Vass A, Süveges G, Érces D, Nógrády M, Varga G, Földesi I, Futakuchi M, Imai M, Okada N, Okada H, Boros M, Kaszaki J
Institute of Surgical Research, University of Szeged, Szeged, Hungary.
Eur Surg Res. 2013;51(1-2):1-13. doi: 10.1159/000352089. Epub 2013 Jul 12.
BACKGROUND/PURPOSE: Cardiac tamponade is a medical emergency situation associated with a high rate of life-threatening complications, even after immediate interventions. Our aim was to characterize the acute inflammatory consequences of this event in a clinically relevant large animal model.
Cardiac tamponade was induced for 60 min in anesthetized, ventilated and thoracotomized minipigs by intrapericardial fluid administration, the mean arterial pressure (MAP) being maintained in the interval of 40-45 mm Hg (n = 8). A further group (n = 7) served as sham-operated control. The global macrohemodynamics, including the right- and left-heart end-diastolic volumes (RHEDV and LHEDV), the pulmonary vascular resistance index (PVRI) and the superior mesenteric artery (SMA) flow, were monitored for 240 min, and the intestinal microcirculatory changes (pCO2 gap) were evaluated by indirect tonometry. Blood samples were taken for the determination of cardiac troponin T and vasoactive inflammatory mediators, including histamine, nitrite/nitrate, big-endothelin, superoxide and high-mobility group box protein-1 levels in association with intestinal leukocyte and complement activation.
The cardiac tamponade induced significant decreases in MAP, cardiac output, LHEDV and SMA flow, while the PVRI and the pCO2 gap increased significantly. After the removal of fluid from the pericardial sac, the MAP and the LHEDV were decreased, while the PVRI and the pCO2 gap remained elevated when compared with those in the sham-operated group. In the posttamponade period, the abrupt release of inflammatory mediators was accompanied by a significant splanchnic leukocyte accumulation and complement activation.
The macrocirculatory and splanchnic microcirculatory disturbances were accompanied by a significant proinflammatory reaction; endothelin and the complement system may be significant components of the inflammatory cascade that is activated in this porcine model of pericardial tamponade.
背景/目的：心脏压塞是一种医疗紧急情况，即使经过立即干预，仍与高发生率的危及生命的并发症相关。我们的目的是在一个具有临床相关性的大型动物模型中，描述该事件的急性炎症后果。
通过心包内注入液体，在麻醉、通气并开胸的小型猪中诱导心脏压塞60分钟，平均动脉压（MAP）维持在40 - 45 mmHg之间（n = 8）。另一组（n = 7）作为假手术对照组。监测240分钟的整体宏观血流动力学，包括右心和左心舒张末期容积（RHEDV和LHEDV）、肺血管阻力指数（PVRI）和肠系膜上动脉（SMA）血流，并通过间接张力测定法评估肠道微循环变化（pCO2差值）。采集血样以测定心肌肌钙蛋白T和血管活性炎症介质，包括组胺、亚硝酸盐/硝酸盐、大内皮素、超氧化物和高迁移率族蛋白-1水平，并与肠道白细胞和补体激活相关联。
心脏压塞导致MAP、心输出量、LHEDV和SMA血流显著降低，而PVRI和pCO2差值显著增加。心包腔内液体清除后，与假手术组相比，MAP和LHEDV降低，而PVRI和pCO2差值仍升高。在心脏压塞后时期，炎症介质的突然释放伴随着显著的内脏白细胞积聚和补体激活。
宏观循环和内脏微循环紊乱伴随着显著的促炎反应；内皮素和补体系统可能是在该猪心包压塞模型中被激活的炎症级联反应的重要组成部分。
