Biomedical subjects
Publications and source records attributed to H Myrvold.
Cholescintigraphy is a simple and reliable way of detecting a liver injury accompanied by biliary leakage and is also well suited to assess the effectiveness of treatment and to follow recovery. To emphasize these points, a case report of a patient suffering from a severe injury to the liver is presented.
Extraction of lipids from human small intestinal epithelial cells or brush borders removed specific binding sites for cholera toxin completely, but only about 50% of the receptor sites for Escherichia coli heat-labile enterotoxin. Both cholera toxin and E. coli heat-labile enterotoxin bound strongly to ganglioside GM1 in the lipid extract and, to a lesser extent, to another monosialoganglioside and to GD1b. The results suggest that E. coli heat-labile enterotoxin binds to both ganglioside and glycoprotein receptor sites of the human small intestinal epithelium, whereas cholera toxin binding was restricted to the ganglioside receptors.
Two different experimental models for inducing septic shock have been characterized. In one, septic shock was induced by intraperitoneal injection of live Escherichia coli bacteria. This resulted in a dose-dependent mortality. Those animals surviving the first 24 h are considered as permanent survivors. In the other models, septic shock and peritonitis was induced by ligation and needle punctures of the cecum. This resulted in a slower development of shock which was almost invariably lethal within 96 h. Arterial blood pressure remained within the normal range in both models for up to 3 h after inducing peritonitis. Then a rapid deterioration was noticed in animals injected with live E. coli. White blood cells and platelets in arterial blood were reduced compared to controls in both groups. This reduction was more pronounced in animals injected with live E. coli. Both models are considered as useful tools in further studies of the pathophysiology of peritonitis and septic shock.
The pathogenesis of small intestinal mucosal damage in septic shock was explored in experiments on 15 cats given live E coli i.v. Villous (absorptive site) blood flow was studied by the carbon monoxide uptake technique using isolated small intestinal segments. In eight of the cats, segments were perfused intraluminally with oxygenated or nitrogenated saline. The main part of the small intestine was unperfused and served as control. Nine cats (60%) developed mucosal damage. They had significantly lower arterial blood pressure at the end of septicemia (56 +/- 6) than cats without mucosal damage (76 +/- 3 mmHg). Total intestinal blood flow was similar before or during septicemia. Villous blood flow before septicemia was 3.7 +/- 0.5 ml/min X 100 g intestine and 5.1 +/- 1.0 (n.s.) in the two groups, respectively, and remained unchanged. Intraluminal perfusion with oxygenated but not with nitrogenated saline prevented the development of mucosal damage. It was concluded that the small intestinal mucosal damage is due to hypoxia in spite of unchanged villous blood supply.
After a two-hour period of regional intestinal shock (arterial inflow pressure 30 to 35 mm Hg; electrical stimulation of regional vasoconstrictor fibers at 6 Hz) a pronounced cardiovascular derangement is observed as reflected in a rapid fall in arterial blood pressure. In this study, central hemodynamics and lung function were investigated to elucidate if functional changes in the thoracic organs might explain the cardiovascular collapse. No alteration of pulmonary function was observed. A negative inotropic influence on the heart was, however, noted as judged by a decreased left ventricular stroke volume and left ventricular maximal pressure change in the face of an increased left ventricular end diastolic pressure. Based on earlier observations with the same shock model, it is proposed that the cardiac effects were caused by cardiotoxic material released from the hypoxic gut.