[Pathogenesis of acute hypercapnic hyperammoniaemia (author's transl)].
Alterations in the ammonia concentration in arterial blood due to drug-induced portal vasoconstriction (oxprenolol 1 mg/kg) or vasodilatation (phentolamine 0.5 mg/kg) were studied in anaesthetized and artificially respirated mongrel dogs during normal air ventilation, during hypercapnia induced by ventilation with an appropriate gas mixture, and during episodes. The NH3 values in arterial-blood plasma were in the region of 41 microgram/100 ml and those in portal-blood plasma 3--4 times higher. The induction of progressive levels of hypercapnia opened the portal-to-systemic venous shunt, producing an increase in arterial NH3 and, to a lesser extent, NH3 in the CSF. The portal vasoconstriction caused by oxprenolol 1 mg/kg i.v. resulted in the functional elimination of the shunt during normoxia or hypercapnia, leading to a decrease in the NH3 concentration in the arteral blood and hence also in the CSF. The vasodilating effect of phentolamine 0.5 mg/kg i.v., on the other hand, caused a transient, stastically significant increase in arterial NH3 during normoxia; during hypercapnia the NH3 values did not differ from the controls.
D000641:Ammonia / Q000097:blood* / Q000134:cerebrospinal fluid; D000818:Animals; D004285:Dogs; D006935:Hypercapnia / Q000097:blood*; D010096:Oxprenolol / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D014661:Vasoconstriction; D014664:Vasodilation
D010096:Oxprenolol; D000641:Ammonia; D010646:Phentolamine
Pathogenese einer akuten hyperkapnischen Hyperammoniämie.