心脏移植供心保护方案及心脏保存液改良研究
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摘要
目的：针对心脏移植手术的临床特点,重新设计心脏移植的供心保护方案,对采用改良供心保护方案进行心肌保护病例的心肌保护效果进行分析,评价新方案的临床价值。
方法：阜外医院自2008年1月至2011年12月期间进行的181例心脏移植,心肌保护采用改良供心保护方案。供心心肌保护为从主动脉根部灌注冷4℃St.Thomas液1000mL使供体心脏迅速停搏,再经主动脉根部一次灌注4℃HTK液2000mL进行脏器保护。所有患者均接受同种原位心脏移植术,术前常规行实验室生化检查,内分泌学检查,相关细菌学和病毒学检查以及各种物理辅助检查。
结果：热缺血时间7.1±1.9min,冷缺血时间285.7±114.5min,体外循环时间185.9±52.6min,体外循环并行辅助时间73.3±17.6min,开放升主动脉后59%(107/181)的心脏自动复跳。有16例患者术后停机困难,经体外膜式氧合器氧合(extracorporeal membrane oxygenation,ECMO)支持后脱离体外循环。术后存活出院177例,死亡4例。
结论：有效的供体心脏保护措施对心脏移植的成功起着非常关键的作用,改良供心保护方案对心脏移植供心有优良的保护效果。
目的：分析心脏移植术后早期移植物衰竭体外膜肺氧合(extracorporeal membrane oxygenation, ECMO)支持的临床临床效果,总结心脏移植患者ECMO支持的管理经验。
方法：自2008年1月至2011年12月,共进行心脏移植181例,其中16例患者在心脏移植术后使用ECMO进行循环支持治疗。记录ECMO运行期间相关参数,机械辅助时间、并发症等指标。观察ECMO建立时、辅助24小时和撤机时患者血浆乳酸值,ECMO辅助前和ECMO辅助24小时多巴胺及肾上腺素的使用量。
结果：16例心脏移植围手术期接受ECMO辅助治疗患者中脱机14例,存活出院13例,2例因心脏功能无改善不能脱机放弃治疗,1例脱机后发生慢性排斥反应,出现多器官功能衰竭死亡。所有患者均采用动脉—静脉(A-V)ECMO辅助方式,患者ECMO前,ECMO运行24小时和停止ECMO血浆乳酸值分别为：8.36±3.41、2.42±1.53.2.25±2.17mmol/L。运行24小时及停止ECMO时,血浆乳酸值较安装前明显下降(P<0.05)。ECMO前和运行24小时多巴胺用量分别为：7.38±3.42和5.29±1.93μg/min/kg,两者之间比较无统计学差异。ECMO前和运行24小时肾上腺素用量分别为：0.17±0.11和).02±0.03μg/min/kg,运行24小时较ECMO前肾上腺素用量明显减小(P<0.05)。
结论：ECMO是一种有效的循环呼吸衰竭辅助支持疗法,能明显降低终末期心脏病患者心脏移植术后早期死亡率。
目的心脏保存液在心脏移植供体心脏保护中起着非常关键的作用,在现有心脏保存液的基础上,引入“心肌保护±血管保护”的供心保护策略,以加强离体供心冠状动脉保护效果。通过改良心脏保存液对离体鼠心低温保存效果的研究,评价新设计保存液的心脏保存效果。
方法15只雄性Wistar大鼠随机分为三组：正常对照组、改良保存液组、HTK液组。除正常对照组外,其余各组取大鼠心脏后,立即分别用4℃各保存液灌注至心脏停搏,并置于相应的4℃心肌保护液中在保存8h,使用Langendorff模型测定心脏功能、检测冠脉流出液的心肌酶、观察心肌的形态学改变以评价各组心肌保护效果。
结果与正常对照组比较,各实验组心功能指标均有明显下降。HTK组LVDP, dp/dtmax, dp/dtmin,均低于改良保存液组(P<0.01),而HTK组CF的高于改良保存液组(P 结论离体低温保存8h后,心肌功能均有很大程度下降；改良保存液对离体鼠心的低温保存效果略优于HTK液。
目的探讨深低温下改良器官保护液对保存猪冠状动脉内皮舒张功能的影响。
方法取猪冠状动脉的左前降支中下1/3段,截成长度为2mm的血管环,连接与血管张力模型上,随机分为三组,分别用改良保存液、HTK液、Krebs-Henseleit重碳酸盐缓冲液(KH)液在4℃缺氧条件下保存8小时,光镜观察血管内皮结构变化及用器官槽法,检测在环加氧酶阻断剂indomethacin(7μ mol/L)和一氧化氮合成酶阻断剂LNNA(300μ mol/L)作用下,前列腺素F2a (U4661930nmol/L)及非受体介导钙离子载体(A2318710-10-10-6mol/L)引发的收缩舒张反应。
结果A23187(10-6mol/L)引发的血管最大舒张反应程度,改良保存液组(65.89%±10.42%)、HTK组(63.92%±11.31%)高于正常对照组(42.57%±12.04%,P<0.05)。
结论深低温下改良心脏保存液对猪冠脉内皮有较好的保护作用。
目的探讨改良器官保存液对缺血缺氧心肌细胞快钠通道(INa)的影响。
方法实验分为缺血再灌注组(I/R, Ischemia/reperfusion)、 Histidine-tryptophan-ketoglutarat液组(HTK)和改良器官保存液组。选择培养至18-48h的SD乳鼠心肌细胞用于实验。I/R组细胞经模拟缺血缺氧3h、再灌1h处理；HTK组和改良保存液组在模拟I/R过程中,分别加HTK液和改良保存液于细胞培养基中进行干预。用全细胞膜片钳技术检测INa的电流强度和门控特性。
