TY - JOUR
T1 - Pathophysiological and Histopathological Ailments in Asphyxial Cardiac Arrest Induced Ischemic Renal Injury
AU - Cho, Jeong-Hwi
AU - Islam, Anowarul
AU - Kim, In-Shik
AU - Lee, Jun Ho
AU - Yoo, Yeo-Jin
AU - Kim, So Eun
AU - Jawad, Ali
AU - Tian, Weishun
AU - Ahn, Dongchoon
AU - Park, Byung-Yong
AU - Kim, Kyunghwa
AU - Lee, Jeong Ho
AU - Lee, Eui-Yong
AU - Shin, Ha-Young
AU - Akanda, Md Rashedunnabi
AU - Tae, Hyun-Jin
AU - Yoon, Jae Chol
PY - 2021
Y1 - 2021
N2 - 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. Cardiacarrest 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. Theseresults direct that COX-2 takes part in the asphyxial CA-induced ischemic renal injury.
AB - 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. Cardiacarrest 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. Theseresults direct that COX-2 takes part in the asphyxial CA-induced ischemic renal injury.
KW - Cardiac arrest
KW - Cyclooxygenase-2
KW - Histopathology
KW - Kidneys
KW - Rats
KW - Renal ischemia
KW - Cardiac arrest Cyclooxygenase-2 Histopathology Kidneys Rats Renal ischemia
UR - http://www.scopus.com/inward/record.url?scp=85101395038&partnerID=8YFLogxK
U2 - 10.29261/pakvetj/2020.080
DO - 10.29261/pakvetj/2020.080
M3 - Article
VL - 41
SP - 64
EP - 70
JO - Pakistan veteinary Journal
JF - Pakistan veteinary Journal
IS - 1
ER -