Autolysehemmung an Nierengewebe durch den Kallikrein-Inaktivator Trasylol

Goslar, H. G.; Grigoriadis, P; Grundmann, E.

doi:10.1007/bf00277385

Cited by 3 publications

(2 citation statements)

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“…Accounting half-lives and protein binding, the dosages used in this experiment, i.e., aprotinin, 2 X 40,000 KJU/kg body weight, and gabex ate-mesilate, 2 X 7 mg/kg body weight, are approxi mately equipotent in vivo. Aprotinin has a potentially beneficial effect on the kidney's ischemia tolerance, be cause it inhibits the proteolytic enzymes released during autolysis [23], while the enzymes involved in energy metabolism, i.e., cytochrome oxidase, cytochrome c re ductase (NADH), lactic dehydrogenase, glucose-6-phosphodehydrogenasc and succinic dehydrogenase, are less markedly affected [23], Filipp [24] showed the epithelium in the S3 segment and the interstitium to be most sensi tive to short-term ischemia of the kidney [24]. In these same cells antiprotease administration was found to im prove the enzyme activities after ischemia [23].…”

Section: Discussionmentioning

confidence: 99%

“…Aprotinin has a potentially beneficial effect on the kidney's ischemia tolerance, be cause it inhibits the proteolytic enzymes released during autolysis [23], while the enzymes involved in energy metabolism, i.e., cytochrome oxidase, cytochrome c re ductase (NADH), lactic dehydrogenase, glucose-6-phosphodehydrogenasc and succinic dehydrogenase, are less markedly affected [23], Filipp [24] showed the epithelium in the S3 segment and the interstitium to be most sensi tive to short-term ischemia of the kidney [24]. In these same cells antiprotease administration was found to im prove the enzyme activities after ischemia [23]. In addi tion, aprotinin is capable of suppressing kallikrein-induced prostaglandin E release, but has no effect on kinin-induced prostaglandins [25].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Antiproteases (Aprotinin and Gabexate-Mesilate) on the Postischemic Vascular Response of the Kidney

1983

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Both under physiologic conditions and after short-term ischemia (1–3 min) kallikrein and locally synthesized prostaglandins contribute to control renal blood flow. In the present experiment the antiproteases aprotinin and gabexate-mesilate were administered to rabbits in an attempt to show whether the hemodynamic changes produced by 60 min of normothermic ischemia, i.e., postischemic hyperemia and reduction of vascular resistance, were equally mediated by kallikrein. Vascular responses were evaluated by determining renal cortical blood flow using radioactively labelled microspheres, by calculating vascular resistances, and by measuring the diameters of renal medullary vessels. Kidneys exposed to normothermic ischemia and sham-operated control organs of animals treated with aprotinin (2 × 40,000 KlU/kg body weight) and gabexate-mesilate (2X7 mg/kg body weight) were compared with those of rabbits which were analogously operated, but did not receive any drugs. As the antiproteases used did not significantly affect the hyperemia and the reduction of renal cortical vascular resistance seen after 60 min of normothermic ischemia, these phenomena are apparently not mediated by kallikrein. Renal medullary vasodilatation (arteriolae rectae) was significantly lower under aprotinin than in untreated ischemic kidneys, and was not longer demonstrable in gabexate-mesilate-treated animals. Thus, the effect of gabexate-mesilate was superior to that of aprotinin. Whether the antiprotease action is due to an unspecific membrane-stabilizing, to a general ezyme-inhibiting, or to a specific kallikrein-inhibiting effect, is still unclear.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Antiproteases (Aprotinin and Gabexate-Mesilate) on the Postischemic Vascular Response of the Kidney

1983

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Effects of aprotinin of organ cultures of the rat’s kidney

1976

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Fragments of adult renal tissue were maintained as organ cultures for 7 days in HEPES-buffered medium 199, supplemented with 10% calf serum and antibiotics. Addition of aprotinin (10,000 kallikrein inhibitor units per ml) to the medium resulted in improved survival of the cells of the glomeruli and tubules and preserved the integrity of the glomerular, capsular and tubular basement membranes. Optimal results were obtained when aprotinin was present throughout the period of culturing. Inclusion of aprotinin in the medium for only the first 3 days in vitro slightly increased the numbers of surviving glomerular and tubular cells, but also promoted the growth of connective tissue in the explants and was detrimental to the basement membranes of the tubules. It is suggested that both the antiproteolytic and the carbohydrate-binding properties of aprotinin are involved in the mediation of the observed effects.

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Effects of aprotinin on organ cultures of the cerebellum of the adult rat

Drayton¹,

Kiernan²

1973

Experimental Neurology

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Autolysehemmung an Nierengewebe durch den Kallikrein-Inaktivator Trasylol

Cited by 3 publications

References 10 publications

Effects of Antiproteases (Aprotinin and Gabexate-Mesilate) on the Postischemic Vascular Response of the Kidney

Effects of Antiproteases (Aprotinin and Gabexate-Mesilate) on the Postischemic Vascular Response of the Kidney

Effects of aprotinin of organ cultures of the rat’s kidney

Effects of aprotinin on organ cultures of the cerebellum of the adult rat

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