[Acute hemorrhagic gastritis--diagnosis, clinic and therapy].
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Biomedical subjects
Publications and source records attributed to N Darle.
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The superior mesenteric artery syndrome is a compression of the duodenum. We believe that the diagnostic limitations of the routine barium meal studies can be abolished by hypotonic duodenography. Before surgical treatment other pathological conditions should be excluded. Peptic ulcer disease often coexists. Patients with persisting signs and symptoms after surgery for ulcer should be re-examined with this condition in mind. The adequate treatment is duodenojejunostomy.
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A case of hemorrhage in a pancreatic pseudocyst presenting as massive gastrointestinal bleeding is reported. In the event of an unexplained GI-bleeding in an alcoholic this diagnosis should be considered. Selective angiography during bleeding may lead to correct diagnosis.
We have presented a retrospective study of the surgical management of 299 patients bleeding from duodenal ulcer, gastric ulcer or gastritis. The overall mortality rate was 15%-5% for elective and 25% for emergency operations. The mortality increased with age and reached 50% for emergency operations in patients over the age of 70. Patients with low admission haemoglobin values, who had episodes of hypovolemic shock or who required immediate transfusions were also at risk. A Billroth I gastric resection proved to be the safest operative procedure. Based on our results, we are supporting a program calculated to reduce the mortality attending gastroduodenal bleeding, especially in those patients requiring an emergency operation. The basic principles of this program are constant observation, prompt diagnosis and early surgical intervention.
The effect of intravenous injection of 50 mug/kg of glucagon on the hepatic circulation of the pig was studied in 12 animals. Glucagon caused an arterial pressure reduction of 11 mm Hg after two minutes and 7 mm Hg after ten minutes. The portal pressure and blood flow were not altered. The superior mesenteric arterial flow decreased by 12%. The hepatic arterial blood flow increased by 80% after two minutes and by 58% after ten minutes. There was no difference in response when anesthesia was achieved with small intravenous doses of thiopental (Pentothal) sodium or 70% nitrous oxide in oxygen and tubocurarine chloride.
Hemorrhage amounting to 40% of the calculated blood volume in dogs produced a fall in systemic blood pressure to a level of approximately 50 mm Hg. This was associated with a decline of total liver blood flow of about 60% of normal. Infusion of low molecular dextran (LMD) or saline of a volume, corresponding to 1/7 of the volume of blood taken out, increased the total liver blood flow. This increase was much more pronounced in the LMD group, maybe due to the ability of LMD to simultaneously increase systemic blood pressure, decrease blood viscosity and disaggregate red blood cells in the microcirculation.
It has earlier been shown that the hormone glucagon has the property of increasing liver blood flow both in normotensive dogs as well as in dogs in hemorrhagic shock. This study was done to evaluate the effect of glucagon given in normotensive dogs after occlusion of the hepatic artery. Glucagon was given in a single dose of 50 mug/kg bodyweight. The study shows that glucagon under these circumstances increased total liver blood flow 67% compared to an increase of 3% in a control group. The increase is statistically significant compared to the effect of placebo injection in a control group. A benefit of the hormone is suggested in man in surgical situation where occlusion of the hepatic artery becomes necessary.
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Changes of total liver blood flow (TLBF), portal venous and hepatic arterial flows have been investigated using a hemorrhagic model in dogs. The dogs were bled stepwise from normal blood pressure to a pressure of 50-60 mm Hg. TLBF was measured by the xenon clearance method. Hepatic arterial blood flow was measured by electromagnetic flowmeter. Portal venous flow was calculated by subtracting hepatic arterial blood flow from TLBF. Other parameters studied during the experiment were systemic arterial blood pressure and portal venous pressure. Under normotensive conditions TLBF in mean was registered as 127 ml/min X 100 g liver tissue (25 ml/min X kg body weight). The relation between the flow value in portal vein and hepatic artery was on average 2.3:1. The study shows that there was a pronounced decrease of TLBF flow during hemorrhage. Portal venous flow decreased almost parallel to TLBF, while hepatic arterial flow decreased to a lesser extent which means that there was autoregulation in this flow bed. Hepatic arterial flow successively constituted a larger part of TLBF, during hemorrhage sometimes 65% compared to the normal value of about 30%. During the study there was an increase of vascular resistance in the portal venous system and decreased resistance in the hepatic arterial bed.
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