The mechanism of myocardium and pancreas injury in rabbits with acute renal failure might be related to myeloperoxidase and membrane pump activities

Abstract

LABORATORY STUDYThe mechanism of myocardium and pancreas injury in rabbits with acute renal failure might be related to myeloperoxidase and membrane pump activitiesThe mechanism of myocardium and pancreas injury in acute renal failure Zi-Gang Zhao, Chun-Yu Niu, Yu-Ping Zhang, Rui Han, Ya-Li Hou, Bao-liang Li, and Shu-ting Du Institute of Microcirculation, Hebei North University, Zhangjiakou 075000, Hebei, PR China AbstractThere is increasing evidence indicating that the distant organ injury is a major contributor of high mortality in patients subjected to acute renal failure (ARF). However, sources and mechanisms that ARF causes distant organ injury remain to be determined. The aim of this study is to explore the mechanism from polymorphonuclear neutrophil (PMN) sequestration and membrane pump suppression. To achieve this, we examined myeloperoxidase (MPO), a marker of PMN accumulation in tissues, and membrane pump activities of heart, pancreas, and kidney in two ARF rabbit models. Rabbits are randomly assigned to control, HgCl 2 -treated, and glycerin-treated groups. ARF animal models are established by hypodermic injection of 1% HgCl 2 with 1.3 mL/kg bodyweight (bw) in HgCl 2 -treated group or intramuscular injection of 50% glycerin with 10 mL/kg bw in glycerin-treated group, respectively, and all animals in each group are further divided into 12 h, 24 h, and 48 h subgroups with each consisting of six rabbits. Six healthy rabbits serve as control group. Results have shown that MPO activities of kidney, myocardium, and pancreas in two model groups were significantly increased than control group at diverse time points. Membrane pump activities of kidney in two model groups are significantly lower than the control group at multiple time points. Moreover, Na -ATPase activities of myocardium and pancreas in two model groups are gradually declined with the development of ARF. These findings suggest that PMN sequestration and membrane pump suppression plays an important role in the pathogenesis of ARF and also a major mechanism of myocardium and pancreas injury during the process of ARF.

The Mechanism of Spleen Injury in Rabbits with Acute Renal Failure

“…So, mercury is one of the cytoplasmic toxins and the injury mechanisms of renal tubule are different from that of myoglobin to some extent. 21 The results of this study indicate that spleen injury was present in both ARF induced by exogenous mercury and endogenous myoglobin, which suggests that the spleen injury is induced neither by HgCl 2 nor glycerin purely. These results imply that the internal environment disorders following ARF may be one of the main reasons of spleen injury, which may be the common image of immunity dysfunction in the pathogenesis of ARF.…”

Polymorphisms in the myeloperoxidase gene locus are associated with acute kidney injury–related outcomes

“…These end-products are powerful oxidants that can exert biological effects in the kidney 30 . Indeed, in situ MPO activity has been used as an index of neutrophil kidney parenchymal infiltration in experimental models of ischemia-reperfusion injury 31-35 and nephrotoxicity 36,37 .…”

Mesenteric lymph duct ligation after hemorrhagic shock enhances the ATP level and ATPase activity in rat kidneys

“…9,12,14,15 One unit of ATPase activity represents the amount of enzyme that will produce 1 mmol/h of organic phosphorus from the hydrolysis of ATP into ADP. The protein content of the homogenate was quantified via the Coomassie brilliant blue colorimetric method using a kit (Jiancheng Biotechnology, Nanjing, China).…”

“…Thus, enhancing membrane pump activity could alleviate kidney injury. [9][10][11] However, the effects of MLDL on the ATP level and membrane pump activity in the kidneys after hemorrhagic shock remain unclear. Therefore, the present study aims to examine the effects of MLDL on the ATP level and the ATPase activity in renal tissue after hemorrhagic shock, and to determine the mechanism by which MLDL alleviates renal injury.…”