结果与I/R组和HTK组相比,改良保存液组的INa的峰值电流密度明显降低(-305.9±64.1pA/pF vs-617.2±74.2pA/pF和-547.3±20.8, P<0.05),Ⅰ-Ⅴ曲线上移。HTK组较I/R组峰值电流密度降低,但两者没有统计学差异。与I/R组和改良保存液组相比,HTK组的稳态激活曲线和失活曲线左移。各组半激活电压、激活曲线斜率、半失活电压、失活曲线斜率、失活后恢复曲线时间常数均无显著性差异。
结论改良心脏保存液可抑制乳鼠心肌细胞I/R损伤后的INa通道电流,但不影响快钠通道的门控特性,这有利于减少细胞内钠钙超载,减轻I/R导致的心肌损伤。
Objective:
To design an improved donor heart preservation program on the basis of the clinical characteristic of the heart transplantation. Analyze the cardioprotective effects of the improved program and evaluate its clinical value.
Methods:
We summarized the181heart transplantation cases from January2008to December2011that used the improved program as the donor-heart preservation strategy. The organ preservation procedure was as follows:first, the donor hearts were arrested with aortic perfusion using St. Thomas'solution at4℃; then the donor hearts were perfused with2,000ml4℃HTK solution and preserved in icy saline. All the patients received orthotopic heart transplantation. Regular experimental biochemical and hemadenology tests as well as the bacteriology and virology tests were conducted.
Results:
The CPB, warm ischemia and cold ischemia time was185.9±52.6min,7.1±1.9min and285.7±114.5min, respectively. After releasing the aorta-clamp,59%of the patients recovered heart beat automatically. The16patients, who could not retrieve from CPB immediately after transplantation, turned to the extracorporeal membrane oxygenation (ECMO) support and retrieved from the mechanical support ultimately.177patients survived, and4patients died.
Conclusion:
Proper donor-heart protection strategy is indispensable for heart transplantation. The improved heart protective program can protect the organ heart properly.
Objectives:
To analyze the clinical effectiveness of the application of ECMO to the patients who suffered primary graft failure. To summarize the ECMO administration experience during heart transplantation.
Methods:
From January2008to December2011,181heart transplantation cases were studied retrospectively.16cases of them had received ECMO treatment after the transplantation. Data of the relevant parameters during ECMO, mechanism assistant duration and complications of the patients were collected. The lactic acid (LA) level at the onset and24hours of ECMO were measured. The dosages of dopamine and adrenergic pre and after24hours of ECMO were recorded.
