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L-精氨酸可保护肠系膜血管循环,使其免受体外循环引起的血管功能障碍的影响。

L-arginine protects the mesenteric vascular circulation against cardiopulmonary bypass-induced vascular dysfunction.

作者信息

Andrási Terézia Bogdana, Soós Pál, Bakos Gellért, Stumpf Nicole, Blazovics Anna, Hagl Siegfried, Szabó Gábor

机构信息

Department of Cardiac Surgery, University of Heidelberg, Germany.

出版信息

Surgery. 2003 Jul;134(1):72-9. doi: 10.1067/msy.2003.208.

Abstract

BACKGROUND

The aim of our study was to determine whether addition of the nitric oxide donor l-arginine at reperfusion may prevent the cardiopulmonary bypass (CPB)-induced vascular alterations in the intestine.

METHODS

Twelve dogs underwent 90-minute hypothermic CPB. After 60 minutes, the cardiac arrest-treated group (n = 6) received 40 mg/kg intravenous bolus l-arginine, followed by 3 mg/kg/min infusion for 20 minutes. Hemodynamic parameters, blood gases, lactate, and glucose were monitored. Reactive hyperemia (RH) in response to superior mesenteric artery ischemia and vasorelaxation to systemically administered vasoactive drugs (acetylcholine [ACH] and sodium nitroprusside) were assessed before and after CPB and defined as percent change of vascular resistance.

RESULTS

In the control group, CPB reduced reactive hyperemia (RH) (-26 +/- 15% vs -53 +/- 5%), and the response to ACH (-30 +/- 3% vs -42 +/- 7%). In the treated group, the post-CPB endothelial dysfunction was reversed (-37 +/- 1%, P <.05 vs control group) and RH partially recovered (-34 +/- 4%, P <.05). Administration of l-arginine resulted in a higher mesenteric oxygen delivery, increased nitrite/nitrate production, and lower lactate release from the mesenteric vascular circulation after reperfusion.

CONCLUSIONS

CPB disrupts some of the regulatory functions of the endothelial cell in the mesenterium and these are mostly related to nitric oxide unavailability. Systemic supplementation of l-arginine at reperfusion prevents the CPB-induced mesenteric endothelial dysfunction in association with an increased blood distribution and a reduced metabolic impairment.

摘要

背景

我们研究的目的是确定在再灌注时添加一氧化氮供体L-精氨酸是否可预防体外循环(CPB)引起的肠道血管改变。

方法

12只犬接受90分钟的低温CPB。60分钟后,心脏骤停治疗组(n = 6)静脉推注40mg/kg的L-精氨酸,随后以3mg/kg/min的速度输注20分钟。监测血流动力学参数、血气、乳酸和葡萄糖。在CPB前后评估对肠系膜上动脉缺血的反应性充血(RH)以及对全身给予血管活性药物(乙酰胆碱[ACH]和硝普钠)的血管舒张情况,并将其定义为血管阻力的变化百分比。

结果

在对照组中,CPB降低了反应性充血(RH)(-26±15%对-53±5%)以及对ACH的反应(-30±3%对-42±7%)。在治疗组中,CPB后的内皮功能障碍得到逆转(-37±1%,与对照组相比P<.05),且RH部分恢复(-34±4%,P<.05)。L-精氨酸的给药导致再灌注后肠系膜氧输送增加、亚硝酸盐/硝酸盐生成增加以及肠系膜血管循环中乳酸释放减少。

结论

CPB破坏了肠系膜中内皮细胞的一些调节功能,这些功能大多与一氧化氮的可用性不足有关。再灌注时全身性补充L-精氨酸可预防CPB诱导的肠系膜内皮功能障碍,同时增加血液分布并减少代谢损伤。

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