Summary： The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly： acute ischem...Summary： The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly： acute ischemia （AI） group and sham operation （SO） group. By using the monophasic action potential （MAP） technique, MAP and effective refractory period （ERP） of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization （TDR） and transmural dispersion of ERP （TDE） were analyzed. The results showed that in the AI group, MAP duration （MAPD） was shortened from 201.67±21.42 ms to 169.50±13.81 ms （P〈0.05）, but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.展开更多
Objective: To study the effect of dexmedetomidine on monophasic action potential amplitude (MAPA) in myocardial ischemia-reperfusion and its correlation with myocardial injury. Methods: SD rats were selected as the ex...Objective: To study the effect of dexmedetomidine on monophasic action potential amplitude (MAPA) in myocardial ischemia-reperfusion and its correlation with myocardial injury. Methods: SD rats were selected as the experimental animals and randomly divided into control group, ischemia reperfusion group (I/R group) and dexmedetomidine group (Dex group);I/R group and Dex group were made into myocardial ischemia-reperfusion injury models, and Dex group were given exmedetomidine intervention;the MAPA of myocardial tunica intima layer, tunica media layer and tunica externa layer were measured in Langendorff perfusion system;myocardial tissue was collected to determine the contents of oxidative stress molecules and the expression of apoptosis genes. Results: The MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of I/R group were significantly lower than those of control group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly higher than those of control group;the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of Dex group were significantly higher than those of I/R group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly lower than those of I/R group;Pearson test showed that the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer were negatively correlated with CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue, and positively correlated with Klotho and SOD contents. Conclusion: Dexmedetomidine can increase the MAPA in myocardial ischemia-reperfusion process, and is closely related to the inhibition of oxidative stress response and apoptosis.展开更多
Objective:To study the correlation between myocardial ischemia-reperfusion-induced monophasic action potential amplitude (MAPA) change and myocardial damage.Methods:New Zealand rabbits were selected as experimental an...Objective:To study the correlation between myocardial ischemia-reperfusion-induced monophasic action potential amplitude (MAPA) change and myocardial damage.Methods:New Zealand rabbits were selected as experimental animals and randomly divided into control group and ischemia-reperfusion group (I/R group), myocardial ischemia-reperfusion injury models were established, then the heart was separated and the MAPA of myocardial intima layer, media layer and outer layer were determined in Langendorff perfusion system;serum samples and myocardial tissue were collected to determine the contents of myocardial injury molecules.Results: MAPA levels of myocardial intima layer, media layer and outer layer of I/R group were significantly lower than those of control group;CK-MB, cTnI, cTnT and MDA contents in serum as well as Bax, Caspase-3 and Caspase-9 mRNA expression in myocardial tissue of I/R group were significantly higher than those of control group and negatively correlated with MAPA levels of myocardial intima layer, media layer and outer layer while SOD, GSH-Px and HO-1 contents in serum as well as Bcl-2 and Bcl-xL mRNA expression in myocardial tissue were significantly lower than those of control group and positively correlated with MAPA levels of myocardial intima layer, media layer and outer layer.Conclusion:Myocardial ischemia - reperfusion can induce the decrease of MAPA and is closely related to myocardial oxidative stress injury and apoptosis.展开更多
Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^＋ channel. In affected individuals, the risk of developing malignant v...Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^＋ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.展开更多
The goal is to help create smooth energy-optimal monophasic pulse waveforms for defibrillation using the Luo-Rudy cardiomyocyte membrane computer model. The waveforms were described with the help of the piecewise line...The goal is to help create smooth energy-optimal monophasic pulse waveforms for defibrillation using the Luo-Rudy cardiomyocyte membrane computer model. The waveforms were described with the help of the piecewise linear function. Each line segment provides a transition from one present level of the transmembrane potential to the next with a minimal energy value. The duration of the last segment was defined as a minimum duration at which an action potential occurs. Monophasic waveforms of segments 3, 10 and 29 were built using different increments of the transmembrane potential. The pulse energy efficiency was evaluated according to their threshold energy ratios in mA2·ms/cm4. There was virtually no difference between the threshold energy ratios of the three waveforms constructed and those of the previously studied energy-optimal half- sine waveform: 241 - 242 and 243 mA2·ms/cm4. The pulse waveform constructed is characterized by a low rise and fall as the duration of the rise is ~1.5 times longer than that of the fall. Conclusion: Energy-optimal smooth monophasic pulse waveforms have the same threshold energy ratio as the optimal half-sine one which was studied before. The latter is equivalent to the first phase of biphasic quasisinusoidal Gurvich-Venin pulse which has been used in Russia since 1972. Thus, the use of the Luo-Rudy cardiomyocyte membrane model appears to offer no possibilities for a substantial increase in the energy efficiency (threshold energy ratio reduction) of the classical monophasic defibrillation pulse waveforms.展开更多
文摘Summary： The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of canine in vivo was investigated. Twelve canines were divided into two groups randomly： acute ischemia （AI） group and sham operation （SO） group. By using the monophasic action potential （MAP） technique, MAP and effective refractory period （ERP） of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization （TDR） and transmural dispersion of ERP （TDE） were analyzed. The results showed that in the AI group, MAP duration （MAPD） was shortened from 201.67±21.42 ms to 169.50±13.81 ms （P〈0.05）, but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis.
