摘要
目的:了解不同 CO2 气腹压力对慢性肾功能衰竭模型大鼠肾功能的影响 ,探讨 CO2 气腹造成肾功能变化在亚细胞水平上损伤的可能机制。 方法:建立 5 / 6肾切除大鼠慢性肾功能衰竭模型 ,分别施加 0 .6 7k Pa(5mm Hg)、1.33k Pa(10 mm Hg) CO2 气腹压 ,检测解除气腹即时、1d、4 d血肌酐 (SCr)、尿素氮 (BU N)水平及各时相点时肾脏组织线粒体 Na2 + - K+ - ATP酶和 Ca2 + - ATP酶活性。结果 :解除气腹即时 SCr开始升高 ,1d时升高显著 ,第 4天时下降 ,接近对照组水平 ;BU N变化不明显。肾脏组织线粒体 Na2 + - K+ - ATP酶和 Ca2 + - ATP酶活性也分别在解除气腹即时及 1d时下降 ,第 4天时渐趋恢复。与 0 .6 7k Pa各组相比 ,1.33k Pa气腹压各组出现的变化更加明显。 结论 :CO2 气腹可引起慢性肾功能衰竭肾脏功能改变 ;气腹压力的直接压迫使肾皮质缺血及解除气腹后血流再灌注损伤可能干扰细胞中线粒体的生物氧化功能 ,从而导致细胞功能障碍 ;
Objective: To investigate the influence of CO\-2 pneumoperitoneum at different pressure on the kidney function of rats with chronic renal failure and the possible mechanism associated with these changes at the subcellular level. Methods: CRF rat models established by 5/6 subnephrectomy were exposed to CO\-2 pneumoperitoneum at the pressure of 0.67 kPa and 1.33 kPa. Serum creatine (SCr) and blood urine nitrogen (BUN) was examined on 0 d?1 d?4 d after desufflation individually. The activity of Na 2+ K\++ ATPase and Ca 2+ ATPase also were determined at the same time point. Results: After CO\-2 gas was released, the concentration of SCr increased slightly immediately, significantly on 1 day. 4 days later, then it returned to baseline. There was no obvious variation in BUN. Compared with control group, decreasing of the activity of Na 2+ K\++ ATPase? Ca 2+ ATPase of mitochondria in renal tissue were significant on 0 day and 1day individually postoperation in 1.33 kPa group, lower but no statistical difference on 4 day. The changes in 0.67 kPa group in the study parameters were more mild compared with that in 1.33 kPa group. Conclusion: Renal function in rats with chronic renal failure had been influenced by CO\-2 pneumoperitoneum and reversible change also had been found during transient period post operation at the experimental condition in our study. It may be the result of the damage of mitochondria due to ischemia and anoxia in renal tissue.
出处
《新疆医科大学学报》
CAS
2002年第2期153-156,共4页
Journal of Xinjiang Medical University
