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Biomedical subjects

K Möhring

Publications and source records attributed to K Möhring.

At least 73 records · Page 4Linked to original sources

Haemodialysis in imipramine poisoning? An experimental study.

In the last several years an increasing number of severe imipramine intoxications have been observed. Though standard principles for the treatment of acute tricyclic poisoning have been established, nonetheless there still exists doubt on the most effective method of tricyclic removal in cases of massive overdose. Haemodialysis was successfully employed until now but has not found general acceptance as only insignificant amounts of imipramine could be recovered from the dialysate. An experimental clearance study was undertaken using radiolabelled imipramine (14C-I) to obtain insight into the usefullness of haemodialysis in imipramine poisoning. 14C-I clearances which were calculated in a closed circuit dialysis system ranged between 18 ml/min and 48 ml/min depending on the constitution of the dialysate, i.e. aqueous or lipid solution. Surprisingly a rapid and significant uptake of imipramine by the plastic material (polyvinylchloride) of the extracorporeal blood line system was detected. This escape of imipramine from the blood into the tubings explains the poor recovery of tricyclics from the dialysate, which discredited haemodialysis as a therapeutical method in imipramine poisoning. The results of our experiments may offer a new method of rapid tricyclic elimination in severe imipramine intoxications.

Absorption↗

[Thrombotic occlusion of an arteriovenous Cimino shunt in acute pancreatitis (author's transl)].

An arteriovenous (Cimino) shunt in both right and left forearms clotted during an episode of acute pancreatitis in two patients on chronic haemodialysis. Systemic hypercoagulability (circulating fibrin monomers, shortening of r and k time in the thrombelastogram and shortening of the PTT-time) occurred in association with inhibition of fibrinolysis (prolongation of euglobulin lysis time). Localized thrombosis at the shunt is thought to be due to superimpostition of systemic hyper-coagulability on a local increase in platelet adhesiveness.

Acute Disease↗

Pathophysiology and therapy of hypercalciuria in patients who form recurrent stones.

There are two alternative mechanisms that might be responsible for idiopathic hypercalciuria in recurrent stone formers: increased intestinal absorption of calcium with parathyroid suppression and overflow hypercalciuria (primary intestinal hyperabsorption) or renal calcium leak with compensatory hyperparathyroidism and intestinal hyperabsorption (primary renal-tubular hypercalciuria). In this study, urinary excretion of cAMP, the intracellular effector substance synthetised under parathyroid hormone stimulation, was found to be in the normal range. This finding would argue against intestinal hyperabsorption of calcium as the primary cause of hypercalciuria.

Benzothiadiazines↗