[Effect of Guanxinkang on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/ reperfusion injury].
Na Zhang, Eu-Rang Chen, Yiyi Zhang
Abstract
Na Zhang, Eu-Rang Chen, Yiyi Zhang
Abstract
UNLABELLED: OBJECTIVE To investigate the effect of Guanxinkang (GXK) on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/reperfusion injury and its possible mechanism for cardiac vascular protection and anti-myocardial ischemia. METHODS: Wistar rats were established into I/R injured models by 10 min perfusion--30 min no-flow ischemia--45 min reperfusion, and divided into 5 groups: the I/R model group and 4 treatment groups treated respectively with glibenclamide, pinacidil, GXK and GXK+glibenclamide. Rats' heart were isolated for detecting Ca(2+)-Mg(2+)-ATPase, Na(+)-K(+)-ATPase activity in myocardial cells, and the changes of current in ATP-sensive potassium channel (K(ATP)) was recorded by whole patch clamp technique. Data were controlled by those taken from normal rats in a control group. RESULTS: K(ATP) in the GXK treated group were higher than that in the I/R model group; and similar to that in the pinacidil treated group (P > 0.05). As compared with the model group, activities of Ca(2+)-Mg(2+)-ATPase and Na(+)-K(+)-ATPase in the GXK treated group were increased significantly (P < 0.05). CONCLUSION: GXK shows definite intervention effect on myocardial I/R injury; which is possibly by way of furthering the opening of K(ATP) channel, decreasing Ca2+ influx, and inhibiting Ca2+ overload.
OpenAlex reports 2 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
UNLABELLED: OBJECTIVE To investigate the effect of Guanxinkang (GXK) on ATP-sensitive potassium channel in myocardial cells of rat with ischemic/reperfusion injury and its possible mechanism for cardiac vascular protection and anti-myocardial ischemia. METHODS: Wistar rats were established into I/R injured models by 10 min perfusion--30 min no-flow ischemia--45 min reperfusion, and divided into 5 groups: the I/R model group and 4 treatment groups treated respectively with glibenclamide, pinacidil, GXK and GXK+glibenclamide. Rats' heart were isolated for detecting Ca(2+)-Mg(2+)-ATPase, Na(+)-K(+)-ATPase activity in myocardial cells, and the changes of current in ATP-sensive potassium channel (K(ATP)) was recorded by whole patch clamp technique. Data were controlled by those taken from normal rats in a control group. RESULTS: K(ATP) in the GXK treated group were higher than that in the I/R model group; and similar to that in the pinacidil treated group (P > 0.05). As compared with the model group, activities of Ca(2+)-Mg(2+)-ATPase and Na(+)-K(+)-ATPase in the GXK treated group were increased significantly (P < 0.05). CONCLUSION: GXK shows definite intervention effect on myocardial I/R injury; which is possibly by way of furthering the opening of K(ATP) channel, decreasing Ca2+ influx, and inhibiting Ca2+ overload.
Key concepts: Glibenclamide, Pinacidil, ATP-sensitive potassium channel, Potassium channel, Perfusion, Potassium, Ischemia, Reperfusion injury