ABSTRACT
Objective: To explore the expression of myocardial levels of connexin 43(Cx43), Cx40 in experimental dog model of sympathomimetic atrial fibrillation (AF). Methods: 15 mongrels dogs were randomly divided into 3 groups: Control group, Rapid atrium pacing (RAP) group and RAP+isoprenaline (ISO) perfusion group. n=5 in each group. The hearts were taken to establish in vitro langendorff cardiac perfusion model. Atrial effective refractory period (AERP) and AF inducing rate were tested;intracellular expression and distribution of nerve growth factor (NGF) and tyrosine hydroxylase (TH) were examined by immunohistochemistry, total protein contents of Cx43 and Cx40 were measured by Western blot analysis, mitochondria morphology was observed by transmission electron microscope and mitochondria reactive oxygen species (ROS) generation was detected by fluorescent colorimetric method. Results: AERP was similar between Control group and RAP group (166±5.1) ms vs (160±3.2) ms which cannot induce AF; while it was shortened in RAP+ISO group (148±3.7) ms, P<0.05 which may successfully induce AF.Compared with Control group, mitochondria was slightly swollen in RAP group and the matrix was intact, while mitochondria was obviously swollen in RAP+ISO group and part of matrix was transparent; total protein contents of Cx43 and Cx40 were lower in both RAP group and RAP+ISO group, P<0.05; in addition, they were even lower in RAP+ISO group than RAP group, P<0.05. Compared with Control group and RAP group, RAP+ISO group had increased expression and distribution of NGF, TH and mitochondria ROS generation, P<0.05; NGF, TH and ROS in RAP group were higher than Control group, P<0.05. Conclusion: Sympathetic AF has been related to the contents and changes of myocardial levels of CX43 and Cx40; sympathetic nerve might trigger AF by oxidative stress induced down-regulation of myocardial CX43 and Cx40 in experimental dog model.
ABSTRACT
BACKGROUND: Cigarette smoking causes cardiovascular disease and activates markers of endothelial dysfunction or injury. We investigated the nailfold capillary blood velocity (NCV) in cigarette smokers compared to non-smokers. METHODS: Forty-eight men (eighteen non-smokers and thirty smokers) were recruited. We measured NCV using nailfold capillary microscopy and exhaled carbon monoxide (ECO) concentration three times (before smoking; NCV0min and ECO0min, and after smoking; NCV5min, ECO5min, NCV30min, and ECO30min), in a condition of fasting in the case of smokers. In non-smokers, the same measurements were taken without smoking. Additionally, personal cigarette smoking and alcohol drinking history were acquired by a self-administrated questionnaire. RESULTS: Mean age, waist circumference, ECO0min, ECO5min, and ECO30min was higher and NCV5min and NCV30min were significantly lower in smokers compared to non-smokers. Total smoking years were negatively correlated with NCV5min. Average pack of the daily smoking, total pack-years, as well as total smoking years were also negatively correlated with NCV30min by regression analysis. After adjustment of significantly different variables, NCV30min was significantly lower in smokers. In the subgroup analysis, the interleukin-6 level was significantly increased in subjects with a long period of cigarette smoking compared with non-smokers. CONCLUSION: Reduction of NCV in smokers is associated with personal smoking history, not with body composition or certain oxidative stress markers.