亚低温对急性脑梗死并脑心综合征大鼠血清一氧化氮水平的影响及意义

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目的探讨亚低温对急性脑梗死并脑心综合征大鼠血清一氧化氮水平的影响及其临床意义。方法 Wistar大鼠95只,连续监测Ⅱ导联标准心电图15min,选取无心电图异常大鼠90只,随机分为亚低温组、常温组和假手术组,每组30只。亚低温组和常温组采用线栓法栓塞大鼠右侧大脑中动脉;假手术组仅分离颈总动脉、颈外动脉、颈内动脉,但不结扎及插入线栓。术后低温组维持亚低温状态2h,余2组维持正常体温。术后连续监测标准Ⅱ导联心电图2h。记录各组脑心综合征发生情况,采用ELISA法检测各组术后2、24、48h血清一氧化氮水平,并进行比较。结果假手术组均未发生脑心综合征,亚低温组脑心综合征发病率(46.7%)低于常温组(76.7%)(P<0.05);术后24、48h时常温组[(57.93±10.38)、(76.78±7.14)μmol/L]和亚低温组一氧化氮水平[(57.57±9.38)、(64.37±6.54)μmol/L]均明显高于假手术组[(51.31±11.22)、(53.02±8.65)μmol/L](P<0.05);术后2h常温组[(53.90±9.40)μmol/L]和亚低温组一氧化氮水平[(53.02±7.83)μmol/L]高于假手术组[(48.87±7.46)μmol/L],但差异无统计学意义(P>0.05);常温组术后48h时一氧化氮水平高于亚低温组(P<0.01),术后2、24h高于亚低温组,但差异无统计学意义(P>0.05)。结论亚低温可降低急性脑梗死大鼠脑心综合征发生率,其可能机制是抑制病理状态下一氧化氮水平的过度增高。 Objective To investigate the effect and its clinical significance of mild hypothermia on serum nitric oxide level in rats with acute cerebral infarction and brain-heart syndrome. Methods Ninety - five Wistar rats were continuously monitored for standard electrocardiogram Ⅱ lead for 15 minutes. Ninety rats without ECG abnormalities were randomly divided into mild hypothermia group, normal temperature group and sham operation group, with 30 rats in each group. In the mild hypothermia group and the normal temperature group, the right middle cerebral artery was embolized by thread occlusion method. Only the common carotid artery, external carotid artery and internal carotid artery were separated in the sham-operated group, but not ligated and inserted. Postoperative hypothermia maintained mild hypothermia state 2h, the remaining two groups to maintain normal body temperature. After continuous monitoring standard Ⅱ lead ECG 2h. The incidence of brain-heart syndrome in each group was recorded. The levels of serum nitric oxide at 2, 24, 48 hours after operation were detected by ELISA and compared. Results No brain-heart syndrome occurred in the sham operation group. The incidence of brainstem syndrome in the mild hypothermia group (46.7%) was lower than that in the normal temperature group (76.7%) (P <0.05) (P <0.05), and the level of nitric oxide in hypothermia group [(57.57 ± 9.38), (64.37 ± 6.54) μmol / L] were significantly higher than those in sham operation group [(51.31 ± 11.22) ± 10.38), (76.78 ± 7.14) (53.02 ± 8.63) μmol / L] in the hypothermia group (53.02 ± 8.63 μmol / L, P <0.05) (48.87 ± 7.46 μmol / L) in sham operation group, but the difference was not statistically significant (P> 0.05). The level of nitric oxide in normal temperature group was higher than that in mild hypothermia group at 48h (P <0.01) 2,24h higher than the mild hypothermia group, but the difference was not statistically significant (P> 0.05). Conclusion Mild hypothermia can reduce the incidence of brain-heart syndrome in rats with acute cerebral infarction, and its possible mechanism is to inhibit the excessive increase of nitric oxide level in the pathological state.
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