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.
Introduction: Cardiac arrest (CA) often leads to severe brain damage, resulting in neurological disorders and high mortality rates. Hypothermia treatment (HT) is commonly used in clinical practice after CA/cardio-pulmonary resuscitation (CA/CPR) because it has been shown to improve neurological outcomes and increase survival rates. Olanzapine, a medication known to induce hypothermia, has not been extensively studied in the context of CA/CPR. This study aimed to investigate the neuroprotective effects and mechanisms of olanzapine-induced hypothermia (OIH) following ROSC. Male Sprague-Dawley rats were subjected to the following conditions: (i) Sham: no asphyxial CA + saline, (ii) CA: asphyxial CA + saline, and (iii) OCA: asphyxial CA + olanzapine treatment after the return of spontaneous circulation (ROSC). Result CA/CPR resulted in high mortality, severe neurological impairments, and hippocampal neuron damage observed after 5 days in the asphyxia CA group. These pathological complications were ameliorated by olanzapine treatment. OIH also protected the pyramidal neurons in the CA1 region of the hippocampus. The expression of antioxidant factors SOD-1, SOD-2, and CAT were upregulated in the olanzapine-treated group compared to the CA group. Moreover, olanzapine treatment following asphyxial CA reduced the expression of the pro-inflammatory factor COX-2 and the nuclear transcription factor NF-κB, which was sustained for up to 5 days compared to the CA group. OIH provides protection against cerebral injury following ROSC by enhancing the expression of antioxidant and anti-inflammatory factors. Conclusion The results of our study demonstrate that Olanzapine, an atypical antipsychotic medication, induces a noteworthy reduction in body temperature in the asphyxial CA rat model. The effectiveness of hypothermia treatment was evident by its antioxidant and anti-inflammatory mechanisms. Therefore, we suggest olanzapine as a promising therapeutic agent for alleviating cerebral injury via hypothermia in patients with CA.
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