Cardiovascular responses of exercises performed within the extreme exercise domain.

Stroke volume (SV), heart rate (HR) and arterio-venous O2 difference (a-vO2diff) responses to heavy and severe-intensity exercise have been well documented; however, there is a lack of information on the SV, HR and a v-O2diff responses of work rates within extreme exercise domain. The aim of this study was, therefore, to focus on central and peripheral components of VO2 responses to exercises performed within the heavy, severe and extreme exercise domain. Eight well-trained male cyclists participated in this study. Maximal O2 consumption (VO2max) and corresponding work rate (P@VO2max) were determined by multisession constant work rate exercises. Cardiovascular responses to exercises were evaluated by nitrous-oxide rebreathing method with work rates from 40 % to 160 % of P@VO2max, VO2max corresponded to 324+/-39.4 W; however, maximal SV responses occurred at 205+/-54.3 W (p<0.01). Maximal cardiac output (Q), HR, and a vO2diff responses were revealed by the P@VO2max. VO2 response to exercise significantly decreased from severe-intense exercises to the first work rate of extreme exercise domain due to significant decreases in Q, SV, and HR responses (p<0.05), except a v-O2diff (p>0.05). Moreover, non-significant decreases in Q, SV, and a v-O2diff were evaluated as response to increase in work rate belonging to extreme work rates (p>0.05), except the HR (p<0.05). Work rates within the lower district of the extreme exercise domain have an important potential to improve peripheral component of VO2, while the P@VO2max seems the most appropriate intensity for aerobic endurance development as it maximizes the central component of VO2max.

Oxidative and antioxidative status in the endometrium of patients with benign gynecological disorders.

AIM: Oxidative stress and impaired antioxidative system are implicated in the development of many disease states including gynecological diseases. In the present study, we aimed to investigate the oxidative-antioxidative status in endometrium of patients diagnosed with benign gynecological disorders. METHODS: Samples of endometria and blood were obtained from 65 patients admitted to our center for abnormal uterine bleeding or postmenopausal bleeding. Endometrial biopsy was performed for the evaluation of histopathology and oxidative-antioxidative status in endometrial tissue. Based on histological examination, subjects were divided into groups as follows: normal controls (n=15); patients with endometrial polyps (n=20); patients with uterine myoma (n=10) patients with chronic endometritis (n=10), and patients with atrophic endometrium (n=10). Activities of superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and total antioxidant status (TOS), total oxidant status (TAS) were assessed. RESULTS: Compared to the normal controls, nonsignificant changes (decrease or increase) were detected in antioxidant enzyme activities, TAS and TOS in the examined groups. Additionally, between TAS and TOS, we also found a strong positive correlation in normal and chronic endomethritis groups and a moderate positive correlation uterine myoma, endometrial polyps and endometrial atrophy groups. CONCLUSION: Even though, our results do not allow to conclude how oxidative and antioxidative status are influenced in benign gynecological disorders, these findings may provide a basis for the further researches.

Prevention of infertility induced by ovarian ischemia reperfusion injury by benidipine in rats: Biochemical, gene expression, histopathological and immunohistochemical evaluation.

INTRODUCTION: Benidipine has been reported to prevent the ischemia/reperfusion (I/R) damage in heart tissue and to suppress oxidant and proinflammatory cytokine production, increased by I/R. However, There was no information about the effects of benidipine on I/R injury in the ovary and the damage of I/R-induced infertility. OBJECTIVES: The aim of the study was to investigate the effects of benidipine on bilateral ovarian I/R injury and whether or not effective in the treatment of I/R-induced infertility in rats. METHOD: Forty-eight females, albino Wistar rats were randomly divided into 4 groups: IRC group (ovarian I/R group, n=12), IRB-2 group (ovarian I/R+2mg/kg benidipine group, n=12), IRB-4 group (ovarian I/R+4mg/kg benidipine group, n=12) and HG group (healthy group with sham operation, n=12). In IRB-2 and IRB-4 groups, two hours ischemia and two hours reperfusion was performed following orally benidipine administration. After this I/R procedure, 6 rats from each group performed bilateral overectomy. Ovarian levels of malondialdehyde (MDA) and total glutathione (tGSH), ovarian gene expressions of interleukin-1 beta (IL-1ß) and tumor necrosis factor-alpha (TNF-α) and also apoptosis were evaluated. The other 6 rats from each group were put in together with six male rats in separated cages for 2 months in order to reproduce. During this period, rats which did not become pregnant were accepted as infertile. RESULTS: MDA levels, expressions of TNF-α and IL-1ß in IRC group were significantly higher than in the SGA group and tGSH was decreased. In total, 4mg/kg benidipine has better prevented ovaries from the increase of oxidants and proinflammatory cytokines, the decrease of antioxidants than 2mg/kg benedipine. In the histopathological examination hemorrhage, congestion, follicle degeneration, neutrophil infiltration and necrosis were seen in ovarian tissue of IRC group. Only dilated and congested blood vessels were found in the IRB-2 group. No histopathological finding was encountered in the IRB-4 group. I/R caused infertility in rats. In total, 4mg/kg benidipine prevented from infertility better than the dose of 2mg/kg benedipine. CONCLUSION: In total, 4mg/kg benidipine reduced I/R injury and I/R-related infertility more significantly compared to 2mg/kg benedipine in rat ovaries.