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Changes of connexin43 and its electrophysiologic effects during acute myocardial ischemia in canine hearts

Author: LinJiJin
Tutor: LiYuGuang
School: Shantou University
Course: Cardiovascular within science
Keywords: Ischemia Connexin 43 Conduction velocity Confocal laser scanning microscope Immunohistochemistry Double labeling
CLC: R541.4
Type: Master's thesis
Year: 2001
Downloads: 90
Quote: 0
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Background and Purpose: Cardiac gap junction (gap junction, GJ) is the connecting passage between the myocardial cells, the channel having a hydrophilic, low selectivity, low resistance, and other characteristics, its main function is completed between the myocardial cells electrochemical information exchange in the heart of the rapid spread of excitement impulse. Ventricular myocardial cell gap junction connexin 43 (connexin 43, Cx43) constitute the normal expression of Cx43 distribution is an important guarantee of electrical activity and coordination of systolic and diastolic cardiac resynchronization. Previous studies have shown that chronic myocardial ischemia, myocardial Cx43 degradation and distribution is closely related to the occurrence of the disorder and arrhythmia, acute myocardial ischemia Cx43 is how to change their changes on cardiac electrophysiological properties impact of, has yet to clear. The purpose of this experiment is to proved acute short period of time (1 to 6 hours) myocardial ischemia of myocardial Cx43 change its cardiac electrophysiological properties. Methods: 20 dogs were randomly divided into a control group (4), 1-hour ischemia group (6), 3-hour ischemia group (5) and 6-hour ischemia group (5) 4 group; through ligation of the left anterior descending coronary artery were 0, 1, 3, 6 hours of left ventricular anterior acute myocardial ischemia, the ischemic myocardium is divided into 16 plots, the application of the 48-lead ECG physiological recorder and with 56 The conduction velocity of the electrode plate of the pair of electrodes of each cell was measured, followed by determination of the ventricular fibrillation threshold; remove cardiac ischemic myocardium is divided into 16 small pieces, then each small piece into endocardial underlayer, an intermediate layer, epicardial lower, confocal laser fluorescence microscopy and double labeling immunohistochemistry were measured layers of each small change ischemic myocardial Cx43 content and distribution; Cx43 pixel density on behalf of Cx43 amount, linear regression analysis Cx43 pixel density dispersion, the dispersion of the cardiac conduction velocity, ventricular fibrillation threshold among the correlation. Results: (1) acute myocardial ischemia, myocardial Cx43 began degradation of ischemia and 1 hour about Shantou University Medical College graduate thesis degradation 22.2 see three hours about degradation of 40 lying six hours about degradation of 5 arc; o normal control group myocardial cells in end-to-end the CX43 content junction is about 1.37 times the side-to-side connections, both content equivalent to approximately one hour of ischemia, ischemia 6 / J ', measured contralateral junction CX43 content but for the end-to-end connection at 1.6 times; u) the normal control group subepicardial myocardial the local CX wheel showed no significant differences, significant differences between the various local CX43 content after ischemia, the longer ischemic time the more obvious differences; layers cardiomyocytes the CX43 content differences K) normal control group was not statistically significant, ischemic the CX \; door) before ischemia, myocardial conduction velocity dispersion smaller conduction velocity dispersion increases after ischemia and highly correlated with Cx43 pixel density dispersion, r = .9132; (P <0.01). ( 6) appears block regional myocardial CX43 degree of degradation of more than 70 theory) of CX43 pixel density dispersion and ventricular fibrillation threshold was negatively correlated with r knife .7833, P 1 .01; ischemic myocardium conduction velocity discrete degree of ventricular fibrillation threshold linear negative correlation, r = 0.8602, P <0.01 Conclusion: *) Acute short time to 6 hours Bu O muscle ischemia CX \dependence; ① Acute ischemic myocardial cells end-to-end connection at CX43 degradation rate than in a side-to-side obviously faster connections of CX43 in the distribution patterns change significantly; o) local, 0 muscle CX43 degradation degree of heterogeneity may and regional myocardial ischemic tolerance and collateral blood supply different; concave acute ischemic myocardial CX43 degradation of the middle layer speed fastest, largest degree of degradation, possibly with the intermediate layer myocardial C 3 easier dephosphorylation or protein digestive enzymes sensitive; the smell regional myocardial CX43 serious degradation will lead to conduction block; similar acute myocardial ischemia CX good heterogeneous degradation conduction velocity dispersion increases, decreased stability of cardiac electrophysiology and myocardial Yi important reason for loss increased.

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Coronary arteries ( atherosclerosis ),heart disease (CHD)
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