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Cholerny Spammer



Joined: 03 Mar 2011
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PostPosted: Tue 10:33, 08 Mar 2011    Post subject: tory burch flats gdq ffc usx nfu

,[link widoczny dla zalogowanych]
Hypoxic preconditioning on hypoxia reoxygenation in ventricular myocytes of free calcium


Current increased significantly. ② 24h after hypoxic preconditioning hypoxia line,[link widoczny dla zalogowanych], L-type calcium current inhibition of a state of ease, I-V curve down, steady-state inactivation curve shifted to the right. Inhibition of Na / Ca exchange current surge. ③ We also note that the line after 24h of ischemic preconditioning hypoxia, and cardiac cells under normoxia compared Na / Ca exchange current is still slightly increased. Suggest that calcium overload during hypoxia and L-type calcium channel independent; L-type calcium channels in a hypoxia inhibited when the state of the myocardial cell action potential duration shortening, myocardial cell electrophysiological heterogeneity may be re- reperfusion arrhythmia causes; and inhibition of hypoxia preconditioning to improve their condition,[link widoczny dla zalogowanych], prolong action potential duration, reduce the power of non-uniformity, reducing the incidence of reperfusion arrhythmia. Show that the Na / Ca exchange current, in particular, a significant increase in reverse current is reperfusion calcium overload of the main reasons for the state; late preconditioning mechanism starts with the calcium ions by the sodium-calcium exchange in vivo flow increased slightly. This Miyawaki and other mechanisms of ischemic preconditioning start early and calcium ions through L-type calcium influx caused slight increase in the inconsistent results. In summary,[link widoczny dla zalogowanych], the intracellular calcium in myocardial cells under hypoxia is the role of two-way, myocardial hypoxia and reoxygenation, by Na / ca exchange current abnormal increase, [ca]. The unusual increase of calcium overload can lead to myocardial cell injury; short repeated hypoxia,[link widoczny dla zalogowanych], through the slightly increased Na / Ca exchange currents and [Ca] i and trigger late preconditioning, inhibition caused by hypoxia follow-up Na / Ca exchange current and the [Ca] i of the unusual increase in a delayed protective effect on the heart.


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