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Biomedical subjects

H C Burck

Publications and source records attributed to H C Burck.

At least 19 recordsLinked to original sources
PubMed1991

[Inferior vena cava compression syndrome in cystic kidney. Duplex ultrasonic diagnosis].

Four months after renal transplantation for polycystic renal degeneration a 38-year-old man developed breathing-related pain in the left upper lung and a sinus tachycardia (130/min). Lung perfusion scintigraphy demonstrated pulmonary emboli from an acute venous thrombosis of the left lower leg. Polycythaemia and impairment of clot-inhibiting factors were excluded. Ultrasound examination of the abdomen revealed stenosis of the inferior vena cava (IVC) distal to the hepatic veins, dorsal to the liver and ventral of a huge right polycystic kidney which had been left in situ at the time of the renal transplantation. Duplex sonography demonstrated a band-like flow profile in the region of the stenosis. Blood flow was clearly increased (0.62 m/s) and not affected by either heart rate or breathing movements. The findings were confirmed by angiography. The right kidney, weighing 5 kg, was removed at surgery. The IVC stenosis was postoperatively found to be relieved and duplex sonography gave normal findings.

Adult↗
PubMed1975

[Acute renal failure after the infusion of hemoglobin solutions with or without red cell ghosts in rabbits (author's transl)].

Out of 85 rabbits 2j received a purified 6% hemoglobin solution free of ghosts (1,8 gHb/Kg) and were compared to 14 animals receiving the same dose of a crude hemoglobin solution containing ghosts. 11 rabbits had 5 infusions with a daily dose of 1,2 g Hb/Kg of the stromafree solution. Controls were partly untreated partly infused with saline. Creatinin, urea, electrolytes, and haptoglobin were determined in the serum oxygen consumption was measured separately in cortex and medulla by Warburg technique, and all kidneys examined histologically. In both groups 20% of the animals died spontaneously. Both groups exhibited the typical morphological and functional signs of acute renal failure. There was an increase in creatinin, urea, and potassium in the serum and a gain in kidney weights. In cortex and medulla we found a 20% drop in O2 consumption in both groups. Thus there was no evidence that ghosts play any role in the pathogenesis of renal failure in hemolysis or in the course of Hb-infusions. even after 5 infusions with lower dose renal damage was demonstrable. The drop in haptoglobin levels indicates, that renal ischemia may be induced by a disturbance in hemoglobin breakdown. The pathogenesis of renal damage has to be elucidated before Hb-solutions come into therapeutical use.

Acute Kidney Injury↗
PubMed1975

[Influence of beta 1-methyl-digoxin to red cell electrolyte contents in healthy normals (author's transl)].

6 healthy controls received daily doses of 0.6 mg beta-methyl-digoxin for 3 days and further 0.3 mg for the following 5 days each. After the first 3 days sodium content in the red cells increased from 4.8 to 6.6 meg/kg significantly in parallel to the glycoside level of 1.5 ng/ml (1.2 times 10-9 M). At the same time magnesium in the cells fell significantly from 4.1 to 3.7 meg/kg. There was no change in the concentration of potassium, calcium or chloride at this time. While the glycoside level dropped during the following 5 days under 0.3 mg of methyl-digoxin to 1.2 ng/ml (1 times 10-9 M), sodium content in the cells increased further up to 8.3 meq/kg and was paralleled by a decrease in potassium content from 84.6 to 82.0 meq/kg. There were no changes in plasma electrolyte concentrations during the experiments. Our results confirm the concept of Hoffman that there are two transport pathways in human red cells which differ basically in their dependencies of the sodium and potassium composition of the external medium and the concentration of glycoside needed to inhibit the transport. Our data evidence that red cell electrolyte contents reflect levels of digoxin. They might be useful to follow up the therapeutical effect of cardiac glycosides.

Adult↗