This study was designed to assess the changes in nonlinear properties of heart rate (HR) variability (HRV) during the menstrual cycle by means of complexity measures, including sample entropy (SampEn) and correlation dimension (CD), and explore probable physiological interpretations for them. In 16 healthy women (mean age: 23.8 +/- 2.7 yr), complexity measures along with the spectral components of HRV (sympathovagal markers) were analyzed over 1,500 R-R intervals recorded during both the follicular phase (day 11.9 +/- 1.4) and the luteal phase (day 22.0 +/- 1.4) of each woman's menstrual cycle. Simultaneously, serum ovarian hormone (estradiol-17 and progesterone) and thyroid-related hormone [free triiodothyronine, free thyroxine (T(4)), and thyroid-stimulating hormone] concentrations were measured. With regard to HRV measures, SampEn, CD, and high-frequency (HF) components decreased from the follicular phase to the luteal phase, whereas normalized low-frequency (LF) components and the LF-to-HF ratio as well as resting HR increased. In regard to hormone levels, whereas progesterone was increased, the other hormone concentrations were unchanged. Furthermore, across the menstrual cycle, both SampEn and CD were well correlated with the spectral indexes and free T(4) concentrations, and SampEn also showed significant correlations with the ratio of estradiol-17 to progesterone concentrations. These results suggest that the nonlinear properties in HRV are altered during the regular menstrual cycle and that the autonomic nervous system, ovarian hormone balance, and free T(4) may be involved in nonlinear HR control in healthy women. All of these factors may enrich the physiological meanings of complexity measures.
The present study was designed to investigate whether arsenic trioxide induced the apoptosis in rat mesenteric arterial smooth muscle cells (SMCs), which provides new insights into mechanisms of arsenic-related vascular diseases. Here, we found that arsenic trioxide significantly decreased the viability of SMCs in a dose-dependent manner. In addition, higher level of arsenic trioxide directly caused cellular necrosis. The Hoechst and AO/EB staining demonstrated that apoptotic morphological change was presented in SMCs exposed to arsenic trioxide. The TUNEL assay displayed that more positive apoptotic signal appeared in SMCs treated with arsenic trioxide. The following result showed that ROS formation was markedly increased in arsenic trioxide-treated SMCs. Pretreatment with N-acetylcysteine, an anti-oxidant reagent, obviously attenuated the enhancement of ROS production and the reduction of cell viability induced by arsenic trioxide in SMCs. Arsenic trioxide also enhanced free intracellular Ca(2+) level in SMCs. BAPTA also significantly prevented the increased intracellular Ca(2+) and decreased cell viability induced by arsenic trioxide in SMCs. These results suggested that arsenic trioxide obviously induced apoptosis in SMCs, and its mechanism was partially associated with intracellular ROS formation and free Ca(2+) increasing.
Resveratrol increases endothelial NO production to improve endothelial dysfunction and lowers BP in hypertensive rats, which depends on calcium-eNOS activation.
It is acknowledged that contrast-induced nephropathy (CIN) is a common cause of acute renal insufficiency after cardiac catheterization and affects mortality and morbidity. To date, it is unknown whether oral N-acetylcysteine (NAC) is able to prevent contrast-induced nephropathy (CIN) in patients undergoing coronary angioplasty. A meta-analysis of randomized controlled trials was performed to assess the effects of NAC in the prevention of CIN in patients following coronary angioplasty. A total of 19 studies published prior to January 2015 that investigated the efficacy of oral NAC for the prevention of CIN were collected from Medline, Cochrane and Embase databases and conference proceedings from cardiology and nephrology meetings. The primary point of investigation was CIN, and the secondary points were renal failure requiring dialysis, mortality and length of hospitalization. The meta-analysis was performed using fixed- or random-effect models according to heterogeneity. Up to January 2015, 19 randomized placebo-controlled clinical trials met the inclusion criteria for the meta-analysis, including 4,514 patients. The pooled data showed that oral NAC did not reduce the CIN incidence [relative risk 0.84, 95% confidence interval (CI) 0.65–1.10; P=0.20], without heterogeneity among trials (I2=29%). Thus, the present meta-analysis suggests that oral NAC therapy is not effective as an alternative treatment to prevent CIN in patients following angioplasty. Further high quality randomized clinical controlled trials are required to confirm the usage and availability of this treatment.
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