To reduce intraoperative blood loss in liver resections surgical bleeding control is often performed by a complete inflow obstruction of the liver called Pringle manoeuvre leading to a portal venous stasis. Platelet aggregability may be affected by this circulatory stasis.A study population of 11 patients (37-67 years old, 7 females and 4 males) with hepatic tumours underwent elective liver resection. Pringle manoeuvre of up to 50 min duration was used in 4 patients. The other 7 patients were operated using selective vascular clamping. Platelets were aggregated before and after liver resection with adenosine diphosphate, collagen and ristocetin (according to Born).Mean maximal amplitudes of platelet aggregation were comparable before and after liver resection. Statistic analysis did not detect a significant difference between the values before and after liver resection as well as between Pringle manoeuvre and selective vascular clamping.Induced platelet aggregability is not affected by the method of surgical bleeding control used in liver resection. Platelet aggregability seems to be resistant even to portal venous stasis of up to 50 min during Pringle manoeuvre.
Hintergrund: Die Umsetzung des Arbeitszeitgesetzes vom 1. Januar 2006 forderte von vielen Abteilungen weitere Rationalisierungen im stationären Arbeitsablauf. Hieraus ergab sich die Schwierigkeit, eine Balance zu finden; einen effektiven Arbeitsablauf zu gewährleisten, aber gleichzeitig auch die Patienteninteressen bei der Visite zu berücksichtigen. Material und Methoden: Seit Januar 2009 wurde die Visitendauer von 45 auf 30 min gekürzt. Stationsoberärzte wurden gleichzeitig in den täglichen Visitenablauf eingebunden. Die prospektiv angelegte Studie wurde über 3 Monate durchgeführt. In diesem Zeitraum konnten 86 Patienten ausgewertet werden. Ergebnisse: 86 Patienten mit einem Durchschnittsalter von 56,7 Jahren wurden in der Studie untersucht. Die durchschnittliche stationäre Verweildauer betrug 7,2 Tage. Die präoperative Patientenerwartung einer Visitenlänge war mit 5,3 min signifikant höher als die beobachtete. Insgesamt konnte eine Patientenzufriedenheit von mehr als 80 % erreicht werden. Schlussfolgerung: Trotz deutlicher Kürzung der Visitenzeiten war es dennoch möglich, eine hohe Patientenzufriedenheit auf einer chirurgischen Station durch Visitenbesetzung mit Entscheidungsträgern und der routinemäßigen Eingliederung der Patienten in clinical pathways, zu gewährleisten.
Background. Renal transplantation in infants is frequently complicated by graft thrombosis and accelerated rejection reactions. We herein tested the hypothesis that the amount of blood required to sustain normal perfusion of an adult renal allograft transplanted into a pediatric recipient would surpass the cardiac output and aortic blood flow of the recipient and that the ensuing low flow in full-size grafts (FSG) would induce a release of thrombogenic substances. Methods. In a porcine renal transplant model, adult FSG were transplanted into pediatric recipients. Macro- and microhemodynamic as well as metabolic data were recorded. Surgically size-reduced grafts (RSG) served as controls. Results. Donor weight was 55.1±4.8 kg and 9.6±0.9 kg for recipients. FSG weight was 122±16 g and 65±14 g for RSG. Blood flow in donor kidneys was 20% higher than the infrarenal aortic blood flow of recipients. After reperfusion, mean arterial pressure in recipients of FSG but not RSG dropped to 64 mmHg, despite an increase in cardiac output by 60%. FSG but not RSG were polyuric and proteinuric. The release of endothelin and thromboxane B2 into the circulation was higher from FSG when compared with RSG (P<0.05 for endothelin after 60 min; NS for thromboxane B2). Conclusions. After transplantation of FSG into pediatric recipients, the macrohemodynamic limitations of the recipient cause microcirculatory disturbances in the graft, which contribute to the release of vasoconstrictive and prothrombotic substances and an impaired early graft function. Some of those effects can be ameliorated by surgically size reducing the renal graft.
