CHANGES IN SERUM RENAL FUNCTION INDEXES, RENAL HISTOPATHOLOGY AND EXPRESSION OF INFLAMMATORY FACTORS IN TISSUES AFTER CARDIOPULMONARY RESUSCITATION IN RATS

Xiaowei Yan^{1, 2}, Peng Xu³, Yan Zhao^{1, *}

¹Department of Emergency Center, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China - ²Department of Emergency, Renmin Hospital of Wuhan University, Wuhan, 430060, China - ³Department of Emergency, Xiangyang No.1 People's Hospital, Hubei University of Medicine, Xiangyang, 441000, China

Objective: This study aims to examine the changes in serum renal function indexes, renal histopathology, and expression of inflammatory factors in tissues after cardiopulmonary resuscitation in rats. 

Methods: 20 healthy male SD rats were selected and randomly divided into the control and cardiopulmonary resuscitation groups. Rats in the control group were subjected to tracheal intubation of artery puncture and indwelling punctured tube and were not established cardiac arrest and cardiopulmonary resuscitation models. Rats in the cardiopulmonary resuscitation group were subjected to tracheal intubation of artery puncture and indwelling punctured tube and were established cardiopulmonary resuscitation model by suffocation. The tracheal tube was clamped to cardiac arrest, and cardiopulmonary resuscitation was performed 7 minutes later. The two groups of rats were sacrificed by anesthesia at 6h (T6) and 24h (T24) time after recovery of spontaneous circulation. Renal specimens were retained and fixed with formaldehyde. HE staining was used to detect the pathological changes of kidney tissue in two groups of rats. Mc Whinnie semi-quantitative method was used to evaluate the degree of renal tubular injury. Furthermore, enzyme-linked immunosorbent assay was used to test the levels of urea nitrogen (BUN), creatinine(Cr), neutrophil gelatinase-associated lipocalin (NGAL) and tumor necrosis factor (TNF-α) at time point T6 and T24 of the two groups of rats. 

Results: In the cardiopulmonary resuscitation group, the renal tissue structure was disordered at the T6 time point after spontaneous circulation recovery with the swollen cells and epithelial vacuole degeneration in the renal tubules. At the T24 time point, the renal tissue structure was significantly disordered, the cells were swollen, the nucleus disappeared, and the film was bared. After spontaneous circulation recovery, the renal tubule scores of the rats in the cardiopulmonary resuscitation group at T6 and T24 were significantly higher than those in the control group (P<0.01). Also, the BUN and Cr levels of the cardiopulmonary resuscitation group at the T24 time point were significantly higher than those at the T6 time point (P <0.05). The levels of BUN and Cr at time point T6 and T24 in the cardiopulmonary resuscitation group were higher than those in the control group (P<0.05). The differences in NGAL and TNF-α at the time point T6 and T24 in the cardiopulmonary resuscitation group were statistically significant (P<0.05). The levels of NGAL at T6 and the levels of TNF-α at T6 and T24 were higher in the cardiopulmonary resuscitation group than in the control group; the differences were statistically significant (P<0.05). 

Conclusions: Rats in the cardiopulmonary resuscitation group have obvious renal histopathological and renal function disorders, suggesting that it is accompanied by acute kidney injury. Among them, inflammation is one of the mechanisms of early kidney development after cardiopulmonary resuscitation.