Purpose: Although radiotherapy (RT) is an important component of cancer treatment, it induces adverse tissue reactions in the around of cancer tissue. Therefore, radioprotectives are needed to protect normal tissues. The aim of the present study was to investigate the radioprotective effect of N-acetylcysteine (NAC) on RT- induced cardiac damage in rats for the acute term. Materials and methods: The animals were divided into four groups. The rats in control group were injected with saline for 7 days; the rats in NAC group were injected NAC at dose of 240 mg/kg day for 7 days; the rats in RT group were injected with saline for 7 days plus was irradiated 1 hour after the last injection and the rats in NAC + RT group were injected with NAC for 7 days and irradiated 1 hour after the last NAC dose. The electrocardiogram was recorded and evaluated PR interval, QRS duration, QT interval, T wave alterations and heart rate. Serum interleukin-4, interleukin-6, tumor necrosis factor-alpha, interleukin 1 beta, galectin-3 levels and creatine kinase and creatine kinase isoenzyme-MB activities were determined in all groups. Also, tissue malondialdehyde and nitric oxide levels, superoxide dismutase, catalase and glutathione peroxidase activities were determined. In addition, histological changes of heart were evaluated. All measurements were performed 24 hours after RT. Results: In the RT group, findings supporting cardiac injury were observed in the electrocardiogram. Also, cytokine levels and oxidative stress were significantly increased. Pretreatment of rats with NAC ameliorated cardiac injury induced by RT. Conclusion: Our findings suggested that NAC may be a potential radioprotector which is capable of preventing cardiac damage.

Neurological impairments are the leading cause of post-stroke mortality, while stroke-related cardiovascular diseases rank second in significance.This study investigates the potential protective effects of MitoTEMPO (2,2,6,6-tetramethyl-4-[[2-(triphenylphosphonio) acetyl] amino]-1-piperidinyloxy, monochloride, monohydrate), a mitochondria-specific antioxidant, against cardiac and neurological complications following stroke. The objective is to assess whether MitoTEMPO can be utilized as a protective agent for individuals with a high risk of stroke. 17-week-old male Wistar Albino rats were randomly assigned to three groups: SHAM, ischemia-reperfusion (IR), and MitoTEMPO + ischemia-reperfusion (MT + IR; MitoTEMPO injection 0.7 mg/kg/day for 14 days). The SHAM group underwent a sham operation, while the IR group underwent 1-hour middle cerebral artery occlusion (MCAO) followed by 3 days of reperfusion. Afterwards, noninvasive thoracic electrical bioimpedance (TEB) and electrocardiography (ECG) measurements were taken, and sample collection was performed for histological and biochemical examinations. Our TEB and ECG findings demonstrated that MitoTEMPO exhibited a protective effect on most parameters affected by IR compared to the SHAM group. Furthermore, our biochemical and histological data revealed a significant protective effect of MitoTEMPO against oxidative damage. The findings suggest that both IR-induced cardiovascular abnormalities and the protective effect of MitoTEMPO may involve G-protein coupled receptor (GPCR)-mediated signaling mechanisms. This study was conducted with limitations including a single gender, a uniform age group, a specific stroke model limited to MCA, and pre-scheduled only one IR period. In future studies, addressing these limitations may enable the implementation of preventive measures for individuals at high risk of stroke.

Cardiovascular abnormalities are widespread when a newborn is exposed to a hypoxic-ischemic injury in the neonatal period. Although the neuroprotective effects of levetiracetam (LEV) have been reported after hypoxia, the cardioprotective effects of LEV have not been documented. Therefore, we aimed to investigate whether levetiracetam (LEV) has a protective effect on cardiac-contractility and ultrastructure of heart muscle in rats exposed to hypoxia-ischemia (HI) during the neonatal period. A total of 49 seven-day-old rat pups were separated into four groups. For HI induction, a combination of right common carotid artery ligation with 8% oxygen in seven-day-old rat pups for 2 h was performed for saline, LEV100, and LEV200 groups. Just after hypoxia, LEV100 and LEV200 groups were administered with 100 mg/kg and 200 mg/kg of LEV, respectively. The arteries of rats in the control group were only detected; no ligation or hypoxia was performed. At the end of the 16th week after HI, cardiac mechanograms were recorded, and samples of tissue were explored by electronmicroscopy.While ventricular contractility in the control group was similar to LEV100, there were significant decreases in both saline and LEV200 groups (p < 0.05). Although ventricular contractile duration of the control and saline groups was found to be similar, durations in the LEV100 and LEV200 groups were significantly higher (p < 0.05). After HI, mitochondrial damage and ultrastructural deteriorative alterations in ventricles and atriums of the LEV-administered groups were significantly less severe than the saline group. The present study showed that neonatal HI caused long-term cardiac dysfunction and ultrastructural deteriorations in cardiac muscles. LEV administration just after HI might possess some protective effects against myocardial damage and contractility.

Advances in Clinical and Experimental Medicine jest oficjalnym pismem Uniwersytetu Medycznego im. Piast?w Sl?skich we Wroc?awiu. Publikowane s? w nim prace naukowe polskie, jak r?wnie? zagraniczne.

Myocardial ischemia–reperfusion (IR) injury remains a major challenge in cardiac surgery, and comparative histological and ultrastructural data on cardioplegia solutions are limited. This study compared the myocardial protective effects of St. Thomas II and del Nido cardioplegia in a controlled rat IR model, focusing on inflammation, mast cell dynamics, and subcellular preservation. Twenty-four Wistar Albino rats were randomized to Control, St. Thomas II, or del Nido groups. After 90 minutes of ischemia and 30 minutes of passive reperfusion, myocardial tissue was analyzed by hematoxylin–eosin, toluidine blue, and transmission electron microscopy. Outcomes included mast cell counts, leukocyte infiltration, karyolysis, and ultrastructural measures (Flameng score, crista density, basement membrane thickness). Both cardioplegia groups preserved myocardial morphology and attenuated inflammatory changes versus control. Light microscopy revealed a consistent mast cell density and reduced karyolysis in hearts treated with cardioplegia, with no significant differences observed between St. Thomas II and del Nido solutions. Conversely, transmission electron microscopy (TEM), the primary endpoint of this study, demonstrated enhanced mitochondrial and endothelial preservation in the del Nido group, as evidenced by significantly lower Flameng scores and increased crista density compared to both St. Thomas II and control groups (p < 0.05). In conclusion, both solutions reduced early IR-related injury, but del Nido provided a significant ultrastructural advantage on TEM despite similar routine light-microscopic findings.

Cardiac damage caused by radiation in the long term varies according to the radiation dose received by the heart. In this study, it was aimed to evaluate the damage caused by different radiation doses in the heart, together with hemodynamic parameters, immunhistochemistry, and histopathological analyzes for long term. The animals were divided into four groups: The rats in control group (Group 1) were not irradiated; the rats in group 2 were irradiated with 5 Gy; the rats in group 3 were irradiated with 10 Gy and the rats in group 4 were irradiated with 20 Gy. Hemodynamic parameters and indices were determined from the impedance cardiography (ICG) recording in the whole groups before they were irradiated with RT and 180 days after RT. And then, interleukin-1β, interleukin-10, TNF-α, apopthosis were determined in all groups. In addition, histological changes of heart and aorta were evaluated. Histopathologic, cytokine and hemodynamic findings supported that cardiac damage increased with increasing radiation dose. it is important in terms of being an alternative and supportive method to other methods to be able to detect heart diseases caused by RT with the ICG method.