[Acute renal failure].
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Biomedical subjects
Publications and source records attributed to M Hörl.
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Neutrophils are activated during sepsis. To find out whether granulocytes are further activated during hemodialysis with cellulosic and noncellulosic membranes, we compared the plasma levels of the main granulocyte components in patients with chronic uremia who were undergoing regular hemodialysis treatment and patients with acute renal failure with and without sepsis. During hemodialysis with cuprophane dialyzers, plasma-granulocyte elastase, in complex with alpha-proteinase inhibitor, and lactoferrin levels increased in patients who were undergoing regular hemodialysis treatment, but these levels increased further in patients with acute renal failure who did not have sepsis. Maximal neutrophil degranulation was observed in patients with acute renal failure and sepsis. There was only mild degranulation in all three groups during dialysis with dialyzers made of polysulfone. Our data demonstrate that neutrophil activation is increased in patients with acute renal failure, and it is increased further by superimposed sepsis. Cellulose-containing dialysis membranes introduce a further activation of neutrophils.
Clinical experience gives evidence of the increasing importance of chronic-abscess-forming peritonitis with a general physical impairment in spite of a well-controlled abdominal situation. The number of unsolved problems led us to develop a standardized and reproducible experimental animal model, using Wistar rats. We induced peritonitis by intraperitoneal injection of a mixture containing a capsulated strain of Bacteroides fragilis and DEV agar. The histologic changes in the parietal and visceral peritoneum, lymphnodes and liver were recorded in the course of the disease. The data largely correlate with those recorded in human peritonitis. Bacteriologic examinations gave evidence of bacteria passing through the intestinal wall into the abdomen. This is the first model for peritonitis which is defined by its histological and bacteriological course. It enables one to examine pathophysiological problems and the consequences of harm and stress for the course of the disease.
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The effect of immobilization and the following mobilization on muscle carbohydrate metabolism was investigated in dogs. Total carbohydrate and glycogen content of skeletal muscle fell during immobilization. The glycogen-degrading enzyme phosphorylase was activated 1 week after immobilization (a/b ratio 40.6 +/- 7.6 vs. 27.1 +/- 6.5%). Thereafter, the enzyme activity decreased and remained significantly lowered even 2 weeks after the following mobilization. In contrast, muscle glucose and lactate concentration were unchanged. Our data indicates glycogen breakdown of dog skeletal muscle during immobilization. Even after 2 weeks of mobilization muscle glycogen content has not reached glycogen values of the untreated dogs.
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Our physical, chemical and clinical findings - especially lactate, night pain and peripheral blood flow - have shown that in most cases of AOD stages III and IV, intraarterial infusions with prostaglandine E1 largely improved the peripheral situation. PGE1 seems to meliorate the blood flow - causing better oxygen supply - and to inhibit thrombocyte aggregation. An improvement of the clinical situation will be the result. In most cases a differentiation between responders and non-responders is possible but, on the other hand, it is not possible, however, to give a safe forecast of the success of this treatment in the individual patient.
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Human arteries and veins contract with hypoxia and deprivation of substrate provoked by increasing calcium inflow into the cell and reduced energy. Such spasm may be eliminated by phosphoenolpyruvate which loads up the cell's energy, blocking glycogen reduction at the same time. Reperfusion will then guarantee a sufficient energy stroke. Therapy should pursue the following steps: 1. Phosphoenolpyruvate infusion (1 X 10(-6) up to 1 X 10(-3) gm/ml in tyrodes solution pH 7.3) into the arterial branch, proximal and distal to the injury. 2. Subsequent treatment with vasodilating drugs and rheologically active substances. 3. Failed therapy after more than three hours warm ischemia could be due to autolytic processes and requires resection of the affected vessel. 4. The imbalance of the thrombolytic system with the so-called no reflow phenomenon could be due to a plasminogen activator's inhibitor released during hypoxia. Such cases may reasonably be treated by urokinase or by streptokinase plasminogen complex.
