| Tachyarrhythmia is a cardiovascular disease that threatens humanhealth and safety seriously. Statistics shows, about390,000people died ofcardiac arrhythmia in United States each year, about600,000people diedof sudden cardiac death(SCD) in China each year, more than90%of whichare caused by malignant arrhythmias, such as ventricular tachycardia (VT),ventricular fibrillation (Vf) and atrial fibrillation (Af).Flight crew are a special occupational group, whose workenvironment is characterized by high acceleration, high altitude and lowpressure, high stress, so the occurrence of arrhythmia is more probable.Arrhythmia not only seriously affects the crew’s health, at the same timealso brings great hidden danger to flight safety, and even causes significantflight accidents.There are still no consensuses on the mechanisms of flighttachyarrhythmia now. Shubrooks explained that the heart position waschanged, the sympathetic excited, the speed of diastolic depolarizationaccelerated spontaneously, the catecholamine levels in blood increasedwhen in+Gz exposure, and these factors were all likely to cause arrhythmia.Whinnery thought that+Gz caused the sympathetic to excite, the heartirritability and the purkinje fiber phase4depolarization to increase, thefunctions of conduction and release in sinoatrial node and theatrioventricular node to be suppressed, all of which made the ectopicrhythm of the heart emerge. But these explanations did not reveal the cellelectrophysiologycal mechanism and the molecular basis of tachyarrhythmia under the condition of+Gz exposure.By using Holter monitoring, Burst stimulation, monophasic actionpotentials(MAP) recording and reverse transcription-PCR(RT-PCR)technologyies, the study aimed to observe the incidence of arrhythmia, thechanges of electrophysiological characteristics of ventricular muscle cellsand the expression levels of ion channel proteins Kir2.1, Kv4.3, α1cmRNAand gap junction protein Cx43mRNA in New Zealand white rabbits underthe condition of+Gz exposure, to explore the mechanism of cellularelectrophysiology and molecular basis of tachyarrhythmia, and to provide atheoretical basis for the prevention and cure of crew tachyarrhythmia.The general steps and the results of the experiment were as follows：(1)The rabbits are grouped into control group and+Gz group. Then the+Gz group were given+8Gz exposure,1minute/time,3times/day, andthe interval is3minutes, a total of7days, the two groups of rabbits weregiven Holter monitoring at the same time. The results showed:6rabbits in+Gz group suffered tachyarrhythmia, which included the atrial prematurebeats (APB), various types of ventricular premature beats (VPB),ventricular tachycardia(VT), the comprehensive incidence of arrhythmiabeing55%(6/11), but the arrhythmias didn’t occur to the control group;（2）By using MAP technology to record monophasic action potentialduration of90%repolarization(MAPD90) and transmural dispersion ofrepolarization(TDR) of the rabbits in control group and+Gz group, theresults displayed: comparing with the control group, the+Gz groupMAPD90of endocardial and epicardial cells were significantly decreased (P<0.05), the MAPD90of middle myocardial cells were no significant change(P>0.05), and the TDR was increased obviously (P <0.05).（3）By usingburst stimulation method, the right ventricular anterior wall of the rabbitswas stimulated. The results showed: the tachyarrhythmia occurred to4rabbits in+Gz group, the types of which were atrial premature beat(APB),ventricular premature beat(VPB), and various types of ventricular tachycardia（VT）, the comprehensive incidence of arrhythmia being40%(4/10), but the arrhythmias didn’t occur to the control group;（4）By usingRT-PCR technology, to detect the expression changes of ion channelproteins Kir2.1, Kv4.3, α1cmRNA and gap junction protein Cx43mRNA inthe control and+Gz group rabbits were detected. The results showed:compared with the control group, the expression of Kir2.1, Kv4.3mRNA in+Gz group was significantly raised (P <0.05); the expression of α1c,Cx43mRNA was significantly lowered (P <0.05).The experimental results showed that:1. The incidence oftachyarrhythmias in animals under the condition of repeated+Gz exposurewas increased obviously.2. The MAPD90of ventricular muscle cells wasshortened and the TDR was increased, may be the cellularelectrophysiologic mechanism of tachyarrhythmia induced by+Gz.3. Theexpression level of the Kir2.1, Kv4.3mRNA of ventricular muscleincreased, and that of the α1c, Cx43mRNA decreased, may be themolecular basis of tachyarrhythmia induced by+Gz. |
