Krog M, Ejerblad S, Agren A
Br J Exp Pathol. 1986 Jun;67(3):431-8.
A prominent feature of arterial and myocardial lesions in uraemia is necrosis of the smooth muscle cells. In this study the possibility of detecting metabolic disturbances before necroses appear was investigated. The investigation was made on rats with moderate uraemia (mean serum creatinine 165 mumol/l) of 12 weeks duration. Enzyme activities and concentrations of adenine nucleotides were measured in aorta, heart and skeletal muscles. Histological examination disclosed no changes in these organs. Hexokinase, an important glycolytic enzyme, showed decreased activity in the skeletal muscle and aorta, whereas the hexosemonophosphate shunt enzyme glucose-6-phosphate dehydrogenase remained unchanged. The aspartate aminotransferase was increased in the skeletal muscle. Fat metabolism was not disturbed as reflected by unchanged activity of hydroxyacyl-CoA-dehydrogenase. Adenylatekinase which is important for the energy supply showed markedly increased activities in all tissues examined from the uraemic rats. Decreased ATP levels were found in the heart muscle and the aorta of the uraemic animals, whereas the total pool of adenosine phosphates remained unchanged in all tissues. The animal model described offers a useful means of detecting early changes in uraemia and should be useful for studying the effects of different treatments of uraemic complications.
尿毒症时动脉和心肌损伤的一个显著特征是平滑肌细胞坏死。在本研究中,对坏死出现之前检测代谢紊乱的可能性进行了调查。研究对象为患有持续12周中度尿毒症(平均血清肌酐165μmol/L)的大鼠。对主动脉、心脏和骨骼肌中的酶活性及腺嘌呤核苷酸浓度进行了测定。组织学检查显示这些器官无变化。己糖激酶作为一种重要的糖酵解酶,在骨骼肌和主动脉中的活性降低,而磷酸己糖支路酶葡萄糖-6-磷酸脱氢酶则保持不变。骨骼肌中的天冬氨酸转氨酶升高。羟酰基辅酶A脱氢酶活性未变,这表明脂肪代谢未受干扰。对能量供应很重要的腺苷酸激酶在尿毒症大鼠的所有检测组织中活性均显著增加。在尿毒症动物的心肌和主动脉中发现ATP水平降低,而所有组织中腺苷磷酸的总量保持不变。所描述的动物模型为检测尿毒症早期变化提供了一种有用的手段,并且应该有助于研究尿毒症并发症不同治疗方法的效果。