Pisarenko O I, Studneva I M
Biull Vsesoiuznogo Kardiol Nauchn Tsentra AMN SSSR. 1985;8(2):57-63.
Kinetics of 15N inclusion into amino acids and urea of the intact isolates rat heart and of the rat heart with experimental infarction in the course of 1.6 mM 15N-ammonium acetate perfusion was investigated. The basic mechanism of ammonia binding in the heart is the glutaminsynthetase reaction. 15N inclusion into the glutaminic and asparaginic acids, alanine and urea takes place at a lower rate. In myocardial infarction 15N accumulation by all amino acids is slowed down and its accumulation by the urea is increased. The results suggest that urea synthesis activation in infarcted myocardium is a compensatory change brought about by a disturbance of basic mechanisms of free ammonia binding.
研究了在1.6 mM 15N-醋酸铵灌注过程中,完整离体大鼠心脏和实验性梗死大鼠心脏中15N掺入氨基酸和尿素的动力学。心脏中氨结合的基本机制是谷氨酰胺合成酶反应。15N掺入谷氨酸、天冬氨酸、丙氨酸和尿素的速率较低。在心肌梗死时,所有氨基酸的15N积累减慢,而尿素的15N积累增加。结果表明,梗死心肌中尿素合成的激活是游离氨结合基本机制紊乱引起的一种代偿性变化。