Inflammatory Activation after Experimental Cardiac Tamponade

Abstract

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. Methods: 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. Results: 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. Conclusions: 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.

A pericardialis tamponád kórélettana, klinikuma és állatkísérletes vizsgálati lehetőségei

“…A sebészi beavatkozás egyszerű, könnyen reprodukálható, és jól kontrollálható. A pericardium feltöltésére krisztalloid- [23] vagy kolloidoldat [24,25], esetleg az állat saját vére [26] alkalmas. A kísérletes tamponád kialakításával egyidejűleg invazív nyomásméréssel és perctérfogat-méréssel kontrollálva validálni lehet a kardiogén sokk létrejöttét.…”

Complement C5a inhibition improves late hemodynamic and inflammatory changes in a rat model of nonocclusive mesenteric ischemia

“…In an earlier study with experimental cardiac tamponade, we demonstrated activation of the complement system leading to C3 deposits in the small intestinal capillaries. 11 Accordingly, we set out to characterize the effects of the C5a inhibitor peptide acetyl-peptide-A (AcPepA) 12 on the macrocirculatory and microcirculatory changes and inflammatory reactions 24 hours after the initial insult leading to established low-flow conditions in the splanchnic area.…”

Reduction of perioperative inflammatory reaction with exogenous methane

“…In the first protocol we investigated the overall characteristics and the mesenteric consequences of temporary mechanical compression of the heart leading to microcirculatory I-R of the splanchnic system. Experimental PT is a good model to study the pathomechanism of cardiogenic shock (32,56,65,66). but it has several limitations as well.…”