钙超载

结论慢性Af患者心房肌细胞内存在钙超载。

Conclusion : Chronic Af can lead to intracellular calcium overload in human atrial myocytes .

目的：观察钙超载大鼠心肌肌浆网（SR）功能的变化。

AIM : To study alterations of cardiac sarcoplasmic reticulum ( SR ) function in vitamin D 3-induced calcium overload rats .

结论：钙超载大鼠心肌SR功能下降。

CONCLUSION : The function of cardiac SR in calcium-overload rats was decreased .

戊四氮点燃大鼠海马CA3区钙超载与亚低温对点燃大鼠脑保护作用的研究

Study on the calcium overloading in hippocampal CA_3 region of kindling rats and the cerebral protective effect of mild hypothermia on kindling rats

钙超载又能增加ROS合成，引起细胞自由基损伤。

Furthermore Ca2 + overload can increase ROS synthesis and cause cell injury induced by ROS .

钙超载作为早期的病理事件参与腺泡细胞损伤的发生，钙稳态失衡是LPS致胰腺细胞损伤的主要因素之一。

Calcium homeostasis disorder may be one of the causes or at least an important mediator of LPS-induced pancreatic acinar cell damage .

结论①IP能改善缺血再灌注大鼠心肌的收缩功能，减少线粒体钙超载，保护心肌细胞和线粒体形态和结构的完整，产生心肌保护作用；

Conclusions ① Ischenmic preconditioning can protect the rat heart from ischemia - reperfusion injury by reducing mitochondrial calcium , improving myocardial systolic function and preserving the myocardial and mitochondrial structures .

结果超生理剂量地塞米松可抑制骨骼肌细胞的增殖，降低其SOD水平，提高MDA水平，并造成细胞的损伤与钙超载。

Results Dexamethasone beyond physical dosage could suppress cells proliferation , reduce SOD level , increase MDA , and cause cells injury and Ca 2 + overloading .

结论Dip对铅致原代培养海马神经元损伤具有保护作用，其机制可能与其抑制铅诱导的胞内钙超载有关。

Conclusion Dip holds protective effect against lead-induced injury in cultured hippocampal neurons , which is possibly due to inhibiting the intracellular calcium overload in neurons .

结果缺血再灌注后SEC有损伤，但与OFR和细胞内钙超载无关；

Results HSEC displayed injury after ischemia and reperfusion , but showed no relation with OFR or intracellular calcium overload .

减轻缺血再灌注本身及其所致细胞内钙超载和RAS激活引起的炎症反应对VD大鼠海马神经元的损伤。

Reduce ischemia-reperfusion itself and result in intracellular calcium overload and activation of RAS-induced inflammatory response of VD rat hippocampal neurons damage .

结论：H2O2可引起心肌细胞内钙超载；牛磺酸能显著减轻H2O2诱导的心肌细胞内Ca~（2+）超载。

CONCLUSION : Hydrogen peroxide induces intracellular calcium overload in cardiomyocytes , and taurine decreases [ Ca ~ ( 2 + ) ] I overload in cardiomyocytes induced by hydrogen peroxide .

正常情况下，NMDA受体活性较低从而保证神经细胞不会出现钙超载。

Under normal conditions , the activity of the NMDA receptors is tightly regulated to prevent nerve cells from becoming overloaded with calcium .

氧化损伤和钙超载均能导致心肌细胞凋亡，凋亡通路中Bcl-2和Caspase家族发挥着重要作用。

Oxidize injury and Ca ~ ( 2 + ) overload can lead to cardiomyocyte apoptosis . Bcl-2 and the Caspase family play important role in apoptosis pathway .

细胞钙超载与鸡E.tenella病损伤机制的研究

The Study on Calcium Overloads and Chicken E.tenella Injury Mechanism

最新的研究表明心肌缺血时细胞内发生的钙超载可导致缝隙连接蛋白Cx43的结构和功能发生改变。

Recent studies have shown that calcium overload during cardiocyte-induced ischemia may lead to changes of both structure and function of Cx43 .

结论利多卡因、异丙酚可促进再灌注期间心肌细胞膜Na+K+ATP和肌浆网Ca2+ATP酶活性的恢复，从而抑制钙超载而减轻心肌缺血再灌注损伤。

Conclusion Lidocaine , propofol could attenuate myocardial ischemia-reperfusion injury by increasing the activities of sarcolemmal Na + - K + - ATPase and SR Ca2 + - ATPase during reperfusion .

