Despite advances in intelligent medical care,difficulties remain.Due to its complicated governance,designing,planning,improving,and managing the cardiac system remains difficult.Oversight,including intelligent monitor...Despite advances in intelligent medical care,difficulties remain.Due to its complicated governance,designing,planning,improving,and managing the cardiac system remains difficult.Oversight,including intelligent monitoring,feedback systems,and management practises,is unsuccessful.Current platforms cannot deliver lifelong personal health management services.Insufficient accuracy in patient crisis warning programmes.No frequent,direct interaction between healthcare workers and patients is visible.Physical medical systems and intelligent information systems are not integrated.This study introduces the Advanced Cardiac Twin(ACT)model integrated with Artificial Neural Network(ANN)to handle real-time monitoring,decision-making,and crisis prediction.THINGSPEAK is used to create an IoT platform that accepts patient sensor data.Importing these data sets into MATLAB allows display and analysis.A myocardial ischemia research examined Health Condition Tracking’s(HCT’s)potential.In the case study,75%of the training sets(Xt),15%of the verified data,and 10%of the test data were used.Training set feature values(Xt)were given with the data.Training,Validation,and Testing accuracy rates were 99.9%,99.9%,and 99.9%,respectively.General research accuracy was 99.9%.The proposed HCT system and Artificial Neural Network(ANN)model gather historical and real-time data to manage and anticipate cardiac issues.展开更多
Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associate...Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associated with organ rejection. We hypothesized that it is either passively released from injured tissues during organ procurement, or actively secreted by allograft infiltrating cells contributing to allograft dysfunction. We investigated the impact of IRI in an in vitro study of human heart tissue during the process of transplantation. The mRNA expression levels for both isoforms of the AIF-1, I2 and I3 were significantly increased after 30 minutes reperfusion (AIF-1 I2: p 0.01 vs. AIF-1 I3: p 0.005). Expression levels for IL-18 and the TLRs were increased after 30 minutes of reperfusion. Only IL-18 and TLR-2 were statistically significant (IL-18: p 0.0001 vs. TLR-2: p 0.01). The mRNA expression levels for AIF-1 I2 and IL-18 were decreased from the original levels of ischemia after 60 and 90 minutes reperfusion. The TLR-2 and -4 were presented with minimal levels of reduction after 60 minutes. However, mRNA expression levels for all were decreased to the original levels of ischemia after 90 minutes, except for AIF-1 I3, but the difference was not statistically significant. AIF-1 and IL-18 were specifically detected in myocytes and interstitial tissues by immunohistochemistry (IHC) stain after IRI. TLR-4 was non-specific, and TLR2 was minimally expressed. The study discusses the evidence supporting that the AIF-1 may have therapeutic potential for strategies in the control of innate immune responses early on, after transplantation.展开更多
This study aimed to investigate changes in postmortem urotensin Ⅱ receptor(UTR)levels in brain and kidney tissues in a rat model of cardiac ischemia.The rats were divided into two groups:a control group and a cardiac...This study aimed to investigate changes in postmortem urotensin Ⅱ receptor(UTR)levels in brain and kidney tissues in a rat model of cardiac ischemia.The rats were divided into two groups:a control group and a cardiac ischemia-induced group.Cardiac ischemia was created by an intraperitoneal injection of a single lethal dose of isoproterenol(ISO;850 mg/kg).Plasma UT,blood urea nitrogen,and creatinine levels were determined 0 h postmortem.Brain and kidney UTR mRNA expression levels were determined 0,1,3,6,12,24,4&and 72 h postmortem.The histopathological appearance of brain and kidney tissues was also evaluated.Plasma UT and plasma creatinine levels were increased in the cardiac ischemia-induced group as compared with those in the control group(P<0.001).Ischemia resulted in histopathological changes in brain and cerebellum tissue.The morphological evaluation revealed Purkinje cell degeneration(P=0.037)and dark neurons(P=0.004).The UTR expression level decreased after 1 h postmortem in the brain and after 3 h postmortem in the kidneys in the cardiac ischemia-induced group as compared with that in the control group(P<0.001).The observed changes in UTR expression levels may be valuable in clinical practice in the field of forensic medicine.These changes may be used as a marker in postmortem evaluations of sudden death caused by ischemia-induced cardiac shock.展开更多
Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg...Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL,3.0 mg/mL,5.0 mg/mL) for 24 h.then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h.The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes,respectively.The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot,respectively.Results:Compared to the negative group,pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury(P<0.05).The expression of Bcl-2 in tocilizumab treated group were higher than NC group(P<0.05).while the Bax expression were lower(P<0.05).Conclusions:Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury.Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.展开更多
Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1（PAR1）. However, the role and mechanisms underlying the effects of PAR1 activati...Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1（PAR1）. However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the effects of the PAR1 antagonist SCH79797 in a rabbit model of global cerebral ischemia induced by cardiac arrest. SCH79797 was intravenously administered 10 minutes after the model was established. Forty-eight hours later, compared with those administered saline, rabbits receiving SCH79797 showed markedly decreased neuronal damage as assessed by serum neuron specific enolase levels and less neurological dysfunction as determined using cerebral performance category scores. Additionally, in the hippocampus, cell apoptosis, polymorphonuclear cell infiltration, and c-Jun levels were decreased, whereas extracellular signal-regulated kinase phosphorylation levels were increased. All of these changes were inhibited by the intravenous administration of the phosphoinositide 3-kinase/Akt pathway inhibitor LY29004（3 mg/kg） 10 minutes before the SCH79797 intervention. These findings suggest that SCH79797 mitigates brain injury via anti-inflammatory and anti-apoptotic effects, possibly by modulating the extracellular signal-regulated kinase, c-Jun N-terminal kinase/c-Jun and phosphoinositide 3-kinase/Akt pathways.展开更多
BACKGROUND： Numerous studies have shown that magnetic resonance imaging （MRI） can detect survival and migration of super paramagnetic iron oxide-labeled stem cells in models of focal cerebral infarction. OBJECTIVE...BACKGROUND： Numerous studies have shown that magnetic resonance imaging （MRI） can detect survival and migration of super paramagnetic iron oxide-labeled stem cells in models of focal cerebral infarction. OBJECTIVE： To observe distribution of bone marrow mesenchymal stem cells （BMSCs） in a rat model of global brain ischemia following cardiac arrest and resuscitation, and to investigate the feasibility of tracing iron oxide-labeled BMSCs using non-invasive MRI. DESIGN, TIME AND SETTING： The randomized, controlled, molecular imaging study was performed at the Linbaixin Medical Research Center, Second Affiliated Hospital, Sun Yat-sen University, and the Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, China from October 2006 to February 2009. MATERIALS： A total of 40 clean, Sprague Dawley rats, aged 6 weeks and of either gender, were supplied by the Experimental Animal Center, Sun Yat-sen University, China, for isolation of BMSCs. Feridex （iron oxide）, Gyroscan Inetra 1.5T MRI system, and cardiopulmonary resuscitation device were used in this study. METHODS： A total of 30 healthy, male Sprague Dawiey rats, aged 6 months, were used to induce ventricular fibrillation using alternating current. After 8 minutes, the rats underwent 6-minute chest compression and mechanical ventilation, followed by electric defibrillation, to establish rat models of global brain ischemia due to cardiac arrest and resuscitation. A total of 24 successful models were randomly assigned to Feridex-labeled and non-labeled groups （n = 12 for each group）. At 2 hours after resuscitation, 5 ×10^8 Feridex-labeled BMSCs, with protamine sulfate as a carrier, and 5 ×10^6 non-labeled BMSCs were respectively transplanted into both groups of rats through the right carotid artery （cells were harvested in 1 mL phosphate buffered saline）. MAIN OUTCOME MEASURES： Feridex-labeled BMSCs were observed by Prussian blue staining and electron microscopy. Signal intensity, celluar viability, and proliferative capacity of BMSCs were measured using MRI, Trypan blue test, and M-IT assay, respectively. Distribution of transplanted cells was observed in rats utilizing MRI and Prussian blue staining prior to and 1, 3, 7, and 14 days after transplantation. RESULTS： Prussian blue staining displayed many blue granules in the Feridex-labeled BMSCs. High density of iron granules was observed in the cytoplasm under electron microscopy. According to MRI results, and compared with the non-labeled group, the signal intensity was decreased in the Feridex-labeled group （P 〈 0.05）. The