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Objective To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension. Methods A total of 1 483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1 045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups. Results In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P 79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group. Conclusion Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.
ABSTRACT
OBJECTIVE@#To investigate the relationship between basal ganglia cerebral infarction and paroxysmal atrial fibrillation (PAF) caused by abnormal vagus nerve tension.@*METHODS@#A total of 1483 cases of elder patients with cerebral infarction who received head CT or MRI examination during the period were enrolled, including 830 male and 613 female, with the average age as 78 years. These cases were divided into basal infarction ganglia group (n = 1045) and non-basal ganglia infarction group (n = 438) according to the anatomic site of cerebral infarction. The differences of the incidence of PAF, left atrial diameter and heart rate variability were compared between the two groups.@*RESULTS@#In basal ganglia infarction group, the incidence rate of PAF was significantly higher than that of non-basal ganglia infarction group (P 79 years basal ganglia cerebral infarction group, the incidence of PAF was significantly higher than that of non-basal ganglia infarction group (P < 0.05). There was no significant difference in the left atrial diameter between the basal ganglia infarction group and non-basal ganglia infarction group. Basal ganglia cerebral infarction patients with high PAF had higher heart rate variability than non-basal ganglia infarction group.@*CONCLUSION@#Elderly patients with basal ganglia infarction have high incidence of PAF. Sympathetic nerve damage in cerebral basal ganglia, increased vagal tension and cardiac vagal tension are the direct causes of PAF. The results indicates that the increased central vagal nerve tension mediated PAF probably is an indication of supplying sympathetic neurotransmitter or cardiac vagal denervation treatment.
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Objective: To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose. Methods: CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis. Results: High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (. P<0.05). Conclusions: GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.
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OBJECTIVE@#To investigate the protective effect of glucagon-like peptid-1 (GLP-1) against cardiac microvascular endothelial cell (CMECs) injured by high glucose.@*METHODS@#CMECs were isolated and cultured. Superoxide assay kit and dihydroethidine (DHE) staining were used to assess oxidative stress. TUNEL staining and caspase 3 expression were used to assess the apoptosis of CMECs. H89 was used to inhibit cAMP/PKA pathway; fasudil was used to inhibit Rho/ROCK pathway. The protein expressions of Rho, ROCK were examined by Western blot analysis.@*RESULTS@#High glucose increased the production of ROS, the activity of NADPH, the apoptosis rate and the expression level of Rho/ROCK in CMECs, while GLP-1 decreased high glucose-induced ROS production, the NADPH activity and the apoptosis rate and the expression level of Rho/ROCK in CMECs, the difference were statistically significant (P<0.05).@*CONCLUSIONS@#GLP-1 could protect the cardiac microvessels against oxidative stress and apoptosis. The protective effects of GLP-1 are dependent on downstream inhibition of Rho through a cAMP/PKA-dependent manner, resulting in a subsequent decrease in the expression of NADPH oxidase.