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烧伤中乙酰胆碱诱导及一氧化氮介导的血管舒张

Acetylcholine-induced and nitric oxide-mediated vasodilation in burns.

作者信息

Meng F, Korompai F L, Lynch D M, Yuan Y S

机构信息

Department of Surgery, Texas A&M University Health Science Center, 1901 South First Street, Building 4, Temple, Texas, 76504, USA.

出版信息

J Surg Res. 1998 Dec;80(2):236-42. doi: 10.1006/jsre.1998.5475.

DOI:10.1006/jsre.1998.5475
PMID:9878319
Abstract

Microvascular endothelial cells actively participate in local regulation of blood flow and blood-tissue exchange by producing various vasoactive substances including nitric oxide (NO). This study examined microcirculatory changes in the early stage of thermal injury and the NO-related mechanisms. Resistance arterioles of rat cremaster muscle were observed using intravital microscopy. Arteriolar diameter and flow velocity were measured and flow rate was calculated after administration of various vasoactive agonists in burns. In fluid-resuscitated rats with stable systemic blood pressure, microvascular caliber and blood flow were not significantly altered in the first hour following a 25% total body surface area full-thickness scald burn. Topical application of acetylcholine (ACh), an endothelium-dependent vasodilator, increased arteriolar diameter and flow rate in a dose-dependent fashion. The dose-responsive effects of ACh were significantly greater in burned rats than in sham-burned rats, and the augmentation was blocked by inhibition of NO production with NG-monomethyl-l-arginine (L-NMMA). Topical application of adenosine, an endothelium-independent vasodilator, and sodium nitroprusside, an exogenous NO donor, markedly increased arteriolar diameter and flow rate. The effects were not significantly different in burned and sham-burned animals, and the adenosine-induced vasodilation was not blocked by L-NMMA. These data suggest that endothelium-dependent and NO-mediated arteriolar dilation is enhanced in the early stage of thermal injury. This effect may play an important role in the pathophysiological events of microcirculation and blood-tissue exchange in burns.

摘要

微血管内皮细胞通过产生包括一氧化氮(NO)在内的多种血管活性物质,积极参与局部血流调节和血液与组织的交换。本研究检测了热损伤早期的微循环变化及与NO相关的机制。采用活体显微镜观察大鼠提睾肌的阻力小动脉。在烧伤后给予各种血管活性激动剂后,测量小动脉直径和流速,并计算血流量。在全身血压稳定的液体复苏大鼠中,25%体表面积全层烫伤后第一小时,微血管口径和血流量无明显改变。局部应用内皮依赖性血管舒张剂乙酰胆碱(ACh),可使小动脉直径和流速呈剂量依赖性增加。ACh的剂量反应效应在烧伤大鼠中显著大于假烧伤大鼠,且用NG-单甲基-L-精氨酸(L-NMMA)抑制NO生成可阻断这种增强作用。局部应用非内皮依赖性血管舒张剂腺苷和外源性NO供体硝普钠,可显著增加小动脉直径和流速。在烧伤和假烧伤动物中,这些效应无显著差异,且L-NMMA不能阻断腺苷诱导的血管舒张。这些数据表明,热损伤早期内皮依赖性和NO介导的小动脉扩张增强。这种效应可能在烧伤时微循环和血液与组织交换的病理生理过程中起重要作用。

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