Plasma levels and vascular effects of vasopressin in patients undergoing coronary artery bypass grafting
Plasma levels and vascular effects of vasopressin in patients undergoing coronary artery bypass grafting
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DOI：
10.1016/j.ejcts.2007.03.047
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发表时间：
2007-07-01
影响因子：
3.4
通讯作者：
Benedito, Sara
中科院分区：
文献类型：
--
作者：
Novella, Susana;Cristina Martinez, Ana;Benedito, Sara
目的：近年来研究表明，内源性血管加压素（AVP）在冠状动脉旁路移植术（CABG）中起着促痉挛作用。鉴于AVP可引起移植血管痉挛，我们评估了这种肽的释放过程中，冠状动脉旁路移植术后，并探讨如何抵消其对乳内动脉（IMA）的收缩作用。结果：血浆AVP水平在体外循环（CPB）开始后达到峰值，并与血清渗透压呈正相关（Pearson's r = 0.9490; P < 0.0001; n = 16）。在此阶段记录的血浆AVP水平与AVP在来自相同患者的血管环中引起的体外最大收缩之间观察到负相关（Pearson's r = -0.6968; P < 0.01; n = 16）。去除内皮细胞，暴露于NO前体，（3 x 10（-4）M L-精氨酸），抑制一氧化氮（NO）合酶（3 × 10（-5）M L-NAME）或可溶性鸟苷酸环化酶（3 × 10（-6）M 1H[1，2，4]恶二唑[4，3，-α]喹喔啉-1-酮（ODQ）），清除超氧阴离子（100 U/ml超氧化物歧化酶（SOD）+120 μ g/ml过氧化氢酶）或羟自由基（10（-4）M去铁胺），或特异性α（1）-（10（-6）M哌唑嗪）或内皮素（10（-5）M波生坦）受体拮抗作用。相反，腺苷酸环化酶激活（3 × 10（-8）M毛喉素）减少AVP引起的收缩反应，白色前列腺素合成（3 × 10（-6）M吲哚美辛）抑制和钙激活钾通道阻断（K-ca（10（-3）M四乙铵（TEA））增强AVP收缩。年龄，性别和吸烟也修改了AVP responsibility.Conclusion：我们的研究结果表明，作为一个调制器的血管紧张度在人类IMA的AVP的一个死记硬背。AVP的作用依赖于前列腺素和Ca ~（2+）激活的K ~+通道，因此其在病理生理心血管过程中的功能障碍可能意味着AVP，除其他因素外，在IMA移植物中产生血管痉挛。(c)2007年欧洲胸外科协会。Elsevier B. V.出版，保留所有权利。
Objective: Recent studies have suggested that endogenous vasopressin (AVP) acts as a spasmogen during coronary artery bypass grafting (CABG). Given that AVP could induce vasospasm in the grafted vessel, we assessed the release of this peptide during and after CABG, and explored ways of counteracting its contractile effect on the internal mammary artery (IMA).Methods: Plasma levels of AVP were determined by radioimmunoassay in 16 patients before, during and after CABG. Using isometric force recording techniques, we also investigated the mechanisms involved in the contractile effect of AVID in ring preparations of IMA specimens taken from 95 patients.Results: Plasma AVP levels peaked after the start of cardiopulmonary bypass (CPB) and correlated well with serum osmolality (Pearson's r = 0.9490; P < 0.0001; n = 16). An inverse correlation was observed between plasma AVP levels recorded at this stage and the maximal contraction induced in vitro by AVP in vascular rings from the same patients (Pearson's r = -0.6968; P < 0.01; n = 16). No change in the AVP response was produced by endothelium removal, exposure to the NO precursor (3 x 10(-4) M L-arginine), inhibition of nitric oxide (NO) synthase (3 X 10(-5) M L-NAME) or soluble guanylate cyclase (3 x 10(-6) M 1H[1,2,4]oxadiazol [4,3,-alpha]quinoxalin-1-one (ODQ)), removal of the superoxide anion (100U/ml superoxide dismutase (SOD) plus 120OU/ml catalase) or hydroxyl radical (10(-4) M deferoxamine), or specific alpha(1)- (10(-6) M prazosin) or endothelin (10(-5) M bosentan) receptor antagonism. In contrast, adenylate cyclase activation (3 x 10(-8) M forskolin) reduced the contractile response to AVP, white prostanoid synthesis (3 x 10(-6) M indomethacin) inhibition and blockade of Ca2+-activated potassium channels (K-ca (10(-3) M tetraethylammonium (TEA)) enhanced AVP contraction. Age, gender and smoking also modified the AVP response.Conclusion: Our findings suggest a rote for AVP as a modulator of vascular tone in human IMA. The effect of AVP is dependent on prostanoids and Ca2+-activated K+ channels, so its dysfunction in pathophysiotogical cardiovascular processes could mean that AVP, among other factors, produces vasospasm in IMA grafts. (c) 2007 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.