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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Daniels S, Duncan C J

Department of Environmental and Evolutionary Biology, University of Liverpool, U.K.

Comp Biochem Physiol Comp Physiol. 1993 Jun;105(2):329-32. doi: 10.1016/0300-9629(93)90216-q.

The release of creatine kinase (CK) in the Langendorff-perfused rat heart during the Ca(2+)-paradox, was critically dependent on the duration and [Ca2+]o of the initial Ca(2+)-depletion phase. 2. When [Ca2+]i was raised by perfusion with caffeine or under N2, activation of the protein kinase C pathway (PKC) produced a small but significant release of CK. PKC stimulation is therefore able to substitute for the Cao(2+)-depletion of the Ca(2+)-paradox. 3. The PKC inhibitor, 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine, (2 x 10(-6) M) inhibited both the Ca(2+)-paradox and caffeine-induced release of CK. 4. It is concluded that the PKC pathway has a regulatory role for the damage system of the sarcolemma that is responsible for the release of cytosolic proteins.

在钙矛盾现象期间，Langendorff灌注大鼠心脏中肌酸激酶（CK）的释放严重依赖于初始钙耗竭阶段的持续时间和细胞外钙浓度（[Ca2+]o）。2. 当通过用咖啡因灌注或在氮气条件下升高细胞内钙浓度（[Ca2+]i）时，蛋白激酶C途径（PKC）的激活会导致CK少量但显著释放。因此，PKC刺激能够替代钙矛盾现象中的细胞外钙耗竭。3. PKC抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪（2×10⁻⁶ M）抑制了钙矛盾现象和咖啡因诱导的CK释放。4. 得出的结论是，PKC途径对肌膜损伤系统具有调节作用，该损伤系统负责细胞溶质蛋白的释放。

Daniels S, Duncan C J

Department of Environmental and Evolutionary Biology, University of Liverpool, U.K.

Comp Biochem Physiol Comp Physiol. 1993 Jun;105(2):329-32. doi: 10.1016/0300-9629(93)90216-q.

The release of creatine kinase (CK) in the Langendorff-perfused rat heart during the Ca(2+)-paradox, was critically dependent on the duration and [Ca2+]o of the initial Ca(2+)-depletion phase. 2. When [Ca2+]i was raised by perfusion with caffeine or under N2, activation of the protein kinase C pathway (PKC) produced a small but significant release of CK. PKC stimulation is therefore able to substitute for the Cao(2+)-depletion of the Ca(2+)-paradox. 3. The PKC inhibitor, 1-(5-isoquinolinyl sulphonyl)-2-methyl piperazine, (2 x 10(-6) M) inhibited both the Ca(2+)-paradox and caffeine-induced release of CK. 4. It is concluded that the PKC pathway has a regulatory role for the damage system of the sarcolemma that is responsible for the release of cytosolic proteins.

在钙矛盾现象期间，Langendorff灌注大鼠心脏中肌酸激酶（CK）的释放严重依赖于初始钙耗竭阶段的持续时间和细胞外钙浓度（[Ca2+]o）。2. 当通过用咖啡因灌注或在氮气条件下升高细胞内钙浓度（[Ca2+]i）时，蛋白激酶C途径（PKC）的激活会导致CK少量但显著释放。因此，PKC刺激能够替代钙矛盾现象中的细胞外钙耗竭。3. PKC抑制剂1-（5-异喹啉磺酰基）-2-甲基哌嗪（2×10⁻⁶ M）抑制了钙矛盾现象和咖啡因诱导的CK释放。4. 得出的结论是，PKC途径对肌膜损伤系统具有调节作用，该损伤系统负责细胞溶质蛋白的释放。