| In order to adapt to the need of modern war, high performance fighterplane is becoming to the main battle effectiveness of our air force.Correspondingly, the degree of intensity and difficulty of combat drill areincreasing, which pose a more serious real challenge and demand to thehabitus of our pilots. In other words, with the high speed development ofmodern aircraft, our pilots are confronted with more adverse taskcircumstances. Such kind of adverse task circumstances would producemore adverse impact on many organs such as the heart. Among numerousadverse environmental factors, acceleration is the most evident one. Yearsexperience has showed pilots with excellent constitution are selected tierupon tier by health examinations have high incidence of arrhythmias after along term flight task. In addition, during the past20years, the incidence ofcoronary heart disease (CHD) increased significantly. The affectedpopulation of CHD are becoming younger and younger. CHD is diseasecaused by multi-factors while the flight personnel are faced with more riskfactors of metabolic syndrome in some respects. The prognosis of coronaryheart disease is also affected by multiple factors. CHD not onlycompromises pump function directly, which leading to hemodynamicdisorders, but also causes cardiac electrical instability giving rise toarrhythmias or malignant arrhythmia. Previous studies showed thatacceleration would induce or aggravate arrhythmias. Acceleration not onlyhas effect on coronary blood vessels, but also can result in arrhythmiasdirectly, or facilitate the development of arrhythmias as well. However, thein-depth research work especially the detailed mechanism as this respect is inadequate. To provide theoretical support for the prevention and treatmentof coronary artery disease in patients with cardiac arrhythmias, in this study,we mainly focused on the changes of myocyte channel function and the gapjunction Connexin43expression under normal and ischemic myocardiumsimulated by flight acceleration environment exposure. We also primarilyexplored the main electrophysiological links and mechanisms on conditionthat positive acceleration incorporated myocardial ischemia.In this study,60New Zealand white rabbits were divided into4groups, i.e., control group A, acceleration group B, ischemia group C andacceleration ischemia group D,15rabbits in each group. By usingmonophasic action potential (MAP) technique, we recorded and analyzedthe parameters in each group as following: MAP amplitude (MAPA, mv)and the maximum rate of0phase (Vmax, mv/s) and50%MAPrepolarization (MAPD50) and90%MAP repolarization(MAPD90) and theratio of MAPD50/MAPD90; then we tested the specimens from cardiactissue to detect and analyze the Cx43content for each group by Westernblot. In ventricular tachyarrhythmias aspects, except for no significantdifference between the ischemic group and the acceleration (P>0.05).Compared with the control group, the acceleration group, ischemia group,ischemia and acceleration group were easier to induce ventriculartachyarrhythmias than that of the control group. While the ischemia andacceleration group was easier than that of the acceleration group. Theseresults demonstrated the combined effects of dual factors of accelerationand ischemic to induce ventricular tachyarrhythmias easily. Between thefour groups, the MAPA and Vmaxhas no significant difference (P>0.05),prompting sodium channel function has no significant difference betweenthe four groups; Compared with the control group, MAPD50and MAPD90shortening sequence are: acceleration, ischemia, ischemia and accelerationgroup (P<0.05). Prompting both1,2,3phase of action potentialrepolarization were accelerated and During repolarization both the potassium channels and L-type calcium channels are increased. Comparedwith the control group, the reduction l level in Cx43content from low tohigh sequences are: acceleration, ischemia, ischemia and accelerationgroup (P<0.05). Therefore, the probability of tachyarrhythmias occurredsignificantly increase after ischemic myocardium exposed by positiveacceleration. Possible mechanisms, from the aspect of myocardial cells, theacceleration exposure and ischemic myocardial cause the function ofpotassium and calcium ion channel opening increased in the repolarizationprocess; from the aspects between the myocardial cells, the accelerationexposure and ischemic myocardial reduced the content of connexin43, thusformating reentrant arrhythmias condition. Our findings may provideevidence of cell electrophysiological mechanisms for the prevention ofischemic arrhythmias. |
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