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Preconditioning induced by PKC PKC activation and vascular reactivity in hemorrhagic shock in rats and calcium sensitivity of the mechanism of protection.doc

Preconditioning induced by PKC PKC activation and vascular reactivity in hemorrhagic shock in rats and calcium sensitivity of the mechanism of protection.doc

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Preconditioning induced by PKC PKC activation and vascular reactivity in hemorrhagic shock in rats and calcium sensitivity of the mechanism of protection

 PAGE \* MERGEFORMAT 18 Preconditioning induced by PKC PKC activation and vascular reactivity in hemorrhagic shock in rats and calcium sensitivity of the mechanism of protection Of: Xu Jing, Li Tao, Yang Guangming, Liang-Ming Liu [Abstract] Objective To observe whether ischemic preconditioning through adenosine receptors induced protein kinase C @ (protein kinase C @, PKC @), protein kinase C (protein kinase C, PKC) activation and vascular reactivity in hemorrhagic shock rats and calcium sensitivity of protection. Methods Determination of adenosine during ischemic preconditioning concentration; using western blot technique to observe the A1, A2A, A2B, A3 adenosine receptors (A1, A2A, A2B, A3 adenosine receptor, A1R, A2AR, A2BR, A3R) inhibitors on ischemic preconditioning induced PKC @ and PKC expression and translocation of; tension in isolated microvascular measurement technique to observe the adenosine receptor inhibitor on ischemia preconditioning in hemorrhagic shock induced vascular reactivity and calcium sensitivity of protection. Results (1) 2 hours after shock compared with normal control plasma adenosine concentration was significantly increased, 5% of blood loss shock preconditioning can be further increased after the plasma adenosine concentration to 30 minutes before the shock and ischemic preconditioning group, the highest concentration of adenosine (P lt;0.01); (2) 5% blood loss 30 minutes before shock preconditioning may promote PKC @ and PKC from the cytoplasm to the cell membrane translocation (P lt;0.01), A1R antagonist significantly inhibited the ischemic preconditioning induced PKC @ and PKC translocation, so that PKC @ the membrane / cytosolic part of the ratio back down to 0.583 respectively 1.071, so that PKC in the membrane / cytosolic part of the ratio back down from the 1.280 0.606 (P lt;0.01), A2AR, A2BR and A3R antagonist had no obvious effect; (3) 5% blood loss 30 minutes before shock preconditioning induces vascular reactivit

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