No abstract

It is known that the gut may serve as a reservoir for various microorganisms, which under specific circumstances may intrude into the systemic circulation, causing systemic infections. The aim of the present study was to estimate the "critical time" of disruption of the small-intestine mucosal barrier in conditions of experimentally induced intestinal occlusion, based on the histopathological alterations observed under light and electron microscopy. Forty rabbits underwent small-intestine obstruction through ligation with a nonabsorbable suture. Blood cultures from portal vein and inferior vena cava, as well as cultures from the peritoneal fluid, a hepatic fragment, and a mesenteric lymph node, were obtained before the ligation (0 h). The same cultures were repeated at 4 and 8 h (group A, 20 rabbits) and at 6 and 12 h after the ligation (group B, 20 rabbits). Small-intestine specimens proximal to the occlusion were taken for examination under the optic and electronic microscope in the same time intervals. Five of 20 rabbits of group A died within 4 h and 6 of 20 rabbits of group B died within 6 h after the operation. All anaerobic cultures were negative. All aerobic cultures that became positive developed Escherichia coli colonies. Intestinal epithelium of dead animals was transformed to cuboid with destruction of goblet cells and alteration in secretion of acid polysaccharides. The mucosal appearance of all rabbits that survived 12 hours after ligation was the same. The disruption of the mucosal barrier begins 4 h after complete intestinal occlusion. At 12 h after complete intestinal occlusion, the disruption is total with different degrees of severity.

Agenesis or hypoplasia of the right hepatic lobe combined with a floating gallbladder is an extremely rare condition. We report a case of hypoplasia of the right hepatic lobe, discovered in a 65-year old female. This was an incidental finding at CT scan for staging of a right colonic cancer. The CT evidenced the presence of a hypoplastic right lobe, while the left lobe was diffusely enlarged. Furthermore, the gallbladder was described as floating with partially calcified walls. The diagnosis of this rare anomaly was confirmed intraoperatively. The patient underwent right hemicolectomy and cholecystectomy. Biopsies were taken from both right and left hepatic lobes, revealing the presence of normal hepatic parenchyma. Since all causes of acquired atrophy of the liver had been ruled out, we considered this case to be of congenital origin.

Acute tissue ischemia is usually followed by considerable disturbances of cellular metabolism that often lead to cell death. Reperfusion improves cellular function by withdrawing the toxic products of ischemia and providing energy sources, although sometimes it worsens it. The purpose of this experimental work is to study the metabolic disturbances in skeletal muscle tissue of canines after prolonged acute ischemia in relation to the values of certain substances (ATP, lactate, pyruvate, the ratio of lactate to pyruvate [L/P], and glucose) and whether the alterations in the values of these substances could be used as prognostic indices of the magnitude of tissue damage and the possibility of inverting it. We used 15 mongrel dogs. Complete acute ischemia was induced in the right lower limb lasting 12 h. Reperfusion also lasted for 12 h. The left lower limb was used as reference value. Before the beginning of ischemia, at (1/2), 1, 6, and 12 h after the induction of ischemia, and at (1/2), 1, 6, and 12 h after the restoration of circulation, blood samples, and tissue biopsies were obtained from the healthy and the experimental limb for the measurement of ATP, lactate, pyruvate, the ratio of L/P, and glucose. From the statistical analysis of the values of the controlled parameters the following were concluded: The changes in ATP, lactate, pyruvate, and the L/P ratio in the venous blood of the experimental limb and in the intracellular space of the suffering skeletal muscle could be used as indices to evaluate ischemic injury to the skeletal muscles, the course of its development, and the possibility of reversal after reperfusion.

Acute tissue ischemia is usually followed by considerable disturbances of cellular metabolism that often lead to cell death. Reperfusion improves cellular function by withdrawing the toxic products of ischemia and providing energy sources, although sometimes it worsens it. The purpose of this experimental work is to study the metabolic disturbances in skeletal muscle tissue of canines after prolonged acute ischemia in relation to the values of certain substances (ATP, lactate, pyruvate, the ratio of lactate to pyruvate [L/P], and glucose) and whether the alterations in the values of these substances could be used as prognostic indices of the magnitude of tissue damage and the possibility of inverting it. We used 15 mongrel dogs. Complete acute ischemia was induced in the right lower limb lasting 12 h. Reperfusion also lasted for 12 h. The left lower limb was used as reference value. Before the beginning of ischemia, at (1/2), 1, 6, and 12 h after the induction of ischemia, and at (1/2), 1, 6, and 12 h after the restoration of circulation, blood samples, and tissue biopsies were obtained from the healthy and the experimental limb for the measurement of ATP, lactate, pyruvate, the ratio of L/P, and glucose. From the statistical analysis of the values of the controlled parameters the following were concluded: The changes in ATP, lactate, pyruvate, and the L/P ratio in the venous blood of the experimental limb and in the intracellular space of the suffering skeletal muscle could be used as indices to evaluate ischemic injury to the skeletal muscles, the course of its development, and the possibility of reversal after reperfusion.