The effect of acute Carbon Monoxide intoxication on cardiac necrosis in rats: in relation to Adiponectin levels
Abstract
In order to investigate the effects of acute CO poisoning and subsequent oxygen therapy on cardiac necrosis in rats, with a specific focus on adiponectin levels, twenty–one male Wistar albino rats were divided into three groups (Control, CO, CO+O2). The Control group was placed in a container and exposed to room air for 30 min. Acute CO poisoning was induced in the CO group and CO+O2 group by exposing the rats to CO gas for 30 min. Following CO exposure, the CO+O2 group received oxygen therapy for 30 min, while the CO group did not receive any additional intervention. The animals were euthanized by cardiac puncture under anesthesia, following the approved ethical procedures. Carboxyhemoglobin (COHb), serum levels of creatine kinase (CK), creatine kinase myocardial band (CK–MB), C–reactive protein (CRP) and lactate dehydrogenase (LDH), as well as cardiac and serum adiponectin levels were measured. CO poisoning caused necrosis in cardiac tissue however, oxygen therapy alleviated the negative effect of CO on cardiac injury. COHb and LDH levels in CO group were increased, whereas both cardiac and serum adiponectin levels were decreased (all, P<0.05). There were no changes in CK, CK–MB, CRP levels among groups (all, P>0.05). Oxygen therapy decreased COHb, but increased both cardiac and serum adiponectin levels (all, P<0.05). Adiponectin and LDH may serve as potential biomarkers for early diagnosis of cardiac necrosis caused by acute CO poisoning. The assessment or quantification of adiponectin can also be useful for the early prognosis of cardiac necrosis after oxygen therapy.
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