No protection of the porcine kidney by ischaemic preconditioning

被引:15
作者
Behrends, M
Walz, MK
Kribben, A
Neumann, T
Helmchen, U
Philipp, T
Schulz, R
Heusch, G
机构
[1] Univ Essen Gesamthsch, Sch Med, Dept Pathophysiol, D-45122 Essen, Germany
[2] Univ Essen Gesamthsch, Sch Med, Dept Gen Surg, D-45122 Essen, Germany
[3] Univ Essen Gesamthsch, Sch Med, Dept Nephrol, D-45122 Essen, Germany
[4] Univ Hamburg, Dept Pathol, D-20246 Hamburg, Germany
关键词
D O I
10.1111/j.1469-445X.2000.02073.x
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
One or more episodes of sublethal ischaemia and reperfusion delay infarct development during subsequent, sustained ischaemia in the heart and skeletal muscle. The present study tested whether or not such ischaemic preconditioning (IP) also protects the kidney. Enflurane-anaesthetized pigs underwent 60 min of right renal vessel occlusion (RVO), Followed by 8 h of reperfusion without (placebo group, n = 8) or with three preceding cycles of 10 min RVO and 10 min reperfusion (IP group, n = 8). After 8 h of reperfusion, kidneys were oliguric in both groups (placebo group: 23 +/- 21 ml h(-1), IP group: 24 +/- 27 ml h(-1)). A transient polyuric phase occurred in the IP group at 2 h reperfusion. The reperfused kidneys did not excrete inulin, creatinine or urea in both groups, although renal blood flow during reperfusion was similar to baseline. Morphological damage ranged in both groups from single cell necrosis to disseminated patchy necrosis; the number of pyknotic cells tended to be higher in the IP group than in the placebo group (27.0 +/- 7.1 vs. 15.6 +/- 5.6%, n.s.). In anaesthetized pigs, IP did not therefore attenuate renal dysfunction and morphological damage resulting from 60 min of renal normothermic ischaemia followed by 8 h of reperfusion.
引用
收藏
页码:819 / 827
页数:9
相关论文
共 50 条
[1]   MECHANISMS OF FILTRATION FAILURE DURING POSTISCHEMIC INJURY OF THE HUMAN KIDNEY - A STUDY OF THE REPERFUSED RENAL-ALLOGRAFT [J].
ALEJANDRO, V ;
SCANDLING, JD ;
SIBLEY, RK ;
DAFOE, D ;
ALFREY, E ;
DEEN, W ;
MYERS, BD .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (02) :820-831
[2]   NON-OLIGURIC ACUTE RENAL-FAILURE [J].
ANDERSON, RJ ;
LINAS, SL ;
BERNS, AS ;
HENRICH, WL ;
MILLER, TR ;
GABOW, PA ;
SCHRIER, RW .
NEW ENGLAND JOURNAL OF MEDICINE, 1977, 296 (20) :1134-1138
[3]   MECHANISMS OF ISCHEMIC ACUTE-RENAL-FAILURE [J].
BONVENTRE, JV .
KIDNEY INTERNATIONAL, 1993, 43 (05) :1160-1178
[4]   COMPLICATIONS OF NEPHRON SPARING SURGERY FOR RENAL TUMORS [J].
CAMPBELL, SC ;
NOVICK, AC ;
STREEM, SB ;
KLEIN, E ;
LICHT, M .
JOURNAL OF UROLOGY, 1994, 151 (05) :1177-1180
[5]   IMPROVED FUNCTIONAL RECOVERY BY ISCHEMIC PRECONDITIONING IS NOT MEDIATED BY ADENOSINE IN THE GLOBALLY ISCHEMIC ISOLATED RAT-HEART [J].
CAVE, AC ;
COLLIS, CS ;
DOWNEY, JM ;
HEARSE, DJ .
CARDIOVASCULAR RESEARCH, 1993, 27 (04) :663-668
[6]   Protective mechanism of preconditioning hypoxia attenuates apoptosis formation during renal ischemia/reperfusion phase [J].
Chien, CT ;
Chen, CF ;
Hsu, SM ;
Lee, PH ;
Lai, MK .
TRANSPLANTATION PROCEEDINGS, 1999, 31 (05) :2012-2013
[7]   Ischemic preconditioning attenuates functional, metabolic, and morphologic injury from ischemic acute renal failure in the rat [J].
Cochrane, J ;
Williams, BT ;
Banerjee, A ;
Harken, AH ;
Burke, TJ ;
Cairns, CB ;
Shapiro, JI .
RENAL FAILURE, 1999, 21 (02) :135-145
[8]   PRECONDITIONING CAUSES IMPROVED WALL MOTION AS WELL AS SMALLER INFARCTS AFTER TRANSIENT CORONARY-OCCLUSION IN RABBITS [J].
COHEN, MV ;
LIU, GS ;
DOWNEY, JM .
CIRCULATION, 1991, 84 (01) :341-349
[9]   FUNCTIONAL AND MORPHOLOGICAL EFFECTS OF DEFIBROTIDE ON RENAL ISCHEMIA [J].
COMANDELLA, MG ;
RIGOTTI, P ;
VALENTE, M ;
PITTONI, G ;
BALDAN, N ;
GANZ, E ;
AMODIO, P ;
ANCONA, E .
RESEARCH IN EXPERIMENTAL MEDICINE, 1993, 193 (02) :65-71
[10]  
FINN WF, 1981, J LAB CLIN MED, V98, P21