Stepanek J
Respiration. 1979;37(2):79-84. doi: 10.1159/000194010.
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.
在正常空气通气、通过适当气体混合物通气诱导的高碳酸血症期间以及发作期间，对麻醉并人工呼吸的杂种犬研究了药物诱导的门静脉血管收缩（氧烯洛尔1毫克/千克）或血管扩张（酚妥拉明0.5毫克/千克）引起的动脉血氨浓度变化。动脉血浆中的NH₃值在41微克/100毫升范围内，门静脉血浆中的值高3至4倍。逐渐增加高碳酸血症水平会打开门静脉至体静脉分流，导致动脉NH₃增加，脑脊液中的NH₃也有较小程度增加。静脉注射1毫克/千克氧烯洛尔引起的门静脉血管收缩导致在常氧或高碳酸血症期间分流功能消除，导致动脉血中NH₃浓度降低，从而脑脊液中的NH₃浓度也降低。另一方面，静脉注射0.5毫克/千克酚妥拉明的血管舒张作用在常氧期间导致动脉NH₃短暂、统计学上显著增加；在高碳酸血症期间，NH₃值与对照组无差异。