结果：赤芍总苷对3种钙超载损伤模型大鼠神经细胞均具有明显保护作用，可显著提高损伤模型神经细胞的存活数并降低细胞释放LDH的水平。

Results : TPG possessed obvious protective effects on the nerve cells in rat models , increased the number of survival nerve cells and reduced the content of LDH released nerve cells .

另10只胎鼠在再灌注30分钟后处死进行Fura－2AM法检测，结果显示脑细胞内出现钙超载。

Examination with FUra - 2 revealed that there were intracellular calcium overloads in cerebral cells .

方法实验SD大鼠26只。随机分为两组：第一组19只，为钙超载检测组，第二组7只，为组织病理学检查组。

Methods 26 adult male rats were randomly divided into two groups , one group containing 19 rats was used to measure calcium overloading , the other containing 7 rats was used to observe the histopathological changes .

目的观察丹参酮ⅡA（TSN）、硫酸镁（MS）及二者联合应用对兔脑急性缺血细胞钙超载的影响。

Objective To investigate the protective effect of tanshinone ( TSN ), magnesium sulfate ( MSC ) and TSN combined with MS on the acute ischemic cerebral injury in rabbits .

结论：缺氧缺血可致脑细胞胞浆及线粒体Ca2+浓度增加，硫酸镁和MK-801可抑制缺氧后胞浆钙超载，苯巴比男钠效果不著。

Conclusion : Hypoxic-ischemia induced increase of cytosol and mitochondrial Ca2 + concentration . MK-801 and magnesium sulfate can inhibit cytosol calcium overload after hypoxic-ischemia .

结论：银杏内酯对抗PAF加重离体豚鼠心肌缺血再灌注损伤的作用与拮抗PAF受体、抑制自由基产生、减少心肌细胞钙超载、防止心律失常的发生有关。

Conclusion : Ginkgolides protects occurrence of arrhythmia during the MI / R by antagonizing activities of PAF and generation of free radicals to reduce the overload of calcium in myocardial cells .

结论：CGRP对缺氧再给氧的血管内皮细胞具有直接保护作用，其作用可能与CGRP具有抗脂质过氧化，减轻细胞内钙超载以及减少镁与酶的丢失有关。

CONCLUSION : These results showed that CGRP might have a direct protective function to endothelial cells afflicted with anoxic-reoxygenation injury by inhibiting lipid peroxidation , attenuating calcium overload and loss of magnesium and enzyme .

缺氧和LPS均可引起大鼠皮层神经元细胞的严重损伤，病理损害包括细胞内钙超载、能量代谢异常、细胞膜通透性增加，以及促进神经元细胞的凋亡和死亡。

Conclusion : Anoxia and LPS can lead to severe damages of cultured cortical neurons , which include intracellular calcium overload , abnormal energy metabolism , increased permeability of cellular membrane and increase in neuron apoptosis and death .

间断多次低温发挥神经保护作用的机制为抑制OGD后活性氧及超氧阴离子自由基产生，减轻细胞内钙超载，保护线粒体膜电位损伤。

The neuroprotective mechanisms were as follows : inhibiting ROS and superoxide anion radical generation , alleviating intracellular calcium overload , protecting mitochondrial membrane potential damage .

因此，探讨房颤、细胞钙超载和CaMKⅡ三者之间的关系可能有助阐明房颤的确切发病机理。

Therefore , the study of atrial fibrillation , calcium overload and the relationship between CaMK ⅱ may help the prevention and treatment of atrial fibrillation .

结论肾衰合剂通过拮抗肾小管上皮细胞钙超载、抑制炎症介质释放达到减轻肾组织病变、防治ATN的功效。

Conclusion It was indicated that SSM could antagonize calcium overload in TEC and clear away initiate inflammatory medium , consequently alleviate renal pathological changes , prevent and treat ARF .

方法：采用组织培养法，以原代大鼠大脑皮层神经细胞为材料，制备咖啡因、KCI及NMDA诱导的钙超载损伤模型。

Methods : Three injured models induced by caffeine , KCI , and NMDA , respectively , were used to assay the action of tanshinone in cultured primary cortex neurone of baby rats .

脑出血后PKC表达上调及胞内钙超载与凋亡现象成正相关，表明脑细胞信号转导途径参与脑出血后神经元损伤的病理生理改变。

In our research , the expression of PKC isoenzyme were related to cellular apoptosis and intracellular free calcium overload around the hematoma and this indicted that PKC signal transduction pathway participated in physiopathological process of neuronal injury after ICH .