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Biomedical subjects

T Hau

Publications and source records attributed to T Hau.

At least 73 records · Page 4Linked to original sources
PubMed1978

Evaluation of the mechanism of zymosan-induced resistance to experimental peritonitis.

Three injections of intraperiotoneal (IP) zymosan-induced profound resistance to E. coli peritonitis in Sprague-Dawley rats. IP zymosan had minimal effects on organ weights and systemic phagocytic clearance ability, suggesting that this mode of administration had few systemic reticuloendothelial system (RES) effects. Hemoglobin (a known inhibitor of local phagocytosis) reduced the protection induced by zymosan, giving further evidence that IP zymosan acts locally. IP zymosan stimulation results in an initial marked influx of polymorphonuclear cells followed by a greater percentage replacement of mononuclear cells by the third day. Examination of these cells via chemiluminescence studies demonstrated that the phagocytic capacity of zymosan-stimulated peritoneal cells was markedly greater than the control group on a cell-for-cell basis. IP zymosan also gave some protection against intravenous (IV) E. coli, but IV zymosan did not significanly protect against IP E. coli. Possible mechanisms of action are discussed. These findings suggest that a technique of local RES stimulation could have a place in preparation of certain high-risk patients for elective abdominal surgery where peritoneal contamination is likely.

Animals↗
PubMed1978

Prognostic factors of peritoneal infections in transplant patients.

Twenty-eight cases of peritoneal infections occurring in 686 transplant patients (4%) are reported. The mortality was 78.5% (22 of 28 patients) and accounted for 13.2% of all transplant deaths. Recipients of cadaver kidneys were more prone to develop intraperitoneal infection, whereas the age, the presence of diabetes, and the tissue typing had no influence on the likelihood to develop intraperitoneal infections. Sixteen patients developed intraperitoneal infection secondary to the transplantation or another operation, whereas the intraperitoneal infection was due to a disease process unrelated to previous surgery in 12 patients. Only 64% of the patients presented with abdominal symptoms, 24 presented with septic shock, and 11 with a wound infection without peritoneal signs. The uncharacteristic clinical findings resulted in a delay of 8.7 days between the onset of symptoms and the recognition of the peritoneal infection and made a preoperative diagnosis possible in only 22 patients. It became clear that patients with generalized peritonitis, concomitant distant infections, opportunistics organisms in the peritoneal cavity, and the infections caused by postoperative complications have a poorer prognosis than the remainder of the group. Early recognition of the problem, especially after operation, and vigorous treatment seem to be the keys for improved results in the treatment of this serious condition.

Adult↗
PubMed1977

Inhibition of granulocyte chemotaxis by hemoglobin in experimental peritonitis.

We have shown in in vivo experiments that hemoglobin interferes with the attraction of polymorphonuclear granulocytes into the peritoneal cavity of rats in response to a bacterial inoculum and thus permits bacterial growth. These findings are proportional to the intraperitoneal concentration of hemoglobin. In in vitro experiments the chemotactic response of human polymorphonuclear granulocytes to zymosan activated serum as well as E. coli bacterial factor is inhibited by hemoglobin. While hemoglobin added in a concentration of 4% to the chemotactic factor causes a significant depression of granulocyte chemotaxis concentrations of only 0.01% are sufficient to cause inhibition of chemotaxis when hemoglobin is added to the cell suspension. The spontaneous migration of the cells is not influenced in either experiment.

Animals↗
PubMed1977

Lung preservation techniques.

Some of the barriers to successful lung transplantation include the lack of acceptable methods for ischemic protection and the absence of reliable systems for preservation. The lung response to 60 minutes of warm ischemia basically consists of alveolar-capillary edema and disruption, mitochondria swelling, interstitial hemorrhage, significantly depressed pulmonary function, elevation of pulmonary vascular resistance, and considerable drop in levels of glucose, phospholipids, and adenosine triphosphate. The tolerance to warm ischemia increases to several hours with the use of different systems of ventilatory assistance with or without positive end-expiratory pressure. Several methods of preservation have been attempted: hypothermia, hyperbaria, and hypothermic pulsatile or nonpulsatile perfusion. Hypothermic pulsatile perfusion appears to offer longer periods of protection than the other methods. Longer periods of ischemia and extended preservation may be made possible by advances in the use of drug protection during warm ischemia and the utilization of intracellular colloid or noncolloid solutions for hypothermic storage or hypothermic pulsatile perfusion.

Animals↗
PubMedDate not supplied

Bacteria, toxins, and the peritoneum.

Intraperitoneal infections are caused by members of the gastrointestinal flora, mainly Escherichia coli, enterococci, Klebsiella, Enterobacter, Proteus, Bacteroides, anaerobic cocci, Clostridia, and Fusobacteria. The Gram-negative aerobic bacteria exert their pathogenic potential mainly through endotoxin which acts by way of mediators, causing systemic septic response and, initially, the local response of the peritoneal cavity. The main virulence factors of anaerobic bacteria are exoenzymes and capsular polysaccharides. Peritoneal infections are truly synergistic infections. The most important synergistic mechanisms are protection against host defense and creation of a suitable environment by one member of the flora for another. Aside from bacteria, certain adjuvant substances, i.e., bile, gastric juice, blood, and necrotic tissue, play a role in the pathogenesis of peritonitis. The peritoneum deals with an infection in 3 ways: first, the direct absorption of bacteria into the lymphatics via the stoma of the diaphragmatic peritoneum; second, the local destruction of bacteria through phagocytosis by either resident macrophages or polymorphonuclear granulocytes attracted to the peritoneal cavity; and third, the localization of the infection in the form of an abscess.

Bacteria, Aerobic↗
PubMedDate not supplied

Peritonitis: pathophysiology and local defense mechanisms.

The peritoneal cavity can be divided in the supracolic infracolic and paracolic spaces, the lesser sack and the pelvis. The peritoneum is a semipermeable membrane which allows a flux of solutes into and from the peritoneal cavity. In addition, particles can be absorbed through the stomata of the diaphragmatic peritoneum. Secondary peritonitis is always a polymicrobial infection. The flora consists of aerobic enterobacteriaeceae and anaerobs mainly B. fragilis. These two groups of bacteria act synergistically. Besides unspecific defence mechanisms, i.e. the direct absorption of bacteria and the entrapment of bacteria in fibrin, the immunological defence mechanisms of the peritoneal cavity are triggered by endotoxin contained in the cell wall of the invading bacteria leading to the production of cytokines by macrophages, activation of complement and as a result the migration of granulocytes from the intervascular space into the peritoneal cavity.

Animals↗