decrease was most significant in the 50 pg/mL Feridex-labeled group （P 〈 0.01）. There were no significant differences in celluar viability and proliferation of BMSCs between the Feridex-labeled and non-labeled groups after 1 week （P 〉 0.05）. Low-signal lesions were detected in the rat hippocampus and temporal cortex at 3 days after transplantation. The low-signal lesions were still detectable at 14 days, and positively stained cells were observed in the hippocampus and temporal cortex using Prussian blue staining. There were no significant differences in signal intensity in the non-labeled group. CONCLUSION： BMSC transplantation traversed the blood-brain barrier and distributed into vulnerable zones in a rat model of cardiac arrest-induced global brain ischemia. MRI provided a non-invasive method to in vivo dynamically and spatially trace Feridex-labeled BMSCs after transplantation.展开更多
Aim: To observe the effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) induced changes of cardiac sympathetic discharges and the effects of some related receptors in the spinal cord. Methods: A total...Aim: To observe the effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) induced changes of cardiac sympathetic discharges and the effects of some related receptors in the spinal cord. Methods: A total of 53 rabbits anesthetized with mixture solution of 25% urethane (420 mg/kg) and 1.5% chloralose (50 mg/kg) were used in this study. AMI was induced by occlusion of the ventricular branch of the left coronary artery. Discharges of the left cardiac sympathetic nerve were recorded by using a bipolar platinum electrode. Bilateral "Ximen"(PC 40) and "Kongzhui"(LU 6) were stimulated electrically by using an EA therapeutic apparatus or an electrical stimulator. DPDPE δ opiate receptor agonist, 20 nmol, 10 μL, n=8), Naltrindole Hydrochloride (δ opiate receptor antagonist, 20 nmol, 10 μL, n=8), DAP5 (NMDA receptor antagonist, 5 nmol, 10 μL, n=9) and CNQX (non NMDA receptor antagonist, 5 nmol, 10 μL, n=8) were respectively injected into the thoracic subarachnoid space of the spinal cord in different groups, followed by observing their effects on changes of sympathetic activity evoked by EA of the abovementioned acupoints. Results: ① After AMI, sympathetic discharges increased (200.56±79.89%) in 10 cases and decreased (-59.34 ±7.06%) in other 9 cases in comparison with their individual basal values. After EA of "Ximen" (PC 4) and "Kongzhui"(LU 6), AMI induced increase and decrease changes of the sympathetic activity were suppressed significantly, but the effect of EA of LU 6 was weaker than that of EA of PC 4. ② Following EA of PC 4 and LU 6, sympathetic discharges increased significantly in 2 and 4 cases, decreased apparently in 7 and 3 cases, and had no striking changes in 1 and 3 cases respectively. The mean reaction threshold of sympathetic activity after EA of PC 4 and LU 6 were 2.1±0.65 mA and 3.28±1.13 mA separately. ③ After pre treatment with DPDPE, the reaction threshold of the cardiac sympathetic activity to EA of PC 4 elevated significantly (35.89±6.12%); while after pre treatment with Naltrindole, this reaction threshold decreased considerably (84.88±26.58%). Following intrathecal injection of DAP5 (n=9) and CNQX (n=9) , the reaction thresholds of the cardiac sympathetic activity to EA of PC 4 increased obviously (142.06±60.27% and 112.54±28.58% separately). It suggests that spinal δ opioid receptor, NMDA and non NMDA receptors are involved in EA induced changes of sympathetic activity. Conclusion: ① EA could regulate AMI induced changes of cardiac sympathetic activity; and ② spinal δ opioid receptors, NMDA and non NMDA receptors participate in the effect of EA on the cardiac sympathetic activity.展开更多
The effect of ischemia like solution and high concentration of isoprenaline and Phenylephrine in that solution on normal pacemaker current If of sheep cardiac Puekinje fibres were observed After perfusing the preparat...The effect of ischemia like solution and high concentration of isoprenaline and Phenylephrine in that solution on normal pacemaker current If of sheep cardiac Puekinje fibres were observed After perfusing the preparations with “ischemia” solution 15, 30, and 60 min, the amplitude of If current at all measured membrane potentials (from -60 to -120 mV) decreased (n=7,p<0.05)and the activation curve of If current shiftea to left side,E0.5 changed from control value -85.0±3.7 mV to -91.7±4.1 mV at 30 min. Isoprenaline 1×10-6mol/L could increase the amplitude of If current in “ischemia” solution (n= 10, P<0.05) and shift the activation curve of If current back to right side, but it could not completely reverse the inhibitory effect of“ ischemia“. In the presence of propranolol 5 ×10-7 mol/L, 5×10-5 mol/L phenylephrine decreased the amplitude of If current further in “ischemia” solution (n= 7, P<0.05-0.01), the activatior curve of If current shifted to left side further. The above results indicate that the normal pacemaker current was inhibited in “ischemia” condition even in the presence of high concentration of beta and alpha adrenoceptor agonists so the genesis of ischemic ventricular arrhythmia is hardly due to the abnormal enhancement of normal ventricular pacemaker activity.展开更多
