Ayaz, MuratGuney, OnderErdi, FatihKucukbagriacik, Yusuf2020-03-262020-03-2620091383-875X1572-8595https://dx.doi.org/10.1007/s10840-009-9400-0https://hdl.handle.net/20.500.12395/23508Although subarachnoid hemorrhage (SAH) serves as a good model to study heart-brain interactions, neither the changes on the single ventricular action potential (SVAP) and contraction nor the effects of possible cardioprotective agents have been investigated. A total of 18 male rabbits were used for the three experimental groups. SAH was induced by replacing the cerebrospinal fluid (CSF) with fresh autologous blood at the ratio of 1 mL to the 1-kg body mass (N = 6). In the control (CON; N = 6) group, the CSF was replaced with serum physiologic at the same ratio. The treated SAH group (SAH+NAC) received daily intraperitoneal N-acetylcysteine (NAC; 150 mg/kg for 3 days) starting from just before SAH was induced by CSF replacement. On the fourth day, animals were examined for the single action potential and contraction recordings from the left ventricular papillary muscle. At the end of 3 days, the overshoot decreased together with increased time to reach the peak potential. Additionally, the resting membrane potential was depressed and repolarization was slowed during SVAPs. On the other hand, peak tension depressed and time to peak increased. NAC treatment, which protects infarction in the brain, prevented these pathological changes in the cardiac muscle. SAH-induced cardiac changes can be attributed to adenosine triphosphate depletion through mitochondrial dysfunction. Pretreatment of NAC to SAH on the other hand had a positive effect on these cardiac changes. But the exact mechanism by which NAC treatment protects the cardiac muscle needs further investigation.en10.1007/s10840-009-9400-0info:eu-repo/semantics/closedAccessSubarachnoid hemorrhagePapillary muscleElectrophysiologyN-acetylcysteineArticle2629510019399602Q2WOS:000272174700002Q4