Spontaneous Epstein-Barr virus (EBV)-transformed lymphoblastoid cell lines (SP-LCLs) can be easily obtained from latently EBV-infected cancer patients and used as a source of antigen-presenting cells (APCs) for immunotherapy. Using point-mutated (codon 12) p21(ras) (muRas) as a model tumor antigen, we evaluated the practicability of using genetically modified SP-LCLs as cancer vaccines for patients with pancreatic cancer expressing mutated Ras (muRas). The repeated stimulation of peripheral blood mononuclear cells (PBMCs) from patients with muRas-LCLs elicited a strong, muRas-specific T cell response. A significant cytotoxic activity against EBV virus proteins or components of the expression vector was not observed. The T cells were able to recognize naturally presented muRas, as shown by their cytotoxicity against muRas (Gly-12 to Val-12 or Asp-12)-expressing tumor cells. The T cell response was mainly MHC class I restricted, and peptides containing amino acids 5 to 14 of muRas-Val-12 and muRas-Asp-12 were identified as immunogenic peptides for HLA-A2. In contrast to the situation in patients with putatively muRas-primed T cells, muRas-LCLs were not able to prime naive T lymphocytes from healthy controls. Vaccination of a pancreatic cancer patient with muRas-LCL induced muRas-specific T cells in PBMCs after 4 weeks. We conclude that genetically modified muRas-LCLs can efficiently present tumor antigens to the immune system and induce antigen-specific cytotoxic T cell responses in vitro and in vivo.
The use of the stomach is still the preferred substitute for the esophagus requiring only the anastomosis to reestablish food passage. Furthermore the gastric substitute acquires spontaneous propulsive contractility and is associated with good long-term functional results. In Western populations, tubular transformation of the stomach following lesser curvature resection, as described by Akiyama occasionally results in a short gastric tube with perfusion deficiencies at the cranial part of the tube.
Background: Extrahepatic cholestasis by biliary obstruction is known to induce an acute phase reaction in the liver. The activation of acute phase proteins was related to the increase of oxidative stress. Hemeoxygenase (HO)-1 catalyses not only the degradation of endogenously produced heme, but represents also a stress protein which modulates acute inflammatory states by carbon monoxide and biliverdin formation. We have already shown that acute bile duct ligation (BDL) leads to HO-1 expression in liver tissue. In this study we focused on the contribution of HO-1 to the bilirubin production during BDL. Moreover we examined whether HO-1 has any protective role in the BDL model. Methods: Sprague Dawley rats (6 of each group) underwent BDL or Sham operation. One group with BDL or with Sham operation received additionally 10 μmol/kgKG Tin(IV)-mesoporphyrin IX (SnMP) i. v. for functional blockade of HO-1. After 3 days liver microcirculation was determined by laser Doppler flowmetry (LDF) and blood as well as liver samples were taken for further analysis (liver chemistry, histological analysis, HO-1 RT-PCR and immunohistochemistry). Results: HO-1 RNA was 2.5-fold increased after SnMP administration. Immunochemistry demonstrated 11 ±� 1% HO-1 positive hepatocytes compared to 1 ±� 0.4 % in sham operated animals. Administration of SnMP further increased the percentage of HO-1 positive hepatocytes after BDL (16 ±� 1 %) and even in sham operated controls (4 ±� 1 %). HO-1 blockade diminished endogeneous bilirubin formation after BDL (Bilirubin BDL-group: 9.6 ±� 0.4 mg/dl, BDL+SnMP-group: 6.7 ±� 0.5 mg/dl). Liver injury markers such as AST and LDH were lower in the BDL+SnMP group compared to animals with BDL only. LDF showed decreased flux values in BDL compared to sham controls. Of interest, microcirculatory blood flow was even more decreased in the BDL+SnMP group. In general, liver architecture was preserved in all groups. However, there were signs of leukocyte infiltration and damage in the periportal regions in BDL and BDL+SnMP animals. Conclusions: These findings illustrate that the bilirubin increase after BDL is partially caused by increased HO-1 induction. In contrast to a large body of studies showing protective effects of HO-1 induction, our findings also suggest some detrimental effects of cholestatic HO-1 expression. Einleitung Die extrahepatische Cholestase fuhrt aufgrund eines erhohten oxidativen Stress zu einer Akut-Phase Reaktion in der Leber [1]. Diese bewirkt unter anderem die Expression des unter Stressbedingungen induzierbaren Enzyms Hamoxygenase (HO)-1. Nachdem wir bereits gezeigt haben, dass eine akute Gallengangsligatur eine HO-1 Expression in der Leber verursacht, haben wir in der vorliegenden Untersuchung die Bedeutung der HO-1 Induktion fur die endogene Bilirubinproduktion sowie deren funktionelle Auswirkung bei Cholestase untersucht.
