The Mechanism of Spleen Injury in Rabbits with Acute Renal Failure

Abstract

Immune function disorders are common during acute renal failure (ARF), but the mechanisms are unknown. As the spleen is the largest organ of the immune system, we aimed to observe if there are morphological changes in the spleen in rabbits with ARF. In addition, we tried to explore its mechanism from the perspective of oxygen free radicals, nitric oxide (NO), myeloperoxidase (MPO), and membrane pump activities. ARF animal models were established by either hypodermic injection of 1.3 mL/kg bw 1% HgCl2 or intramuscular injection of 10 mL/kg bw 50% glycerin. Animals were divided into 12 h, 24 h, and 48 h treatment groups with six rabbits in each group. Compared with control animals, congestion was found in the spleen and splenic trabeculae were increased in the two ARF model groups at multiple time points. The malonaldehyde, NO, nitric oxide synthase, and MPO levels in the ARF models were increased compared with the control group at 24 h or 48 h, and the superoxide dismutase and adenosine triphosphatase activities were significantly lower than the levels in the control group at multiple time points. These indices of free radical damage were induced gradually with ARF development, and there were statistically significant differences at different time points. These data suggested that histological damage of spleen during ARF may lead to immune disorders, which might be related to free radical injury, NO excessive release, polymorphonuclear neutrophils (PMN) sequestration, and membrane pump dysfunction.