scholarly journals Acute Lethal Toxicity, Hyperkalemia Associated with Renal Injury and Hepatic Damage after Intravenous Administration of Cadmium Nitrate in Rats

2007 ◽  
Vol 49 (1) ◽  
pp. 17-24 ◽  
Author(s):  
Emi Dote ◽  
Tomotaro Dote ◽  
Hiroyasu Shimizu ◽  
Yukari Shimbo ◽  
Michiko Fujihara ◽  
...  
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Hepatic Damage ◽  
Cadmium Nitrate ◽  
Lethal Toxicity

Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation

Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 3781-3787 ◽  
Author(s):  
Akio Mizutani ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Takayuki Noguchi
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Protein C ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Activated Protein C ◽  
Factor Xa ◽  
Renal Tissue ◽  
Tissue Blood Flow ◽  
Leukocyte Activation

We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tissue blood flow and the increase in the vascular permeability, whereas neither DEGR-FXa, heparin, nor DIP-APC produced such effects. Renal I/R-induced increases in plasma levels of fibrin degradation products were significantly inhibited by APC, DEGR-FXa, and heparin. These observations suggest that APC reduces I/R-induced renal injury independently of its anticoagulant effects but in a manner dependent on its serine protease activity. Renal levels of tumor necrosis factor- (TNF-), rat interleukin-8, and myeloperoxidase were significantly increased after renal I/R. These increases were significantly inhibited by APC but not by DEGR-FXa, heparin, or DIP-APC. Leukocytopenia produced effects similar to those of APC. These findings strongly suggest that APC protects against I/R-induced renal injury not by inhibiting coagulation abnormalities but by inhibiting activation of leukocytes that play an important role in I/R-induced renal injury. Inhibition of leukocyte activation by APC could be explained by the inhibitory activity of TNF-.

scholarly journals Accumulation of Clostridium perfringens Epsilon-Toxin in the Mouse Kidney and Its Possible Biological Significance

2003 ◽  
Vol 71 (9) ◽  
pp. 5371-5375 ◽  
Author(s):  
Eiji Tamai ◽  
Tetsuya Ishida ◽  
Shigeru Miyata ◽  
Osamu Matsushita ◽  
Hirofumi Suda ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clostridium Perfringens ◽  
Host Defense ◽  
Renal Injury ◽  
Biological Significance ◽  
Mouse Kidney ◽  
Bilateral Nephrectomy ◽  
Lethal Toxicity ◽  
Collecting Ducts ◽  
Epsilon Toxin

ABSTRACT In this paper we show that Clostridium perfringens epsilon-toxin accumulates predominantly in the mouse kidney, where it is distributed mainly in glomeruli, capillaries, and collecting ducts. Although some pycnotic and exfoliated epithelial cells were observed in distal tubuli and collecting ducts, there were no findings indicative of severe renal injury. Bilateral nephrectomy increased the mouse lethality of the toxin, suggesting that the kidney contributes to the host defense against the lethal toxicity of epsilon-toxin.

Activated protein C reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation

Blood ◽  
2000 ◽  
Vol 95 (12) ◽  
pp. 3781-3787 ◽  
Author(s):  
Akio Mizutani ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Takayuki Noguchi
Keyword(s):  
Intravenous Administration ◽  
Renal Injury ◽  
Protein C ◽  
Degradation Products ◽  
Ischemia Reperfusion ◽  
Activated Protein C ◽  
Factor Xa ◽  
Renal Tissue ◽  
Tissue Blood Flow ◽  
Leukocyte Activation

Abstract We examined whether activated protein C (APC) reduces ischemia/reperfusion (I/R)–induced renal injury by inhibiting leukocyte activation. In a rat model, intravenous administration of APC markedly reduced I/R-induced renal dysfunction and histological changes, whereas intravenous administration of dansyl glutamylglycylarginyl chloromethyl ketone–treated factor Xa (DEGR-FXa; active-site–blocked factor Xa), heparin or diisopropyl fluorophosphate–treated APC (DIP-APC; inactive derivative of ARC) had no effect. Furthermore, APC significantly inhibited the I/R-induced decrease in renal tissue blood flow and the increase in the vascular permeability, whereas neither DEGR-FXa, heparin, nor DIP-APC produced such effects. Renal I/R-induced increases in plasma levels of fibrin degradation products were significantly inhibited by APC, DEGR-FXa, and heparin. These observations suggest that APC reduces I/R-induced renal injury independently of its anticoagulant effects but in a manner dependent on its serine protease activity. Renal levels of tumor necrosis factor- (TNF-), rat interleukin-8, and myeloperoxidase were significantly increased after renal I/R. These increases were significantly inhibited by APC but not by DEGR-FXa, heparin, or DIP-APC. Leukocytopenia produced effects similar to those of APC. These findings strongly suggest that APC protects against I/R-induced renal injury not by inhibiting coagulation abnormalities but by inhibiting activation of leukocytes that play an important role in I/R-induced renal injury. Inhibition of leukocyte activation by APC could be explained by the inhibitory activity of TNF-.

105: Renal Injury Mechanisms in Motor Vehicle Collisions: Analysis of the Crash Injury Research and Engineering Network (CIREN) Dataset

2007 ◽  
Vol 177 (4S) ◽  
pp. 37-37
Author(s):  
James K. Kuan ◽  
Robert Kaufman ◽  
Jonathan L. Wright ◽  
Charles Mock ◽  
Avery B. Nathens ◽  
...  
Keyword(s):  
Renal Injury ◽  
Motor Vehicle ◽  
Motor Vehicle Collisions ◽  
Vehicle Collisions ◽  
Injury Mechanisms ◽  
Injury Research

Intravenous administration of furosemide in heart failure

JAMA ◽  
1967 ◽  
Vol 200 (10) ◽  
pp. 824-829 ◽  
Author(s):  
M. Davidov
Keyword(s):  
Heart Failure ◽  
Intravenous Administration
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