Our previous studies demonstrated that CD151 gene promoted neovascularization in ischemic heart model.To improve the delivery efficacy and target specificity of CD151 gene to ischemic heart,we generated an adeno-assoc...Our previous studies demonstrated that CD151 gene promoted neovascularization in ischemic heart model.To improve the delivery efficacy and target specificity of CD151 gene to ischemic heart,we generated an adeno-associated virus（AAV） vector in which CD151 expression was controlled by the myosin light chain（MLC-2v） promoter to achieve the cardiac-specific expression of CD151 gene in ischemic myocardium and to limit unwanted CD151 expression in extracardiac organs.The function of this vector was examined in rat ischemic myocardium model.The protein expression of CD151 in the ischemic myocardium areas,liver and kidney was confirmed by using Western blot,while the microvessels within ischemic myocardium areas were detected by using immunohistochemistry.The results showed that MLC-2v significantly enhanced the expression of CD151 in ischemic myocardium,but attenuated its expression in other organs.The forced CD151 expression could increase the number of microvessels in the ischemic myocardium.This study demonstrates the AAV-mediated and MLC-2v regulated CD151 gene is highly expressed in the ischemic myocardium and cardiac-specific delivery that is more efficiently targets CD151 to the ischemia myocardium after myocardial infarction.展开更多
文摘Despite advances in intelligent medical care,difficulties remain.Due to its complicated governance,designing,planning,improving,and managing the cardiac system remains difficult.Oversight,including intelligent monitoring,feedback systems,and management practises,is unsuccessful.Current platforms cannot deliver lifelong personal health management services.Insufficient accuracy in patient crisis warning programmes.No frequent,direct interaction between healthcare workers and patients is visible.Physical medical systems and intelligent information systems are not integrated.This study introduces the Advanced Cardiac Twin(ACT)model integrated with Artificial Neural Network(ANN)to handle real-time monitoring,decision-making,and crisis prediction.THINGSPEAK is used to create an IoT platform that accepts patient sensor data.Importing these data sets into MATLAB allows display and analysis.A myocardial ischemia research examined Health Condition Tracking’s(HCT’s)potential.In the case study,75%of the training sets(Xt),15%of the verified data,and 10%of the test data were used.Training set feature values(Xt)were given with the data.Training,Validation,and Testing accuracy rates were 99.9%,99.9%,and 99.9%,respectively.General research accuracy was 99.9%.The proposed HCT system and Artificial Neural Network(ANN)model gather historical and real-time data to manage and anticipate cardiac issues.
文摘Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associated with organ rejection. We hypothesized that it is either passively released from injured tissues during organ procurement, or actively secreted by allograft infiltrating cells contributing to allograft dysfunction. We investigated the impact of IRI in an in vitro study of human heart tissue during the process of transplantation. The mRNA expression levels for both isoforms of the AIF-1, I2 and I3 were significantly increased after 30 minutes reperfusion (AIF-1 I2: p 0.01 vs. AIF-1 I3: p 0.005). Expression levels for IL-18 and the TLRs were increased after 30 minutes of reperfusion. Only IL-18 and TLR-2 were statistically significant (IL-18: p 0.0001 vs. TLR-2: p 0.01). The mRNA expression levels for AIF-1 I2 and IL-18 were decreased from the original levels of ischemia after 60 and 90 minutes reperfusion. The TLR-2 and -4 were presented with minimal levels of reduction after 60 minutes. However, mRNA expression levels for all were decreased to the original levels of ischemia after 90 minutes, except for AIF-1 I3, but the difference was not statistically significant. AIF-1 and IL-18 were specifically detected in myocytes and interstitial tissues by immunohistochemistry (IHC) stain after IRI. TLR-4 was non-specific, and TLR2 was minimally expressed. The study discusses the evidence supporting that the AIF-1 may have therapeutic potential for strategies in the control of innate immune responses early on, after transplantation.
