Bari Gábor, Szűcs Szilárd, Érces Dániel, Boros Mihály, Varga Gabriella
Department of Cardiac Surgery, Szeged University, Szeged, Hungary.
Institute of Surgical Research, Szeged University, Szeged, Hungary.
Turk J Surg. 2018 Sep 1;34(3):205-211. doi: 10.5152/turkjsurg.2018.4181. eCollection 2018.
Pericardial tamponade is a life-threatening medical emergency, when the hemodynamic consequences of low cardiac output severely disturb the perfusion of the peripheral tissues. Our aim was to design a reliable large animal model to reproduce the clinical scenario with the relevant pathophysiological consequences of pericardial tamponade -induced cardiogenic shock.
Anesthetized Vietnamese mini pigs were used (n=12). Following laparotomy, a cannula was fixed into the pericardium through the diaphragm without thoracotomy. A sham-operated group (n=6) served as control, while in the second group (n=6) pericardial tamponade was induced by intra-pericardial injection of heparinized own blood. Throughout the 60-min pericardial tamponade and the 180-min reperfusion, macro hemodynamics, renal circulation and the mesenteric macro- and micro-circulatory parameters were monitored. Myeloperoxidase activity was measured to detect neutrophil leukocyte accumulation and in vivo histology was performed by confocal laser scanning endomicroscopy to observe the structural changes of the intestinal mucosa.
PT increased the central venous pressure, heart rate, and decreased mean arterial pressure. The mesenteric artery flow (from 355.5±112.4 vs 182.0±59.1 mL/min) and renal arterial flow (from 159.63±50.7 vs 35.902±27.9 mL//min) and the micro-circulation of the ileum was reduced. The myeloperoxidase activity was elevated (from 3.66±1.6 to 7.01±1.44 mU/mg protein) and manifest injury of the ileal mucosa was present.
This experimental model suitably mimics the hemodynamics and the pathology of clinical pericardial tamponade situations, and on this basis, it provides an opportunity to study the adverse macro- and micro-circulatory effects and biochemical consequences of human cardiogenic shock.
心包填塞是一种危及生命的医疗急症,此时低心输出量的血流动力学后果会严重干扰外周组织的灌注。我们的目的是设计一种可靠的大型动物模型,以重现心包填塞所致心源性休克的临床情况及其相关病理生理后果。
使用麻醉后的越南小型猪(n = 12)。开腹后,通过膈肌将套管固定于心包,无需开胸。一组假手术组(n = 6)作为对照,另一组(n = 6)通过心包内注射肝素化自体血诱导心包填塞。在整个60分钟的心包填塞和180分钟的再灌注过程中,监测宏观血流动力学、肾循环以及肠系膜的宏观和微观循环参数。测量髓过氧化物酶活性以检测中性粒细胞积聚,并通过共聚焦激光扫描内镜进行体内组织学检查,以观察肠黏膜的结构变化。
心包填塞增加了中心静脉压、心率,并降低了平均动脉压。肠系膜动脉血流量(从355.5±112.4降至182.0±59.1 mL/分钟)和肾动脉血流量(从159.63±50.7降至35.902±27.9 mL/分钟)以及回肠微循环减少。髓过氧化物酶活性升高(从3.66±1.6升至7.01±1.44 mU/毫克蛋白),回肠黏膜出现明显损伤。
该实验模型能很好地模拟临床心包填塞情况的血流动力学和病理学,在此基础上,为研究人类心源性休克的不良宏观和微观循环影响及生化后果提供了机会。