Results:
Fourteen patients (87.5%) were successfully weaned from ECMO and13(81.3%) survived to hospital discharge. Among the16cases of ECMO,2cases abandoned therapy for no cardiac function promotion was obtained.1of them died of multiple organ failure (MOF) and chronic rejection were the main cause of death. All patients had received artery-vein (A-V) ECMO. The average level of LA at before,24hours and the end of ECMO were8.36±3.41、2.42±2.25±2.17mmol/L, respectively. The LA level was significantly decreased at the24hours and the end of ECMO, compared with pre ECMO period (P<0.05). The dosage of dopamine pre and after24hours of ECMO were7.38±3.42、5.29±1.93μg/min/kg, no significant differences were observed. However, after24hours of ECMO, the dosage of adrenergic significantly decreased0.17±0.11、0.02±0.03μg/min/kg,(P<0.05).
Conclusions:
ECMO is an effective mechanism support treatment for circulation and respiration failure. It could significantly decrease the early postoperative mortality rate of the patients who were at the terminal stage of cardiac diseases and received heart transplantation.
Objective:
The heart preservation solution is indispensable for the donor-heart preservation during transplantation. We combined "the cardiac protection and the coronary protection" together to intensify the isolated heart preservation effects. We used the isolated rat heart perfusion model to assess the hypothermic preservation effects of the newly designed solution.
Methods:
We randomly divided the male Wistar rats (n=15) to3groups as follow:Control, FW and HTK. The hearts, except the control group, were preserved by simplely immersion them for8hours at4℃in each solution. At the end of the storage period, the hearts were perfused immediately in the Langendorff model. Some indices of myocardial function were measured, every kind of myocardial enzymes were measured in the coronary effluent. Myocardium was reserved to observe the changes of myocardial ultra-structure to assess the quality of heart preservation.
Results:
The heart function of the experimental group decreased to a different degree. Group FW and HTK had a lower mean left ventricular developed pressure (LVDP)、 dp/dtmax、 dp/dtmin compared with the Control group (P<0.01). Group HTK showed better coronary flow (CF) compared to group FW (P<0.05). Group FW showed remarkably decreased release of every kind myocardial enzymes compared to group HTK (P<0.01, respectively) in cTnI、GOT and CK.
Conclusion:
After the preservation in the three kind of profound hypothermia cardioplegia solution for8hour, the heart function decrease. Cardioprotection effects of FW solution is better than the HTK solution in the isolated rat heart model during hypothermic preservation.
Objective:
To assess the effect of Fuwai organ preservation solution on endothelia relaxation and morphology in isolated rat thoracic aortic arteries.
Methods:
After rat thoracic aortic artery rings were incubated in FW (nicorandil0.1mmol/L), HTK, UW and Krebs solution at4℃for4hours, the structural change of endothelium was evaluated by light and electron microscopy, meanwhile pre-contraction induced by prostaglandin F2a (U4661930nmol/L) and endothelium-dependent relaxation induced by calcium ionophore(A2318710-10-10-6mol/L) were measured in the presence of indomethacin(7μmol/L) and LNNA(300μmol/L) in organ chamber.
Results:
Under light microscopy observation,there was no significant damage of endothelium among the FW group, the HTK group, the UW group and the control (KH) group. Under electron microscopy observation, the of endothelium damages of the group HTK and the FW group were lighter than the UW group. The maximal relaxation response induced by A23187in group FW (65.89%±10.42%) and in group HTK (63.92%±11.31%) was higher than that in group KH(42.57%±12.04%), whereas the maximal relaxation in group UW (32.06%±12.43%) was lower than that in group KH (P<0.05).
Conclusion:
Under deep hypothermia condition, the FW solution is superior to the UW solution in the endothelium preservation in the isolated rat thoracic aortic arteries.
Methods:
To study the effect of the FW solution on sodium channel (INa) in ischemia-reperfusion (I/R) neonatal rat myocytes.
Methods:
Myocytes were primary cultured for18-48h before using in the experiment. Cells were treated with I/R in the I/R group and with I/R plus Histidine-tryptophan-ketoglutarat (HTK) solution or FW solution in the HTK and the FW group, respectively. Whole cell patch clamp was used to record the current and gating.
Results:
The peak current density in the FW group decreased significantly than the I/R and the HTK group (-305.9±64.1pA/pF vs-617.2±74.2pA/pFand-547.3±20.8, P<0.05), the Ⅰ-Ⅴ curve of the FW group up-shifted. The peak current in the HTK group decreased than the I/R group, however no significant difference was observed. Compared with the I/R and the FW group, the activation and inactivation curves of the HTK group left-shifted.
