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L-精氨酸和L-硝基精氨酸治疗对兔内毒素休克模型血压和心输出量的影响。

Effects of L-arginine and L-nitro-arginine treatment on blood pressure and cardiac output in a rabbit endotoxin shock model.

作者信息

Pastor C, Teisseire B, Vicaut E, Payen D

机构信息

Department of Anesthesiology and Intensive Care, Lariboisière University Hospital, Paris, France.

出版信息

Crit Care Med. 1994 Mar;22(3):465-9. doi: 10.1097/00003246-199403000-00017.

Abstract

OBJECTIVE

To verify the effect of nitric oxide system modification during sepsis, not only in terms of pressure but also in terms of perfusion flow.

DESIGN

Experimental, comparative study.

SETTING

Laboratory of a university hospital.

SUBJECTS

Twenty-six New Zealand male rabbits (2 to 2.5 kg body weight) were studied under anesthesia.

INTERVENTIONS

Nitric oxide pathways were modified during shock-induced hypotension, using L-arginine (600 mg/kg) and L-nitro-arginine (7.5 mg/kg), which were infused 75 mins after endotoxin injection.

MEASUREMENTS AND MAIN RESULTS

Mean arterial pressure (MAP) and cardiac output, as well as ascending aortic velocity, were measured and aortic conductance (aortic velocity/MAP in cm/sec/mm Hg) was calculated. Both L-arginine and L-nitro-arginine increased MAP to the pre-endotoxin level, but only L-arginine increased aortic velocity in association with a marked increase in aortic conductance (p < .001). L-nitro-arginine significantly (p < .05) decreased aortic velocity as compared with the control endotoxin group, with an intense vasoconstriction as shown by a significant (p < .001) decrease in aortic conductance.

CONCLUSIONS

These results, along with the high mortality rate in the L-nitro-arginine treated group, challenge the hypothesis that nitric oxide release inhibition has a beneficial effect in septic shock.

摘要

目的

验证脓毒症期间一氧化氮系统调节的效果,不仅要从压力方面,还要从灌注流量方面进行验证。

设计

实验性对比研究。

地点

大学医院实验室。

对象

26只新西兰雄性兔(体重2至2.5千克)在麻醉状态下接受研究。

干预措施

在内毒素注射75分钟后,使用L-精氨酸(600毫克/千克)和L-硝基精氨酸(7.5毫克/千克),在休克诱导的低血压期间对一氧化氮途径进行调节。

测量指标及主要结果

测量平均动脉压(MAP)、心输出量以及升主动脉速度,并计算主动脉传导率(主动脉速度/MAP,单位为厘米/秒/毫米汞柱)。L-精氨酸和L-硝基精氨酸均使MAP升高至内毒素注射前水平,但只有L-精氨酸增加了主动脉速度,同时主动脉传导率显著增加(p <.001)。与内毒素对照组相比,L-硝基精氨酸显著(p <.05)降低了主动脉速度,主动脉传导率显著降低(p <.001),表明出现强烈的血管收缩。

结论

这些结果,连同L-硝基精氨酸治疗组的高死亡率,对一氧化氮释放抑制在感染性休克中有有益作用这一假说提出了挑战。

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