Acute changes in peritoneal morphology and transport properties with infectious peritonitis and mechanical injury

Abstract

Peritoneal clearance studies were performed in rats undergoing acute peritoneal dialysis. Some of these animals were then exposed to laparotomy and mechanical drying of the peritoneum. Peritoneal clearance studies were repeated at intervals up to 11 days. Another group of rats was placed on daily peritoneal dialysis and allowed to spontaneously develop peritonitis which was not treated. These rats underwent peritoneal transport studies at differing durations of infection. In all groups, animals were sacrificed at the time of the last transport studies for morphological assessment of the peritoneum by light microscopy, scanning electron microscopy, and transmission electron microscopy. The results showed similar decreases in drainage volume and increases in glucose absorption and protein losses with both infection and drying. Both types of injury resulted in extensive mesothelial structural changes. While drying caused mainly denudation of the mesothelial surface, infectious peritonitis was associated with separation of mesothelial cells, and the appearance of numerous white blood cells between and on mesothelial cells. Exposure to peritoneal dialysis alone had no obvious effects on anatomy. Although changes in the peritoneal microcirculation and deeper structures cannot be excluded as contributing to peritoneal transport alterations, the findings suggest that alterations of mesothelium might explain some of the changes in peritoneal transport properties under the conditions of these studies.

Hepatocyte Growth Factor/Scatter Factor Released during Peritonitis Is Active on Mesothelial Cells

“…The production of collagen is stimulated also by serum and peritoneal fluid of patients with peritonitis and is prevented by anti-HGF antibody. The collagen proteins produced by mesothelial cells are type III and type I (␣1) 3 , i.e., the two types, especially type III, that are assembled as fibrotic tissue in organs exposed to chronic inflammation. 39 The release of HGF during peritonitis and the evidence that HGF acts on mesothelial cells suggest that HGF influences in several ways the process of healing of the peritoneum, especially in patients undergoing peritoneal dialysis.…”

“…The diagnosis of peritonitis was based on clinical signs (cloudy peritoneal fluid, abdominal pain), leukocyte count Ͼ100/ mm 3 and positive culture in peritoneal fluid. The two groups of patients were matched for age, time on CAPD, number of peritonitic episodes, and index of dialysis adequacy (KT/V).…”

“…1,2 The pathogenic mechanisms accounting for the phenomenon are poorly understood, but loss of mesothelial cell adhesion with separation of cells from one another and detachment from the basal membrane, extracellular matrix deposition, and angiogenesis in the submesothelial layer are characteristic features of the process. 3 Although mesothelial cells are the victim of peritoneal inflammation, recent studies suggest that they participate as culprit in the fibrotic transformation of the peritoneal membrane. In fact, mesothelial cells can release inflammatory cytokines 4 -7 and when exposed to peritoneal effluents obtained from patients on CAPD they can upregulate transcription and expression of collagen.…”

Peritonitis-induced peritoneal injury models for research in peritoneal dialysis review of infectious and non-infectious models

“…We have reported that uremia is associated with inflammation of the peritoneal membrane [12]. Histologically, acute peritonitis can cause morphological damage to the peritoneum [10,13]. Detachment and disintegration of mesothelial cells is observed, along with the appearance of fibrin exudation and numerous infiltrating cells, ultimately resulting in internal structures becoming unrecognizable [6].…”

Expression of Heat Shock Proteins 72/73 in Human Peritoneal Mesothelial Cells in vivo and in vitro

“…However, the local accumulation of leukocytes during peritonitis is associated with marked structural changes of MC, characterized by a cuboid cell shape, hyperplasia of the rough endoplasmatic reticulum, and discontinuity of cell-cell contacts [7, 8, 9]. MC injury is thought to be caused by activated and adherent polymorphonuclear leukocytes which release a number of protease enzymes and free radicals (O – 2 , H 2 O 2 , and HO – ) to create an injurious microenvironment [10, 11].…”