Conclusions:
FW solution could inhibit the Ina current after I/R injury in neonatal rat myocytes without affecting the gating characteristics of the channel. This could help alleviating intracellular Na+and calcium (Ca2+) overload.
方法：阜外医院自2008年1月至2011年12月期间进行的181例心脏移植,心肌保护采用改良供心保护方案。供心心肌保护为从主动脉根部灌注冷4℃St.Thomas液1000mL使供体心脏迅速停搏,再经主动脉根部一次灌注4℃HTK液2000mL进行脏器保护。所有患者均接受同种原位心脏移植术,术前常规行实验室生化检查,内分泌学检查,相关细菌学和病毒学检查以及各种物理辅助检查。
结果：热缺血时间7.1±1.9min,冷缺血时间285.7±114.5min,体外循环时间185.9±52.6min,体外循环并行辅助时间73.3±17.6min,开放升主动脉后59%(107/181)的心脏自动复跳。有16例患者术后停机困难,经体外膜式氧合器氧合(extracorporeal membrane oxygenation,ECMO)支持后脱离体外循环。术后存活出院177例,死亡4例。
结论：有效的供体心脏保护措施对心脏移植的成功起着非常关键的作用,改良供心保护方案对心脏移植供心有优良的保护效果。
目的：分析心脏移植术后早期移植物衰竭体外膜肺氧合(extracorporeal membrane oxygenation, ECMO)支持的临床临床效果,总结心脏移植患者ECMO支持的管理经验。
方法：自2008年1月至2011年12月,共进行心脏移植181例,其中16例患者在心脏移植术后使用ECMO进行循环支持治疗。记录ECMO运行期间相关参数,机械辅助时间、并发症等指标。观察ECMO建立时、辅助24小时和撤机时患者血浆乳酸值,ECMO辅助前和ECMO辅助24小时多巴胺及肾上腺素的使用量。
结果：16例心脏移植围手术期接受ECMO辅助治疗患者中脱机14例,存活出院13例,2例因心脏功能无改善不能脱机放弃治疗,1例脱机后发生慢性排斥反应,出现多器官功能衰竭死亡。所有患者均采用动脉—静脉(A-V)ECMO辅助方式,患者ECMO前,ECMO运行24小时和停止ECMO血浆乳酸值分别为：8.36±3.41、2.42±1.53.2.25±2.17mmol/L。运行24小时及停止ECMO时,血浆乳酸值较安装前明显下降(P<0.05)。ECMO前和运行24小时多巴胺用量分别为：7.38±3.42和5.29±1.93μg/min/kg,两者之间比较无统计学差异。ECMO前和运行24小时肾上腺素用量分别为：0.17±0.11和).02±0.03μg/min/kg,运行24小时较ECMO前肾上腺素用量明显减小(P<0.05)。
结论：ECMO是一种有效的循环呼吸衰竭辅助支持疗法,能明显降低终末期心脏病患者心脏移植术后早期死亡率。
目的心脏保存液在心脏移植供体心脏保护中起着非常关键的作用,在现有心脏保存液的基础上,引入“心肌保护±血管保护”的供心保护策略,以加强离体供心冠状动脉保护效果。通过改良心脏保存液对离体鼠心低温保存效果的研究,评价新设计保存液的心脏保存效果。
方法15只雄性Wistar大鼠随机分为三组：正常对照组、改良保存液组、HTK液组。除正常对照组外,其余各组取大鼠心脏后,立即分别用4℃各保存液灌注至心脏停搏,并置于相应的4℃心肌保护液中在保存8h,使用Langendorff模型测定心脏功能、检测冠脉流出液的心肌酶、观察心肌的形态学改变以评价各组心肌保护效果。
结果与正常对照组比较,各实验组心功能指标均有明显下降。HTK组LVDP, dp/dtmax, dp/dtmin,均低于改良保存液组(P<0.01),而HTK组CF的高于改良保存液组(P
目的探讨深低温下改良器官保护液对保存猪冠状动脉内皮舒张功能的影响。
方法取猪冠状动脉的左前降支中下1/3段,截成长度为2mm的血管环,连接与血管张力模型上,随机分为三组,分别用改良保存液、HTK液、Krebs-Henseleit重碳酸盐缓冲液(KH)液在4℃缺氧条件下保存8小时,光镜观察血管内皮结构变化及用器官槽法,检测在环加氧酶阻断剂indomethacin(7μ mol/L)和一氧化氮合成酶阻断剂LNNA(300μ mol/L)作用下,前列腺素F2a (U4661930nmol/L)及非受体介导钙离子载体(A2318710-10-10-6mol/L)引发的收缩舒张反应。
结果A23187(10-6mol/L)引发的血管最大舒张反应程度,改良保存液组(65.89%±10.42%)、HTK组(63.92%±11.31%)高于正常对照组(42.57%±12.04%,P<0.05)。
结论深低温下改良心脏保存液对猪冠脉内皮有较好的保护作用。
目的探讨改良器官保存液对缺血缺氧心肌细胞快钠通道(INa)的影响。
方法实验分为缺血再灌注组(I/R, Ischemia/reperfusion)、 Histidine-tryptophan-ketoglutarat液组(HTK)和改良器官保存液组。选择培养至18-48h的SD乳鼠心肌细胞用于实验。I/R组细胞经模拟缺血缺氧3h、再灌1h处理；HTK组和改良保存液组在模拟I/R过程中,分别加HTK液和改良保存液于细胞培养基中进行干预。用全细胞膜片钳技术检测INa的电流强度和门控特性。
结果与I/R组和HTK组相比,改良保存液组的INa的峰值电流密度明显降低(-305.9±64.1pA/pF vs-617.2±74.2pA/pF和-547.3±20.8, P<0.05),Ⅰ-Ⅴ曲线上移。HTK组较I/R组峰值电流密度降低,但两者没有统计学差异。与I/R组和改良保存液组相比,HTK组的稳态激活曲线和失活曲线左移。各组半激活电压、激活曲线斜率、半失活电压、失活曲线斜率、失活后恢复曲线时间常数均无显著性差异。
结论改良心脏保存液可抑制乳鼠心肌细胞I/R损伤后的INa通道电流,但不影响快钠通道的门控特性,这有利于减少细胞内钠钙超载,减轻I/R导致的心肌损伤。
Objective:
