Postoperative immunosuppression after open and laparoscopic liver resection: assessment of cellular immune function and monocytic HLA-DR expression.

BACKGROUND AND OBJECTIVES: Major abdominal procedures are strongly associated with postoperative immunosuppression and subsequent increased patient morbidity. It is believed that laparoscopic surgery causes less depletion of the systemic immune function because of the reduced tissue trauma. Various cytokines and monocytic HLA-DR expression have been successfully implemented to assess postoperative immune function. The aim of our study was to show the difference in immunologic profiles after minimally invasive versus conventional liver resection. METHODS: Ten animals underwent either laparoscopic or conventional open left lateral liver resection. Flow cytometric characteristics of HLA-DR expression on monocytes and lipopolysaccharide-stimulated cellular secretion of tumor necrosis factor α, interferon γ, interleukin 6, and interleukin 8 were measured and analyzed in ex vivo whole blood samples. Intraoperative and postoperative clinical outcome parameters were also documented and evaluated. RESULTS: All animals survived the procedures. Postoperative complications were fever (n = 3), wound infections (n = 2), and biloma (n = 1). Open surgery showed a morbidity rate of 80% compared with 40% after laparoscopic surgery. Laparoscopic liver resection showed no postoperative immunoparalysis. Major histocompatibility complex class II expression in this group was elevated, whereas the open surgery group showed decreased major histocompatibility complex class II expression on postoperative day 1. Postoperative secretion of tumor necrosis factor , interleukin 6, and interferon was lower in the open surgery group. Elevated transaminase levels after laparoscopy might have resulted from an ischemia/reperfusion injury caused by the capnoperitoneum. CONCLUSION: Major immunoparalysis depression was not observed in either group. Laparoscopic surgery shows a tendency to improve immunologic recovery after liver resection.

In a porcine model of mixed acidemia HES 130/0.4 may support more stable hemodynamics during CVVH when compared to gelatine.

PURPOSE: Continuous veno-venous hemofiltration (CVVH) and mixed acidemia often occur simultaneously in critically ill patients. In a previous study in non-acidemic pigs we found that colloids and CVVH interact specifically with respect to hemodynamic stability, with favorable effects for 6% HES 130/0.4 versus 4% gelatine (GEL) infusion. In a porcine model, we investigated whether these colloid-type associated differences are still dominant under acidemic conditions. METHODS: We utilized 5 groups, a non-acidemic reference group receiving HES130 and CVVH; two acidemic groups receiving HES130 infusion (one with and one without CVVH); and two acidemic groups receiving GEL infusion (one with and one without CVVH). Mixed acidemia (pH ~7.20) was established by low tidal volume ventilation and acid infusion. Stable acidemia/CVVH application was maintained for 3 hours. Hemodynamics and blood gases were recorded. RESULTS: Mixed acidemia led to a significant decrease in MAP and increase in MPAP in all groups. CVVH led to a further decrease in MAP but improved MPAP. During CVVH, HES130 ensured significantly higher MAP, Hb, and DO2 values than GEL infusion. In the groups without CVVH these differences between HES 130/0.4 and GEL were not observed. CONCLUSIONS: As in a previous study in non-acidemic pigs, we found a colloid-specific influence of HES130 versus GEL on hemodynamics during CVVH under acidemia. Again, HES130 infusion may lead to favorable effects. In contrast, acidemia without CVVH application was dominant over the impact of a respective colloid. The application of a CVVH seems to be an important trigger for the overall circulatory response to a particular colloid.

Prolonged hypoxemia and acidemia in anesthetized pigs: a model for research on extracorporeal organ support in an intensive care setting.

PURPOSE: Hypoxemia and acidemia (hypoxemia/acidemia) are serious complications in the critically ill and often occur in unstable patients exposed to extracorporeal organ support. Still, little is known about the biocompatibility interactions of hypoxemia/acidemia with extracorporeal circuits (ECC). Existing animal models often include the release of mediator cascades (sepsis-, lung injury models) or are based on small laboratory animals. We established a porcine model of hypoxemia/acidemia without an underlying disease and further challenged the situation with an extracorporeal circuit (ECC). METHODS: Hypoxemia/acidemia were induced (3.5 h) and maintained (3 h) in anesthetized pigs (40 kg) by a stepwise reduction in oxygenation, infusion of 0.4 mol.l⁻¹ lactic and hydrochloric acid and by low tidal volume ventilation, targeting an PaO2 < 70 mmHg, SvO2 < 65%, pH ~ 7.2. Venovenous hemofiltration (CVVH) operated in recirculation mode without volume exchange was chosen to prove the suitability of the model for studies on ECCs under clinical conditions (ECC group, n=6). Another 6 animals underwent the same protocol except for the CVVH (reference group, n=6). RESULTS: The median PaO2 during hypoxemia/acidemia was 62 mmHg, the median SvO2 was 38%, and the median pH was 7.22. Hypoxemia/acidemia was successfully induced and maintained for 6.5 h in all pigs. CVVH could be performed for 3 h with blood flow rates up to 300 ml.min⁻¹ and filtrate rates up to 60 ml.min⁻¹. CONCLUSIONS: Our model provides hypoxemia/acidemia with blood gas values comparable to critically ill adult patients for several hours, during which it is possible to perform CVVH. Thus, it enables research on the biocompatibility reactions of extracorporeal circuits under intensive care conditions.