| Background Sleep deprivation (SD) means a complete lack of sleep time or less than optimal sleep time. Research results showed that sleep deprivation or lack of sleep time can lead to immune function reduced. Especially in the war time, wartime stress such as continuous fighting, night fighting, fighting across time zones can cause the body's sleep-wake rhythm disorders,disruption and loss of sleep time, which can lead to mental fatigue,depression and reduce the cognitive function. Consequently, the combat capability of troops will be affected.Objective The aims of the study are to observe the basic state, the level of oxidative stress and inflammatory reaction, the severity of the myocardial damage and cardiac electrophysiological changes in rats after SD; to research the mechanisms of myocardial damage and arrhythmia caused by SD, and to further research the effect of drug intervention on myocardial injury after SD; to provide the basis for the establishment of control strategies.Method Adult male Sprague-Dawley rats were used as research objects. They were randomly divided into 8 groups:large platform group fed with saline (TC group), large platform group fed with L-carnitine (LCTC group), sleep deprivation 1 day,3 days,5 days groups fed with L-carnitine (LC1d, LC3d, LC5d group); sleep deprivation 1 day,3 days,5 days groups fed with saline (SD1d, SD3d, SD5d group). SD were established by modified multiple platform method of sleep deprivation model.1.The concentration of MDA, SOD, IMA, hs-CRP in myocardium after SD were monitored, and the changes of these index which were influenced by L-carnitine were observed.2.Patch clamp technique was used to record transient outward potassium current (Ito) and inward potassium current order (Ik1) changes after SD. Results1.MDA was increased and SOD activity was decreased with the progress of SD. Inflammatory marker hs-CRP was increased progressively after SD. IMA was increased at early time after SD, and its increase trend was clearly accelerated with the prolongation of SD.2.With the influence of L-carnitine, the concentration of MDA decreased with the progress of SD, and SOD activity increased. Inflammatory marker hs-CRP decreased significantly. Compare with SD group, IMA decreased with the influence of L-carnitine.3.The electric current densities of Ito in SD1d,SD3d,SD5d groups were 38.84±3.01,27.37±2.42,21.37±1.47 (pA/pF), but in TC group was 41.63±4.14 (pA/pF), which was obviously higher.4.The outward rectification of Ito reduced or disappeared after SD. The activation of Ito decreased and inactivation increased. The recover time of inactivation was prolonged. The speed of closed state inactivation was increased.5.The electric current densities of Ik1 in TC,SD1d,SD3d,SD5d groups were-89.23±4.36,-85.46±6.65,-82.55±5.45,-85.46±4.46 (pA/pF), respectively. They were not influenced by SD.Conclusions1,SD could cause myocardial oxidative stress and inflammatory reaction. The longer the SD period, more serious the reaction.2,SD could cause myocardial ischemic and hypoxic injury, which became serious with the SD period prolongation.3,L-carnitine could reduce myocardial oxidative stress and inflammatory injury after SD, and provent the damage of myocardium.4,SD could inhibit the Ito of myocardium, and affect the early repolarization of myocardium, and cause the occurrence and development of arrhythmia.
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