To design an improved donor heart preservation program on the basis of the clinical characteristic of the heart transplantation. Analyze the cardioprotective effects of the improved program and evaluate its clinical value.
Methods:
We summarized the181heart transplantation cases from January2008to December2011that used the improved program as the donor-heart preservation strategy. The organ preservation procedure was as follows:first, the donor hearts were arrested with aortic perfusion using St. Thomas'solution at4℃; then the donor hearts were perfused with2,000ml4℃HTK solution and preserved in icy saline. All the patients received orthotopic heart transplantation. Regular experimental biochemical and hemadenology tests as well as the bacteriology and virology tests were conducted.
Results:
The CPB, warm ischemia and cold ischemia time was185.9±52.6min,7.1±1.9min and285.7±114.5min, respectively. After releasing the aorta-clamp,59%of the patients recovered heart beat automatically. The16patients, who could not retrieve from CPB immediately after transplantation, turned to the extracorporeal membrane oxygenation (ECMO) support and retrieved from the mechanical support ultimately.177patients survived, and4patients died.
Conclusion:
Proper donor-heart protection strategy is indispensable for heart transplantation. The improved heart protective program can protect the organ heart properly.
Objectives:
To analyze the clinical effectiveness of the application of ECMO to the patients who suffered primary graft failure. To summarize the ECMO administration experience during heart transplantation.
Methods:
From January2008to December2011,181heart transplantation cases were studied retrospectively.16cases of them had received ECMO treatment after the transplantation. Data of the relevant parameters during ECMO, mechanism assistant duration and complications of the patients were collected. The lactic acid (LA) level at the onset and24hours of ECMO were measured. The dosages of dopamine and adrenergic pre and after24hours of ECMO were recorded.
Results:
Fourteen patients (87.5%) were successfully weaned from ECMO and13(81.3%) survived to hospital discharge. Among the16cases of ECMO,2cases abandoned therapy for no cardiac function promotion was obtained.1of them died of multiple organ failure (MOF) and chronic rejection were the main cause of death. All patients had received artery-vein (A-V) ECMO. The average level of LA at before,24hours and the end of ECMO were8.36±3.41、2.42±2.25±2.17mmol/L, respectively. The LA level was significantly decreased at the24hours and the end of ECMO, compared with pre ECMO period (P<0.05). The dosage of dopamine pre and after24hours of ECMO were7.38±3.42、5.29±1.93μg/min/kg, no significant differences were observed. However, after24hours of ECMO, the dosage of adrenergic significantly decreased0.17±0.11、0.02±0.03μg/min/kg,(P<0.05).
