A STUDY IN THE MAINTENANCE PHASE OF ISCHEMIC ACUTE-RENAL-FAILURE IN THE RAT

被引:4
作者
BAYATI, A
机构
[1] Dept. of Phys./Med. Biophys., University of Uppsala, S-751 23 Uppsala
来源
ACTA PHYSIOLOGICA SCANDINAVICA | 1990年 / 138卷 / 03期
关键词
Acute renal failure; Diffusion half-time; Erythrocyte trapping; Semipermeable membrane; Tamm-Horsfall protein; Tubular blockade;
D O I
10.1111/j.1748-1716.1990.tb08857.x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The fate of the trapped deformed erythrocytes seen in the early recirculation phase after ischaemia and the generation of long Tamm-Horsfall (TH) cylinders in the renal medulla during the first week after recirculation was studied in rats. In an in-vitro study the effects of different concentrations of TH protein on the permeability to Na+ of a semipermeable membrane were also investigated. The trapping of erythrocytes was found to be a reflow phenomenon, as there was no increase in the capillary area of the medulla in kidneys subjected to ischaemia but with no recirculation. This area increased to a maximum of 34.6 ± 2.07% 20 min after recirculation and decreased to a normal value of 3.3 ± 0.74% 1 day after the primary ischaemia. The area occupied by cylinders increased to a maximum of 19.2 ± 1.4% 2 days after the primary damage and was as large as 16.7 ± 1.47% after 1 week. It was also shown that the diffusion half-time of Na+ ions across a semipermeable membrane increased from 11.4 ± 0.45 min to a maximum of 32.2 ± 2.19 min with a protein concentration of 1 mg ml-1. It was concluded that the trapping of erythrocytes alone could not explain the decrease in renal function 1 week after the primary damage, but that the blockade of the tubules by the long homogeneous TH cylinders could be responsible for this decrease.
引用
收藏
页码:349 / 357
页数:9
相关论文
共 29 条
[1]   NEPHRON STOP-FLOW PRESSURE RESPONSE TO OBSTRUCTION FOR 24 HOURS IN RAT-KIDNEY [J].
ARENDSHORST, WJ ;
FINN, WF ;
GOTTSCHALK, CW .
JOURNAL OF CLINICAL INVESTIGATION, 1974, 53 (05) :1497-1500
[2]   THE LONG-TERM OUTCOME OF POSTISCHEMIC ACUTE-RENAL-FAILURE IN THE RAT .2. A HISTOPATHOLOGICAL STUDY OF THE UNTREATED KIDNEY [J].
BAYATI, A ;
NYGREN, K ;
KALLSKOG, O ;
WOLGAST, M .
ACTA PHYSIOLOGICA SCANDINAVICA, 1990, 138 (01) :35-47
[3]   MECHANISM OF ERYTHROCYTE TRAPPING IN ISCHEMIC ACUTE-RENAL-FAILURE [J].
BAYATI, A ;
CHRISTOFFERSON, R ;
KALLSKOG, O ;
WOLGAST, M .
ACTA PHYSIOLOGICA SCANDINAVICA, 1990, 138 (01) :13-23
[4]   THE LONG-TERM OUTCOME OF POSTISCHEMIC ACUTE-RENAL-FAILURE IN THE RAT .1. A FUNCTIONAL-STUDY AFTER TREATMENT WITH SOD AND SUCROSE [J].
BAYATI, A ;
KALLSKOG, O ;
WOLGAST, M .
ACTA PHYSIOLOGICA SCANDINAVICA, 1990, 138 (01) :25-33
[5]   PREVENTION OF ISCHEMIC ACUTE-RENAL-FAILURE WITH SUPEROXIDE-DISMUTASE AND SUCROSE [J].
BAYATI, A ;
HELLBERG, O ;
ODLIND, B ;
WOLGAST, M .
ACTA PHYSIOLOGICA SCANDINAVICA, 1987, 130 (03) :367-372
[6]  
BAYATI A, 1990, IN PRESS ACTA PHYSL
[7]   THE VISCOMETRIC BEHAVIOUR OF A MUCOPROTEIN ISOLATED FROM HUMAN URINE [J].
CURTAIN, CC .
AUSTRALIAN JOURNAL OF EXPERIMENTAL BIOLOGY AND MEDICAL SCIENCE, 1953, 31 (03) :255-265
[8]   EFFECTS OF 24-HOUR UNILATERAL URETERAL OBSTRUCTION ON GLOMERULAR HEMODYNAMICS IN RAT-KIDNEY [J].
DALCANTON, A ;
CORRADI, A ;
STANZIALE, R ;
MARUCCIO, G ;
MIGONE, L .
KIDNEY INTERNATIONAL, 1979, 15 (05) :457-462
[9]  
HAMLIN LM, 1977, INT J PEPT PROT RES, V10, P270
[10]  
HELLBERG O, 1985, ACTA PHYSL SCAN S542, V142, P382