The effect of peritoneal dialysate on the capacity of peripheral blood polymorphonuclear (PMNL) and mononuclear leukocytes (MNC) to release leukotriene B₄ (LTB₄) and tumor necrosis factor alpha (TNFα) was investigated in vitro. Following density gradient separation, aliquots of 5 × 10⁶ PMNL or MNC were incubated in peritoneal dialysis fluid containing 1.5% glucose or Hanks’ buffer ( = control) for 1–2 h at 37^°C. TNFα and LTB₄ production was stimulated with Escherichia coli lipopolysaccharide (LPS) and calcium ionophore A23187, respectively. MNC incubated in buffer and LPS produced (mean ± SD) 1,006 ± 522 pg TNFα/5 × 10⁶ cells; no significant amounts of TNFα were detectable in the presence of dialysate. An inhibition of TNFα release was also observed in MNC exposed to bicarbonate-buffered dialysates (pH 7.40) and 4.25% and 1.5% glucose solution with physiologic osmolality. Incubation of PMNL in Hanks’ buffer followed by A23187 stimulation led to production of 29.1 ± 19.2 ng LTB₄/5 × 10⁶ cells, whereas glucose-incubated cells were refractory to ionophore stimulation ( < 0.l ng LTB₄/5 × 10⁶ cells). The failure of dialysate-exposed leukocytes to release inflammatory mediators in response to adequate stimuli may contribute to the impairment of cellular host defense in the setting of continuous ambulatory peritoneal dialysis.

During continuous ambulatory peritoneal dialysis (CAPD), peritoneal host defence mechanisms are repeatedly exposed to dialysis solutions (with unphysiological composition) which may compromise peritoneal immune cell functions. In this context, the current study focused on the capacity of peripheral and peritoneal PMN to release leukotrienes following exposure to conventional CAPD dialysates. PMN were obtained from peripheral blood of healthy volunteers and from the peritoneal effluent of CAPD patients with acute peritonitis. Following isolation, cells were incubated in fresh CAPD dialysates or control buffer, and calcium ionophore A23187-stimulated leukotriene synthesis was measured. Additional experiments included RP-HPLC analysis and radioactivity monitoring of lipoxygenase products in PMN labelled with 14C-arachidonic acid. Leukotriene B4 and leukotrienes C4/D4/E4 were determined by radioimmunoassay. Ionophore-triggered leukotriene release from cells exposed to control buffer was pronounced in inflammatory peritoneal PMN (70.4 +/- 31.3 ng/5 x 10(6) cells LTB4 and 13.4 +/- 19.8 ng/5 x 10(6) cells LTC4/D4/E4, mean +/- SD, n = 14) when compared to healthy peripheral PMN (26.6 +/- 16.9 ng/ml LTB4 and 6.3 +/- 6.6 ng/ml LTC4/D4/E4, n = 12). Incubation in fresh solutions for peritoneal dialysis severely depressed leukotriene release from both cell populations. These results indicate a severe inhibition of cellular responsiveness as a consequence of dialysate exposure which could contribute to the impairment of host defence early in the CAPD cycle.

No abstract

The importance of partial liver resection as a therapeutic option to cure hepatic tumors has increased over the last decades. This has been influenced on the one hand by advances in surgical and anesthetic management resulting in a reduced mortality after surgery and on the other hand by an increased incidence of hepatocellular carcinoma. Nowadays, partial resection of the liver is performed safely and as a routine operation in specialized centers. This article describes the pathophysiological changes secondary to liver failure and assesses the perioperative management of patients undergoing partial or extended liver resection. It looks in detail at the preoperative assessment, the intraoperative anesthetic management including fluid management and techniques to reduce blood loss as well as postoperative analgesia and intensive care therapy.