Conclusions:
ECMO is an effective mechanism support treatment for circulation and respiration failure. It could significantly decrease the early postoperative mortality rate of the patients who were at the terminal stage of cardiac diseases and received heart transplantation.
Objective:
The heart preservation solution is indispensable for the donor-heart preservation during transplantation. We combined "the cardiac protection and the coronary protection" together to intensify the isolated heart preservation effects. We used the isolated rat heart perfusion model to assess the hypothermic preservation effects of the newly designed solution.
Methods:
We randomly divided the male Wistar rats (n=15) to3groups as follow:Control, FW and HTK. The hearts, except the control group, were preserved by simplely immersion them for8hours at4℃in each solution. At the end of the storage period, the hearts were perfused immediately in the Langendorff model. Some indices of myocardial function were measured, every kind of myocardial enzymes were measured in the coronary effluent. Myocardium was reserved to observe the changes of myocardial ultra-structure to assess the quality of heart preservation.
Results:
The heart function of the experimental group decreased to a different degree. Group FW and HTK had a lower mean left ventricular developed pressure (LVDP)、 dp/dtmax、 dp/dtmin compared with the Control group (P<0.01). Group HTK showed better coronary flow (CF) compared to group FW (P<0.05). Group FW showed remarkably decreased release of every kind myocardial enzymes compared to group HTK (P<0.01, respectively) in cTnI、GOT and CK.
Conclusion:
After the preservation in the three kind of profound hypothermia cardioplegia solution for8hour, the heart function decrease. Cardioprotection effects of FW solution is better than the HTK solution in the isolated rat heart model during hypothermic preservation.
Objective:
To assess the effect of Fuwai organ preservation solution on endothelia relaxation and morphology in isolated rat thoracic aortic arteries.
Methods:
After rat thoracic aortic artery rings were incubated in FW (nicorandil0.1mmol/L), HTK, UW and Krebs solution at4℃for4hours, the structural change of endothelium was evaluated by light and electron microscopy, meanwhile pre-contraction induced by prostaglandin F2a (U4661930nmol/L) and endothelium-dependent relaxation induced by calcium ionophore(A2318710-10-10-6mol/L) were measured in the presence of indomethacin(7μmol/L) and LNNA(300μmol/L) in organ chamber.
Results:
Under light microscopy observation,there was no significant damage of endothelium among the FW group, the HTK group, the UW group and the control (KH) group. Under electron microscopy observation, the of endothelium damages of the group HTK and the FW group were lighter than the UW group. The maximal relaxation response induced by A23187in group FW (65.89%±10.42%) and in group HTK (63.92%±11.31%) was higher than that in group KH(42.57%±12.04%), whereas the maximal relaxation in group UW (32.06%±12.43%) was lower than that in group KH (P<0.05).
Conclusion:
Under deep hypothermia condition, the FW solution is superior to the UW solution in the endothelium preservation in the isolated rat thoracic aortic arteries.
Methods:
To study the effect of the FW solution on sodium channel (INa) in ischemia-reperfusion (I/R) neonatal rat myocytes.
Methods:
Myocytes were primary cultured for18-48h before using in the experiment. Cells were treated with I/R in the I/R group and with I/R plus Histidine-tryptophan-ketoglutarat (HTK) solution or FW solution in the HTK and the FW group, respectively. Whole cell patch clamp was used to record the current and gating.
Results:
The peak current density in the FW group decreased significantly than the I/R and the HTK group (-305.9±64.1pA/pF vs-617.2±74.2pA/pFand-547.3±20.8, P<0.05), the Ⅰ-Ⅴ curve of the FW group up-shifted. The peak current in the HTK group decreased than the I/R group, however no significant difference was observed. Compared with the I/R and the FW group, the activation and inactivation curves of the HTK group left-shifted.
Conclusions:
FW solution could inhibit the Ina current after I/R injury in neonatal rat myocytes without affecting the gating characteristics of the channel. This could help alleviating intracellular Na+and calcium (Ca2+) overload.
引文
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