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Biomedical subjects

K Elsebach

Publications and source records attributed to K Elsebach.

4 recordsLinked to original sources

[Veno-occlusive dysfunction as a cause of erectile impotence: therapy of venous leak with retrograde embolization of the internal pudendal vein].

"Venous leak impotence" remains a therapeutic challenge as long term success rates with all interventions are only 50%. Surgical venous ligation is a well established procedure, yet not all pathological venous groups can always be occluded. Retrograde embolisation of angiographically identified pathological venous groups represent a promising alternative to surgical isolation and antegrad embolisation of deep dorsal penile veins. Four young men (19-42 years) presented with complete loss of erection. Vaginal intercourse was impossible. Pharmaco-duplex sonography with Prostaglandin E, 10-20 micrograms demonstrated normal arterial flow in all 4 penile arteries but even after intra-cavernosoal injection of Prostaglandin E, 20 micrograms no complete erection was achieved. Dynamic infusion cavernosometry showed increased maintenance flow. Cavernosography showed a venous leak involving the deep dorsal penile vein in all four cases. Embolisation was carried out via the femoral vein by coaxial technique using Histoacryl-Lipiodol solution in order to embolise all angiographically identified insufficient veins. At one year follow up all 4 patients still achieved spontaneous erections without any additional medical treatment.

Adult↗

Paraurethral actinomycosis.

Actinomycosis of the genitourinary tract is rare. Herein we report a case of actinomycosis of the urethra following staged hypospadia repair. Pathophysiology and treatment options of this rare lesion are discussed.

Actinomycosis↗

Effect of pancreatic atrophy and hypertrophy on the small intestine.

Intestinal enzyme activities were investigated in mice with spontaneously occurring exocrine pancreatic insufficiency (EPI), in rats after induction of pancreatic insufficiency by intraductal injection of oleic acid, and in rats after feeding a proteinase inhibitor (Camostate) which induced a marked pancreatic hypertrophy. An increase in saccharase activity and in vitro uptake of L-phenylalanine was found in EPI mice, while activities of alkaline phosphatase and lactase were not altered. In oleic acid induced pancreatic insufficiency and in pancreatic hypertrophy no alterations in enzyme activities were observed. Morphometric analysis revealed no alterations in mucosal surface of EPI mice. It was suggested that the small intestine adapts fuctionally to severe and long lasting pancreatic insufficiency, but not to pancreatic hypertrophy.

Adaptation, Physiological↗

Endocrine pancreatic morphology and function in exocrine insufficiency in rats.

Exocrine pancreatic insufficiency was induced in rats by injection of oleic acid into the pancreatic duct. Six weeks after a single injection of 50 microliters oleic acid, the exocrine tissue was reduced by 98%. The islets of Langerhans remained intact and showed no changes in the relative distribution of beta-, alpha-, D-, and PP-cells. In rats fed ad libitum, plasma insulin levels and pancreatic insulin content did not differ between oleic acid-treated animals and controls. The dynamic insulin response was evaluated in the isolated perfused pancreas. The biphasic pattern of insulin release after stimulation by glucose was preserved. The half-maximal (10 mM) glucose-induced insulin release was reduced to 49% after onset of exocrine atrophy. After stimulation of insulin secretion by a maximal glucose load (20 mM), the insulin output from the perfused pancreas was reduced to 56%. A reduction in insulin release to 24% occurred with respect to the arginine (15 + 10 mM glucose)-stimulated secretion. To evaluate the significance of these findings in intact animals, glucose tolerance tests were performed. There were no differences between oleic acid-, saline-, or untreated animals with respect to serum glucose or plasma insulin levels during the oral glucose tolerance test. The insulin response after intravenous glucose in oleic acid-treated rats was not statistically different from controls. Nevertheless, the serum glucose levels in rats with exocrine atrophy were above controls, indicating a slight impairment of glucose tolerance.

Animals↗