Bomberg Hagen, Bierbach Benjamin, Flache Stephan, Novák Matous, Bandner-Risch Doris, Menger Michael D, Schäfers Hans-Joachim
Department of Thoracic and Cardiovascular Surgery, University Hospital of Saarland, Homburg/Saar, Germany.
Eur Surg Res. 2015;54(1-2):75-86. doi: 10.1159/000368355. Epub 2014 Nov 5.
BACKGROUND/AIM: Upper gastrointestinal bleeding (UGIB) is one of the most frequent gastrointestinal complications after cardiac surgery with cardiopulmonary bypass (CPB). Endothelin expression and microcirculatory dysfunction have been shown to be involved in UGIB. The aim of this study was to analyze the effect of vasopressin during CPB on the gastric mucosal microcirculation and the involvement of the endothelin system.
Eighteen pigs were randomized into three groups (n = 6 each): group I = sham, group II = CPB (1-hour CPB) and group III = CPB + vasopressin (1-hour CPB and vasopressin administration during CPB to maintain baseline arterial pressure). All animals were observed for a further 90 min after termination of CPB. Systemic hemodynamics as well as blood flow and oxygen saturation of the gastric mucosa were measured continuously. At the end of the experiment, the gastric mucosal expressions of endothelin-1 (ET-1) and its receptor subtypes A (ET(A)) and B (ET(B)) were determined by polymerase chain reaction. Gastric mucosal injury, apoptotic cell death and leukocytic infiltration were determined by histology and immunohistochemical analyses of cleaved caspase-3 and myeloperoxidase.
CPB decreased gastric microvascular perfusion, which was associated with an increased expression of ET-1 and ET(A). Vasopressin aggravated the CPB-associated malperfusion, whereas it completely abrogated the upregulation of ET-1 and ET(A). Interestingly, vasopressin did not induce gastric mucosal morphologic injury, leukocytic infiltration or apoptotic cell death.
Vasopressin aggravates CPB-associated microvascular malperfusion of the gastric mucosa but does not induce gastric mucosal injury.
背景/目的：上消化道出血（UGIB）是体外循环心脏手术后最常见的胃肠道并发症之一。内皮素表达和微循环功能障碍已被证明与UGIB有关。本研究的目的是分析体外循环期间血管加压素对胃黏膜微循环的影响以及内皮素系统的参与情况。
18只猪随机分为三组（每组n = 6）：第一组为假手术组，第二组为体外循环组（体外循环1小时），第三组为体外循环 + 血管加压素组（体外循环1小时并在体外循环期间给予血管加压素以维持基线动脉压）。在体外循环结束后，所有动物再观察90分钟。连续测量全身血流动力学以及胃黏膜的血流量和血氧饱和度。实验结束时，通过聚合酶链反应测定胃黏膜内皮素-1（ET-1）及其受体亚型A（ET(A)）和B（ET(B)）的表达。通过组织学以及对裂解的半胱天冬酶-3和髓过氧化物酶的免疫组织化学分析来确定胃黏膜损伤、凋亡细胞死亡和白细胞浸润情况。
体外循环降低了胃微血管灌注，这与ET-1和ET(A)表达增加有关。血管加压素加重了与体外循环相关的灌注不良，而它完全消除了ET-1和ET(A)的上调。有趣的是，血管加压素并未诱导胃黏膜形态学损伤、白细胞浸润或凋亡细胞死亡。
血管加压素加重了与体外循环相关的胃黏膜微血管灌注不良，但并未诱导胃黏膜损伤。
