[Effects of free oxygen radical and nitric oxide in multiple organ dysfunction syndrome induced by acute renal...

To observe the changes in free oxygen radical and nitric oxide (NO) in the liver, lung, and heart homogenate in rabbits with acute renal failure (ARF), and inquire into the mechanism of multiple organ dysfunction syndrome (MODS) subsequent to ARF.

Sixty rabbits were randomly divided into four groups (n=15 in each group). In the group I ARF was reproduced by hypodermic injection of 1% HgCl(2) in a dose of 1.3 ml/kg, and in group II ARF was reproduced by intramuscular injection of 50% glycerin in a dose of 10 ml/kg. In the control groups I and II the rabbits received an equal volume of normal saline. After 24 hours, blood samples were obtained from all the rabbits, and the liver, lung and heart were harvested and 10% homogenates were made. The blood urea nitrogen and serum creatinine were determined by automatic biochemical analyzer (Aeroset), superoxide dismutase (SOD), malondialdehyde (MDA), NO, nitric oxide synthase (NOS), and inducible nitric oxide synthase (iNOS) in tissue homogenate were also determined.

It showed that SOD activity was significantly lowered and the MDA, NO, NOS and iNOS were significantly increased in heart homogenate of ARF groups I and II compared with control group I and II (P<0.01 or P<0.05). But these indexes in the liver and lung homogenates were not significantly different between the groups (all P>0.05). The levels of NO, NOS and iNOS in serum of ARF groups I and II were significantly increased compared with control group I and II (P<0.05 or P<0.01), and the NO contents in renal homogenate of ARF groups I and II were significantly increased compared with control group I and II (P<0.01).

There is sign of damage of the myocardium in ARF, resulting in MODS. Its possible pathogenic mechanism might be attributable to free oxygen radical injury and increase in NO production. NO plays a dual role of protection and damage in the pathogenesis of ARF.