文摘Objective: To study the effect of dexmedetomidine on monophasic action potential amplitude (MAPA) in myocardial ischemia-reperfusion and its correlation with myocardial injury. Methods: SD rats were selected as the experimental animals and randomly divided into control group, ischemia reperfusion group (I/R group) and dexmedetomidine group (Dex group);I/R group and Dex group were made into myocardial ischemia-reperfusion injury models, and Dex group were given exmedetomidine intervention;the MAPA of myocardial tunica intima layer, tunica media layer and tunica externa layer were measured in Langendorff perfusion system;myocardial tissue was collected to determine the contents of oxidative stress molecules and the expression of apoptosis genes. Results: The MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of I/R group were significantly lower than those of control group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly higher than those of control group;the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer as well as Klotho and SOD contents in myocardial tissue of Dex group were significantly higher than those of I/R group whereas CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue were significantly lower than those of I/R group;Pearson test showed that the MAPA levels of myocardial tunica intima layer, tunica media layer and tunica externa layer were negatively correlated with CaMKII, NOX2, NOX4 and MDA contents as well as CaSR, USP14, JNK, Bax, Fas and Caspase-3 mRNA expression in myocardial tissue, and positively correlated with Klotho and SOD contents. Conclusion: Dexmedetomidine can increase the MAPA in myocardial ischemia-reperfusion process, and is closely related to the inhibition of oxidative stress response and apoptosis.
文摘Objective:To study the correlation between myocardial ischemia-reperfusion-induced monophasic action potential amplitude (MAPA) change and myocardial damage.Methods:New Zealand rabbits were selected as experimental animals and randomly divided into control group and ischemia-reperfusion group (I/R group), myocardial ischemia-reperfusion injury models were established, then the heart was separated and the MAPA of myocardial intima layer, media layer and outer layer were determined in Langendorff perfusion system;serum samples and myocardial tissue were collected to determine the contents of myocardial injury molecules.Results: MAPA levels of myocardial intima layer, media layer and outer layer of I/R group were significantly lower than those of control group;CK-MB, cTnI, cTnT and MDA contents in serum as well as Bax, Caspase-3 and Caspase-9 mRNA expression in myocardial tissue of I/R group were significantly higher than those of control group and negatively correlated with MAPA levels of myocardial intima layer, media layer and outer layer while SOD, GSH-Px and HO-1 contents in serum as well as Bcl-2 and Bcl-xL mRNA expression in myocardial tissue were significantly lower than those of control group and positively correlated with MAPA levels of myocardial intima layer, media layer and outer layer.Conclusion:Myocardial ischemia - reperfusion can induce the decrease of MAPA and is closely related to myocardial oxidative stress injury and apoptosis.
文摘Brugada syndrome is a primary arrhythmia syndrome characterized by loss-of-function mutations in the SCN5A gene, which encodes for the cardiac Na^＋ channel. In affected individuals, the risk of developing malignant ventricular arrhythmias and sudden cardiac death are increased.
文摘The goal is to help create smooth energy-optimal monophasic pulse waveforms for defibrillation using the Luo-Rudy cardiomyocyte membrane computer model. The waveforms were described with the help of the piecewise linear function. Each line segment provides a transition from one present level of the transmembrane potential to the next with a minimal energy value. The duration of the last segment was defined as a minimum duration at which an action potential occurs. Monophasic waveforms of segments 3, 10 and 29 were built using different increments of the transmembrane potential. The pulse energy efficiency was evaluated according to their threshold energy ratios in mA2·ms/cm4. There was virtually no difference between the threshold energy ratios of the three waveforms constructed and those of the previously studied energy-optimal half- sine waveform: 241 - 242 and 243 mA2·ms/cm4. The pulse waveform constructed is characterized by a low rise and fall as the duration of the rise is ~1.5 times longer than that of the fall. Conclusion: Energy-optimal smooth monophasic pulse waveforms have the same threshold energy ratio as the optimal half-sine one which was studied before. The latter is equivalent to the first phase of biphasic quasisinusoidal Gurvich-Venin pulse which has been used in Russia since 1972. Thus, the use of the Luo-Rudy cardiomyocyte membrane model appears to offer no possibilities for a substantial increase in the energy efficiency (threshold energy ratio reduction) of the classical monophasic defibrillation pulse waveforms.
