摘要
目的 探讨血液透析脑型失衡综合征的发生机制。方法 采用急性肾功能衰竭的动物模型,观察血液透析后血浆渗透浓度迅速下降对脑水含量、颅内压、脑脊液生化和酸碱平衡的影响。结果 血液透析使血浆渗透浓度迅速下降,形成明显的脑/血渗透浓度梯度和尿素浓度梯度,使脑水含量明显增加,颅内压显著升高。透析后脑脊液pH下降、碳酸氢根(HCO_3^-)降低、Pco_2升高,与同期血浆相应值比较,差异有显著性意义(P<0.05)。结论 血液透析引起的血浆尿素氮快速下降可以导致脑水增加及颅压增高,其机制主要是由尿素的反向渗透效应引起。
Objective To investigate the pathogenesis of brain-type hemodialysis disequilibrium syndrome(DDS) in dogs with acute renal failure. Methods Seventy-two hours after bilateral ureteral ligation,12 uremic dogs were hemodialyzed for 2 hours,yeilding decreases in plasma urea from (66. 76±
13.70) mmol/L to (17. 85±5. 84)mmol/L( P < 0. 05) and in plasma osmolality from (359. 00 ±17. 54) mmol/L to (304. 00±5. 85) mmol/L ( P < 0. 05) . This group was compared with 12 uremic and 12 nonuremic dogs that were not dialyzed. Results In dialyzed animals after dialysis,intracranial pressures were significantly higher than that in non-dialysis animals ( P < 0. 05); brain tissue dry/wet ratio was 0. 24 which was significantly different from that in non-dialysis animals ( P < 0. 05); gradients of urea concentration and osmolality between cerebrospinal fluid (CSF) and plasma were (21. 63 ±6. 87) mmol/L and (11. 1± 3. 28)mmol/L( P < 0. 05); the CSF pH and HCO3- were 7. 34± 0. 02 and (16. 5± 1. 05)mmol/L,but for plasma,7. 39 ±0.02 and (21. 45 ±1.66) mmol/L,respectively( P < 0. 05) . Conclusions A stable animal model of DDS was successfully established. A 73. 26% decrease of plasma urea and a(55. 9±14.32) mmol/L decline of plasma osmolality after dialysis can successfully induce dialysis disequilibrium syndrome. Pathogenesis of brain-type DDS is relevant with gradient of urea and osmolality between plasma and CSF after hemodialysis. Reverse urea effect may strengthen intracranial pressure and brain edema. In addition,significant acidosis in CSF could increase brain osmolality and worsen brain edema.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
2003年第5期320-322,共3页
Chinese Journal of Nephrology
