A new technique of laparoscopic obturator hernia repair: report of a case.

An 84-year-old woman presented with ileus. Ultrasonography, a computed tomography scan, and small bowel contrast examination showed a Richter-type hernia in her left obturator orifice. Under general anesthesia, laparoscopic surgery with low-pressure (4mmHg) pneumoperitoneum was carried out using a peritoneal needle retractor, and a reduction of the strangulated intestinal loop was thus achieved. Because the hernial opening measured 5mm in diameter, it could be closed with four pieces of End-Universal stapler without polypropylene mesh. The ischemic ileum was resected, and the bowel was anastomosed extracorporeally with a minimal skin incision. She was ambulant on the first postoperative day, and her postoperative course was good. Obturator hernias are rare, but when a definitive diagnosis is made in such elderly patients, laparoscopic repair using the peritoneal needle retractor is recommended for minimally invasive surgery. We recommend doing the repair with an End-Universal stapler, since this procedure is more simple and useful for preventing infection than using polypropylene mesh in such a strangulated case.

Role of nitric oxide in oxygen transport in rat liver sinusoids during endotoxemia.

To evaluate the role of nitric oxide (NO) in hepatic microcirculation and liver injury during endotoxemia, we studied O2 transport in the hepatic microcirculation of endotoxin-infused rats. Rats were continuously infused with Escherichia coli lipopolysaccharide (LPS) (0.8 mg/kg/h) for 7 hours. LPS increased the plasma levels of NO2- + NO3- and aspartate transaminase (AST), and decreased the bile flow rate and hepatic adenosine triphosphate (ATP) level. Hepatic microcirculation was evaluated by two methods: reflectance spectrophotometry showed a decrease in the oxygenation of hemoglobin (Hb) in the liver, and dual-spot microspectroscopy indicated that LPS administration decreased blood velocity, the oxygenation of Hb, and O2 release from sinusoids to hepatocytes. The observed decreases in the O2 transport parameters were prominent in pericentral sinusoids. All of these phenomena were further aggravated by the administration of N(w)-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg/h) plus LPS, and by aminoguanidine (AMG) (5 mg/kg/h) plus LPS, and these could be reversed by the concomitant administration of L-arginine (L-Arg) (100 mg/kg/h). These results suggest that deterioration of hepatic oxygen transport and liver function induced by endotoxin can be ameliorated by NO.

Ca2+ release from mitochondria induces cytosolic enzyme leakage in anoxic liver.

The mechanisms of elevation of cytosolic Ca2+ concentration during anoxia causing cytosolic enzyme leakage were studied in perfused rat liver. Before anoxia the Ca2+ contents in mitochondria of perfused rat liver were varied by addition of noradrenaline and glucagon, lowering Ca2+ concentration in the perfusion medium, and addition of Ca2+ channel blocker, either singly or in combination. The amount of cytosolic enzyme leakage during anoxic perfusion positively correlated with the mitochondrial Ca2+ content just before anoxia and also with Ca2+ release from mitochondria during anoxia. However, the amount of cytosolic enzyme leakage during anoxic perfusion did not correlate with the Ca2+ concentration in the perfusion medium and microsomal Ca2+ content. These data support the hypothesis that in anoxic liver, the cytosolic Ca2+ concentration is elevated to a pathological level mainly by Ca2+ release from mitochondria, causing the cytosolic enzyme leakage.