Monitoring of plasma proteinases, proteinase inhibitors and other selective plasma proteins was evaluated in patients undergoing Y-graft aortofemoral bypass operation. Fast-reacting acute-phase proteins (C-reactive protein, antichymotrypsin, alpha 1-acid glycoprotein) and slow-reacting proteins (haptoglobin, alpha 1-antitrypsin) increased significantly 48-120 h after operation. By contrast, no significant increase was found between plasma ceruloplasmin levels before clamping and after declamping. Activity and concentration of alpha 2-macroglobulin decreased postoperatively and remained significantly lowered throughout the observation period. Plasma levels of granulocyte elastase were elevated significantly 1 h after declamping, whereas trypsin-binding capacity decreased immediately after the release of the clamp. Aprotinin pretreatment caused higher trypsin-binding capacity of the plasma, significantly lower 'unspecific' proteolytic (azocasein-hydrolyzing) activity and significantly lower non-TCA precipitable low molecular weight plasma protein concentration. Our results confirm the data of several authors that monitoring of plasma proteinases, proteinase inhibitors and other selective plasma proteins may be helpful in evaluating surgical patients postoperatively.
The cause for a nonocclusive ischemic enteropathy seems to be a low cardiac output syndrome. There are often signs of a paralytic intestinal obstruction. Parameters of the blood chemistry offer no conclusive data. The angiogram of the mesenteric vessels demonstrates extensive arterial vasoconstriction as well as an obstructed venous outflow. Experimental findings disclose that this venous obstruction may be a result of an ischemic contracture in the course of a low flow state. This rigor initiates finally a thrombosis of the venoles. The rigor can be effectually mastered by energy-rich compounds.
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Metabolic changes in blood and skeletal muscle of dogs before, during and after tourniquet ischaemia were investigated to obtain further information on cellular metabolic abnormalities and restitution during and following long-lasting blood flow interruptions. Total carbohydrate and glycogen contents in the muscle tissue fell during ischaemia and remained significantly decreased even 1 h after recirculation due to inhibition of glycogen synthetase activity. Muscle glucose concentration remained stable during ischaemia and was significantly elevated 1 h after tourniquet release. In contrast, muscle lactate concentration was elevated during ischaemia and normal after recirculation. Blood lactate, pyruvate and serum inorganic phosphate concentrations increased markedly after tourniquet release and were still significantly elevated 1 h after recirculation, whereas ketone bodies and citric acid cycle intermediates remained unchanged. Tourniquet ischaemia had no effect on muscle phosphate concentration or on the activities of proteases, protease inhibitors or hydrolases in the blood. Nevertheless, our results clearly indicate metabolic abnormalities in the blood and skeletal muscle during 5 h of tourniquet ischaemia and even after 1 h of recirculation.
The effect of aprotinin on metabolic changes in blood of 23 patients undergoing Y-graft aortofemoral bypass operation was studied before clamping and after declamping. The right femoral artery was clamped for 122 +/- 15 (-aprotinin) and 115 +/- 10 min (aprotinin group), the left femoral artery 129 +/- 27 (-aprotinin) and 159 +/- 25 min (aprotinin group), respectively. Aprotinin caused a significant decrease of blood lactate, pyruvate, citrate and oxoglutarate levels compared with untreated controls, whereas acetoacetate and beta-hydroxybutyrate concentrations were significantly increased. It is hypothesized that blood lactate and pyruvate levels are lowered due to increased pyruvate oxidation. Limitation of citrate synthesis due to lack of oxaloacetate might explain subsequent formation of ketone bodies.
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Six cases (1981/82) with endometriosis of the bowel are reported on. There was a gynecological and surgical examination after 6-12 months. Intestinal symptoms associated with dysmenorrhea, dyspareunia and nodules, involving the cul-de-sac, the uterosacral ligaments and the anterior surface of the rectum are important symptoms of colonic endometriosis. Problems in diagnosis were illustrated by extramucosal radiologic appearance and normal mucosa and extrinsic pressure by proctosigmoidoscopy. Five patients were treated with resection of the involved bowel. Endometriosis is sufficiently common that it should always be considered in the differential diagnosis of colon lesions of women of childbearing age. In all cases characteristical symptoms were related.