Browsing by Author "Demirtas, Berjan"

Now showing 1 - 2 of 2

The Effect of Acute Carbon Monoxide Intoxication on Cardiac Necrosis in Rats: in Relation To Adiponectin Levels
(Univ Zulia, Facultad Ciencias veterinarias, 2025) Gokdemir, Gul Sahika; Cakmak, Sumeyye; Demirtas, Berjan; Gokdemir, Mehmet Tahir; Sogut, Ozgur; Canpolat-Erkan, Revsa Evin; Yokus, Beran
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+O-2). 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+O-2 group by exposing the rats to CO gas for 30 min. Following CO exposure, the CO+O-2 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.
Effects of acute carbon monoxide posioning on liver damage and comparisons of related oxygen therapies in a rat model
(Taylor & Francis Ltd, 2024) Gökdemir, Gül Şahika; Gokdemir, Gul Sahika; Seker, Ugur; Şeker, Uğur; Demirtas, Berjan; Taskin, Seyhan
Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% NBO with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-alpha, IL-1 beta, and NF-kappa B in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction. [GRAPHICS] .