Local cytokine production and acute coronary events

2000 ◽  
Vol 73 (1) ◽  
pp. 79-81 ◽  
Author(s):  
Juan Carlos Kaski
2012 ◽  
Vol 60 (17) ◽  
pp. B45-B46
Author(s):  
Cameron Donaldson ◽  
David Schneider ◽  
Daniel Bertges ◽  
Julie Adams ◽  
Nader Elgharib ◽  
...  

2018 ◽  
Vol 6 (4) ◽  
pp. 323-335
Author(s):  
Peter Weighardt ◽  
Niels Hayashi

Sepsis is the leading cause of death in critically ill patients, and the incidence of sepsis is increasing causes multiorgan failure, including acute kidney injury (AKI) and patients with both sepsis and AKI have an especially high mortality rate. Several different pathophysiological mechanisms have been proposed for sepsis-induced AKI: vasodilation-induced glomerular hypoperfusion, dysregulated circulation within the peritubular capillary network, inflammatory reactions by systemic cytokine storm or local cytokine production, and tubular dysfunction induced by oxidative stress animal sepsis models have been developed using LPS infusion. Renal dysfunction evaluated by serum creatinine and BUN was found in acute non-survivors (<24 hours) and decreased urine output in subacute non-survivors (24–96 hours). The study show that increased AKI in animal with blood collected heparin (P=0.002) compared to citrate, furthermore; sham mice that received heparin did not develop AKI.


Author(s):  
Mahboob Hossain Qureshi ◽  
Tiantuo Zhang ◽  
Yoshinobu Koguchi ◽  
Kazutoshi Nakashima ◽  
Haruki Okamura ◽  
...  

1994 ◽  
Vol 22 (1) ◽  
pp. 7-8 ◽  
Author(s):  
Richard J. Battafarano ◽  
David L. Dunn

1995 ◽  
Vol 115 (5) ◽  
pp. 689-696 ◽  
Author(s):  
Karin Ågren ◽  
Ulf Andersson ◽  
Britt Nordlander ◽  
Carl-Erik Nord ◽  
Annika Linde ◽  
...  

2017 ◽  
Vol 95 ◽  
Author(s):  
J. Kossl ◽  
B. Hermankova ◽  
E. Javorkova ◽  
P. Bohacova ◽  
A. Zajicova ◽  
...  

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