Research Of Salidroside In Myocardial Ischemia Injury In Cytophysiology

Rhodiola rosea is a perennial herb or subshrub in Rhodiola L. genus,Crassulaceae family; major chemical constituents in root and rhizome includesalidroside (C₁₄H₂₀O₇), tyrosol (C₆H₁₀O₂) and Rhodiola polysaccharide. Manyprevious researches showed salidroside has various pharmacological activitiesincluding anti-fatigue, anti-aging, free-radical scavenging, memory improving, sleepquality promoting, cardiovascular effects, etc. Researches on clinical cases indicatethe therapeutic effects of Rhodiola related drugs on clinical symptoms of anginapectoris, electrocardiogram, TCM symptoms and reduction rate of nitroglycerin areinclined to be more efficient than other medicines.According to the study on the ST segment in surface II leads electrocardiogramsand epicardial potential diagrams of Rhodiola rosea inhibited myocardial ischemiaanimals, myocardial oxygen consumption was lowered, this gave further proof to itseffect of increasing cardiac work in the case of decreased myocardial oxygenconsumption, thus cardiovascular compliance was improved and cardio workefficiency was increased. The mechanism of salidroside’s inhibitory on elevation of Twave and J point in the electrocardiograms of myocardial ischemia animal models hasnot been reported. We designed observation of surface electrocardiograms changes inischemic myocardial injury （organic level）, action potential changes of myocardialcell （cellular level） and changes of ion channel protein molecules on the myocardialcell membrane （molecular level） in this experimental research, to survey the effect ofsalidroside on the electrophysiologic phenomena of myocardial ischemia animalmodels in diversified levels and conclude theoretical mechanism basis of theprotective effect of salidroside on myocardial ischemia animal.BL420system was employed in monitoring ST segment shift in standard II leadssurface electrocardiograms （ECG） of rats. ST segment elevation was led bymyocardial ischemia injury. Afterward salidroside was administrated5mg kg^-1,10 mg kg^-1 and30mg kg^-1 respectively. The results showed ST segment shifts of theischemia group decreased from0.131±0.09mV to0.113±0.04mV,0.08±0.05mV and0.07±0.07mV, suggesting that ST segment shifts were significantly lowered in thesurface electrocardiograms of salidroside administration groups. The results indicatedthat Rhodiola rosea can inhibit ST segment elevation and T wave elevation in II leadselectrocardiograms caused by coronary artery ligation in preparing myocardialischemia rat models. The protective effect of Rhodiola rosea on myocardial ischemiainjury is elucidated from the organic level.The whole-cell Clamp Current method is used to record myocardial cell actionpotential amplitude （APA）, the action potential duration50%,90%（APD50andAPD90）. After myocardial ischemia injury, all the action potential amplitude （APA） aswell as the action potential duration APD50and APD90has declined in differentdegrees. Then, Sal5μmol/L, Sal10μmol/L and Sal30μmol/L of drugs wereadministered, respectively, and the results showed that the myocardial cells APAincreased from ischemic group of78.23±5.21mV to94.43±7.12mV,94.82±5.34Vand95.32±4.34mV. The myocardial cells APD50increased from ischemic group of173.45±20.23to177.54±19.45ms,206.67±17.67ms and263.67±17.37ms. Themyocardial cells APD90increased from ischemic group of203.45±17.65ms to211.65±18.21ms,238.78±17.34ms and298.38±16.85ms. This indicates that Sal doseof every group has significantly increased the action potential amplitude andobviously extended the action potential duration of ischemia group. Experimentalresults show that Rhodiola rosea can inhibit the decrease in action potential amplitude（APA） and the shortening of action potential duration after myocardial ischemiadamage. The protective effect of Rhodiola rosea on myocardial ischemia damage isillustrated on the cellular level.The whole-cell Voltage Clamp mode is used to record the delayed rectifyingpotassium channel current IK⁺of individual cavy ventricle muscle cells. Stimuluspulse increases from-40mV to+50mV, with step voltage of+10mV. Stimulus pulseduration is400ms. After myocardial ischemia injury, the delayed rectifying potassium channel current IK+increased from18.94±18.94nA to25.06±0.124nA. This showsthat the delayed rectifying potassium channel current IK+outflow has increasedduring the myocardial ischemia. Then, Sal5μmol/L, Sal10μmol/L and Sal30μmol/Lof drugs were administered, respectively, and the results showed that the myocardialcells delayed rectifying potassium channel current IK+fell from25.84±0.112nA,25.12±0.115nA and21.56±0.134nA before the dose to23.42±0.117nA,21.56±0.134nA and19.86±0.134nA, respectively. This indicates that Sal dose of every group hassignificantly inhibited ischemic cavy papillary muscle cells rectifying potassiumchannel current IK+from outflow. The protective effect of Rhodiola rosea onmyocardial ischemia damage is illustrated on the molecular level.The above results show that the protective effect of Rhodiola rosea againstmyocardial ischemia injury is related to ventricular muscle cells delayed rectifyingpotassium channel current IK⁺. Rhodiola rosea inhibition of IK⁺can limit theexcessive potassium outflow of cells, thus the action potential duration is extended, sothat the gap between ischemia myocardial cell potential duration and normalmyocardial cell potential duration will be reduced, to prevent arrhythmia aftermyocardial ischemia damage, so as to provide protective effect on myocardialischemia injuries.