerebral metabolic rate of oxygen consumption (CMRO2) has not been well characterized. Accordingly, the relationship between brain temperature and CMRO2 was determined in eight dogs during cooling from 37 to 14 degrees C while the EEG was continuously monitored. Cardiopulmonary bypass was initiated and control measurements were made at 37 degrees C during anesthesia with nitrous oxide 50-60% inspired and morphine sulfate 2 mg.kg-1 intravenously (iv). Upon cooling to 27 degrees C, the nitrous oxide was discontinued and the morphine was antagonized with naloxone 2 mg iv. Measurements were repeated at 27, 22, 18, and 14 degrees C and in four dogs again at 37 degrees C after nitrous oxide 50-60% had been reestablished at 27 degrees C along with administration of morphine sulfate 2 mg.kg-1. For each temperature interval, the temperature coefficient (Q10) for CMRO2 was calculated (Q10 = CMRO2 at x degrees C divided by CMRO2 at [x - 10] degrees C). Between 37 and 27 degrees C the Q10 was 2.23, but between 27 and 14 degrees C the mean Q10 was doubled to 4.53. With rewarming to 37 degrees C, CBF and CMRO2 returned to control levels, and brain biopsies revealed a normal brain energy state. During cooling, the EEG developed burst suppression at or below 22 degrees C. With further cooling, the periods of suppression increased; however, burst activity continued in seven of eight dogs even at 14 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

低温对大脑的保护作用通常归因于大脑代谢抑制。然而,在温度低于28摄氏度时,温度与大脑氧代谢率(CMRO2)之间的关系尚未得到充分描述。因此,在八只狗从37摄氏度冷却至14摄氏度的过程中,在持续监测脑电图(EEG)的同时,测定了脑温与CMRO2之间的关系。启动体外循环,并在麻醉期间,吸入50%-60%氧化亚氮且静脉注射2mg/kg硫酸吗啡时,于37摄氏度进行对照测量。冷却至27摄氏度时,停止吸入氧化亚氮,并用2mg静脉注射纳洛酮拮抗吗啡。在27、22、18和14摄氏度重复测量,并且在27摄氏度重新建立50%-60%氧化亚氮并再次静脉注射2mg/kg硫酸吗啡后,对四只狗在37摄氏度再次测量。对于每个温度区间,计算CMRO2的温度系数(Q10)(Q10 = x摄氏度时的CMRO2除以[x - 10]摄氏度时的CMRO2)。在37至27摄氏度之间,Q10为2.23,但在27至14摄氏度之间,平均Q10翻倍至4.53。随着复温至37摄氏度,脑血流量(CBF)和CMRO2恢复到对照水平,脑活检显示脑能量状态正常。在冷却过程中,脑电图在22摄氏度及以下出现爆发抑制。随着进一步冷却,抑制期增加;然而,即使在14摄氏度时,八只狗中的七只仍有爆发活动。(摘要截短于250字)

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