Effect of therapeutic hypothermia against renal injury in a rat model of asphyxial cardiac arrest: Α focus on the survival rate, pathophysiology and antioxidant enzymes

Mol Med Rep. 2022 Jan;25(1):19. doi: 10.3892/mmr.2021.12535. Epub 2021 Nov 19.

Abstract

Although multi‑organ dysfunction is associated with the survival rate following cardiac arrest (CA), the majority of studies to date have focused on hearts and brains, and few studies have considered renal failure. The objective of the present study, therefore, was to examine the effects of therapeutic hypothermia on the survival rate, pathophysiology and antioxidant enzymes in rat kidneys following asphyxial CA. Rats were sacrificed one day following CA. The survival rate, which was estimated using Kaplan‑Meier analysis, was 42.9% one day following CA. However, hypothermia, which was induced following CA, significantly increased the survival rate (71.4%). In normothermia rats with CA, the serum blood urea nitrogen level was significantly increased one day post‑CA. In addition, the serum creatinine level was significantly increased one day post‑CA. However, in CA rats exposed to hypothermia, the levels of urea nitrogen and creatinine significantly decreased following CA. Histochemical staining revealed a significant temporal increase in renal injury after the normothermia group was subjected to CA. However, renal injury was significantly decreased in the hypothermia group. Immunohistochemical analysis of the kidney revealed a significant decrease in antioxidant enzymes (copper‑zinc superoxide dismutase, manganese superoxide dismutase, glutathione peroxidase and catalase) with time in the normothermia group. However, in the hypothermia group, these enzymes were significantly elevated following CA. Collectively, the results revealed that renal dysfunction following asphyxial CA was strongly associated with the early survival rate and therapeutic hypothermia reduced renal injury via effective antioxidant mechanisms.

Keywords: antioxidant enzymes; asphyxial cardiac arrest; histopathology; hypothermia treatment; kidney; post‑cardiac arrest syndrome.

MeSH terms

  • Acute Kidney Injury / drug therapy*
  • Acute Kidney Injury / genetics
  • Acute Kidney Injury / pathology
  • Animals
  • Antioxidants / pharmacology*
  • Asphyxia / complications*
  • Asphyxia / therapy*
  • Blood Urea Nitrogen
  • Brain / physiopathology
  • Creatinine
  • Disease Models, Animal
  • Heart / physiopathology
  • Heart Arrest / therapy*
  • Hypothermia
  • Hypothermia, Induced / methods*
  • Kidney / drug effects*
  • Kidney / injuries*
  • Kidney / pathology
  • Kidney / physiopathology
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • Survival Rate

Substances

  • Antioxidants
  • Creatinine

Grants and funding

The present study was supported by the Basic Science Research Program through the National Research Foundation of Korea funded by the Ministry of Education (grant nos. NRF-2019R1C1C1002564, NRF-2019R1F1A1062696 and NRF-2021R1F1A1059992).