摘要
目的：探讨亚低温疗法对急性创伤性脑水肿后一氧化氮及其合成酶变化的影响机制。方法：建立大鼠创伤性脑水肿模型，测定伤后不同时间点常温下及亚低温后颈内静脉血一氧化氮、脑组织一氧化氮合成酶和脑含水量。结果：致伤后３０分钟大鼠即出现脑水肿，伤后８小时达高峰（从伤前７７．６３％±０．２１％升至７９．８３％±０．４１％）；一氧化氮具有同步效应〔从伤前（２．４４±０．１２）μｍｏｌ／Ｌ升至（７．８３±０．２７）μｍｏｌ／Ｌ〕；一氧化氮合成酶伤后３０分钟达高峰〔从伤前（３８．８９±４１．３０）μｍｏｌ·ｍｉｎ－１·ｇ－１升至（１０６．５８±５２．４６）μｍｏｌ·ｍｎ－１·ｇ－１〕，以后逐渐下降，伤后８小时〔（５８．２９±１９．４２）μｍｏｌ·ｍｉｎ－１·ｇ－１〕仍高于假手术组。而亚低温（３２～３３℃）能明显减轻脑水肿，减少一氧化氮含量及一氧化氮合成酶的表达〔伤后８小时分别为７９．５６％±０．２７％，（６．８４±０．３７）μｍｏｌ／Ｌ，（５１．０２±２４．５１）μｍｏｌ·ｍｉｎ－１·ｇ－１〕。结论：一氧化氮在创伤性脑水肿发生发展中起作用，而亚低温可能抑制一氧化氮合成酶的表达，减少一氧化氮含量，对创伤性脑水肿有一定保护作用。
Objective:To investigate the influence of subhypothermia on nitric oxide (NO) and nitric oxide synthase (NOS) after acute traumatic brain edema and its potential mechanism(s).Methods:Using a rat model of acute traumatic brain edema,NO levels in blood samples from intrajugulary vein,NOS and water contents in brain tissue were measured in both normoand subhypothermia at 30 minutes,2,4 and 8 hours after head injury .Results:Elevation of NO levels and brain edema were found at 30 minutes,both reaching peaks at 8 hours after injury water content:77 63%±0 21% vs. 79 83%±0 41%;NO:(2 44±0 12)μmol/L vs. (7 83±0 27) μmol/L .NOS activity reached a peak at 30 minutes (38 89±41 30)μmol·min -1 ·g -1 vs. (106 58±52 46) μmol·min -1 ·g -1 ,then it progressively decreased and still marked high (58 29± 19 42)μmol·min -1 ·g -1 compared with shamoperation group at 8 hours after injury.However,treatment with subhypothermia (32～33 ℃) could significantly attenuated brain edema and reduced NO content and NOS expression 79 56%±0 27%,(6 84±0 37)μmol/L,and(51 02±24 51)μmol·min -1 ·g -1 ,respectively . Conclusions :These data suggest that NO may play an important role in the development of traumatic brain edema,subhypothemia has inhibitory effect on NO formation and NOS expression,providing beneficial protection on acute brain edema.
出处
《中国危重病急救医学》
CSCD
1999年第2期87-89,共3页
Chinese Critical Care Medicine
基金
湖北省十堰市科技重点计划项目基金
关键词
脑水肿
创伤性
亚低温
一氧化氮
一氧化氮合成酶
traumatic brain edema\ \ subhypothermia\ \ nitric oxide\ \ nitric oxide synthase
