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Pathophysiological and Histopathological Ailments in Asphyxial Cardiac Arrest Induced Ischemic Renal Injury
Jeong-Hwi Cho1,§, Anowarul Islam1,§, In-Shik Kim1, Jun Ho Lee2, Yeo-Jin Yoo1, So Eun Kim3,4 , Ali Jawad1, Weishun Tian1, Dongchoon Ahn1, Byung-Yong Park1, Kyunghwa Kim4,5, Jeong Ho Lee6,  Eui-Yong Lee1, Ha-Young Shin1, Md Rashedunnabi Akanda7, Hyun-Jin Tae1* and Jae Chol Yoon3,4,*
2Department of Anesthesiology and Pain Medicine, Jeonbuk National University Medical school and Hospital, Jeonju, Korea; 3Department of Emergency Medicine, Jeonbuk National University Medical School, Jeonbuk National University Hospital, Jeonju, 54907, Korea 4Research Institute of Clinical Medicine of Jeonbuk National University and Biomedical Research Institute of Jeonbuk National University Hospital, Jeonju, 54907, Korea; 5Department of Thoracic and Cardiovascular Surgery, Jeonbuk National University Medical School, Jeonbuk National University Hospital, Jeonju, 54907, Korea; 6Sunchang Research Institute of Health and Longevity, Sunchang-gun, 56015, Korea 7Department of Pharmacology and Toxicology, Faculty of Veterinary, Animal and Biomedical Sciences, Sylhet Agricultural University, Sylhet-3100, Bangladesh
§These authors contributed equally to this work.
*Corresponding author:;


Cardiac arrest (CA) is a sudden interruption in the effective blood flow due to heart failure. The current research aimed to conduct the pathophysiological and histopathological analysis in the kidney in asphyxial cardiac arrest rat model. Cardiac arrest was induced by intravenous injection of vecuronium bromide (2 mg/kg), following stop of mechanical ventilation. Rats were kept on the CA condition for 5 minutes. After that, cardiopulmonary resuscitation (CPR) was done to achieve return of spontaneous circulation (ROSC) following intravenous injection of epinephrine bolus (0.005 mg/kg), sodium bicarbonate (1 mEq/kg) and turn on mechanical ventilation. Then Rats were sacrificed after cardiopulmonary resuscitation (CPR) following asphyxial CA at 6 hrs, 12 hrs, 1 day, 2 days, and 5 days. The intensity of renal injury measured by the serum levels of blood urea nitrogen (BUN), creatinine (Crtn). Moreover, Hematoxylin & eosin, and Periodic Acid Schiff staining in the kidney was done for evaluating the renal histopathological changes. Furthermore, COX-2 immunoreactivity and western analysis were performed in the kidney. Survival rate declined following ROSC compared to the sham group, it showed 80% at 6 hrs and decreased time-dependently to 8% at 5 days. In this study, serum BUN and Crtn levels and renal histopathological scores significantly increased after ROSC in CA. Moreover, COX-2 expression also increased after ROSC in comparison to the sham group with its peak level at 5 days following CA. Renal histological damage score and COX-2 expression were upregulated after ROSC following CA. These results direct that COX-2 takes part in the asphyxial CA-induced ischemic renal injury.

To Cite This Article: Cho JH, Islam A, Kim IS, Lee JH, Yoo YJ, Kim SE, Jawad A, Tian W, Ahn D, Park BY, Kim K, Lee JH, Lee EY, Shin HY, Akanda MR, Tae HJ and Yoon JC, 2020. Pathophysiological and Histopathological ailments in asphyxial cardiac arrest induced ischemic renal injury. Pak Vet J.


ISSN 0253-8318 (Print)
ISSN 2074-7764 (Online)