基金This study was part of a dissertation titled^Investigation of postmortem UTR and endothelin 1 levels in brain and kidney tissues in rats that died of ISO toxicity,"which was supported by the Ataturk University Scientific Research Project(BAP 2014/036).
文摘This study aimed to investigate changes in postmortem urotensin Ⅱ receptor(UTR)levels in brain and kidney tissues in a rat model of cardiac ischemia.The rats were divided into two groups:a control group and a cardiac ischemia-induced group.Cardiac ischemia was created by an intraperitoneal injection of a single lethal dose of isoproterenol(ISO;850 mg/kg).Plasma UT,blood urea nitrogen,and creatinine levels were determined 0 h postmortem.Brain and kidney UTR mRNA expression levels were determined 0,1,3,6,12,24,4&and 72 h postmortem.The histopathological appearance of brain and kidney tissues was also evaluated.Plasma UT and plasma creatinine levels were increased in the cardiac ischemia-induced group as compared with those in the control group(P<0.001).Ischemia resulted in histopathological changes in brain and cerebellum tissue.The morphological evaluation revealed Purkinje cell degeneration(P=0.037)and dark neurons(P=0.004).The UTR expression level decreased after 1 h postmortem in the brain and after 3 h postmortem in the kidneys in the cardiac ischemia-induced group as compared with that in the control group(P<0.001).The observed changes in UTR expression levels may be valuable in clinical practice in the field of forensic medicine.These changes may be used as a marker in postmortem evaluations of sudden death caused by ischemia-induced cardiac shock.
基金supported by a grant from the Health Department Foundation of Zhejiang Province(2010KYA102)
文摘Objective:To investigate the protective function of tocilizumab in human cardiac myocytes ischemia-reperfusion injury.Methods:The human cardiac myocytes were treated by tocilizumab with different concentrations(1.0 mg/mL,3.0 mg/mL,5.0 mg/mL) for 24 h.then cells were cultured in ischemia environment for 24 h and reperfusion environment for 1 h.The MTT and flow cytometry were used to detect the proliferation and apoptosis of human cardiac myocytes,respectively.The mRNA and protein expressions of Bcl-2 and Bax were measured by qRT-PCR and western blot,respectively.Results:Compared to the negative group,pretreated by tocilizumab could significantly enhance the proliferation viability and suppress apoptosis of human cardiac myocytes after suffering ischemia reperfusion injury(P<0.05).The expression of Bcl-2 in tocilizumab treated group were higher than NC group(P<0.05).while the Bax expression were lower(P<0.05).Conclusions:Tocilizumab could significantly inhibit apoptosis and keep the proliferation viability of human cardiac myocytes after suffering ischemia reperfusion injury.Tocilizumab may obtain a widely application in the protection of ischemia reperfusion injury.
基金supported by the Natural Science Foundation of Hubei Province of China,No.2010CDB09101
文摘Cerebral ischemia/reperfusion injury is partially mediated by thrombin, which causes brain damage through protease-activated receptor 1（PAR1）. However, the role and mechanisms underlying the effects of PAR1 activation require further elucidation. Therefore, the present study investigated the effects of the PAR1 antagonist SCH79797 in a rabbit model of global cerebral ischemia induced by cardiac arrest. SCH79797 was intravenously administered 10 minutes after the model was established. Forty-eight hours later, compared with those administered saline, rabbits receiving SCH79797 showed markedly decreased neuronal damage as assessed by serum neuron specific enolase levels and less neurological dysfunction as determined using cerebral performance category scores. Additionally, in the hippocampus, cell apoptosis, polymorphonuclear cell infiltration, and c-Jun levels were decreased, whereas extracellular signal-regulated kinase phosphorylation levels were increased. All of these changes were inhibited by the intravenous administration of the phosphoinositide 3-kinase/Akt pathway inhibitor LY29004（3 mg/kg） 10 minutes before the SCH79797 intervention. These findings suggest that SCH79797 mitigates brain injury via anti-inflammatory and anti-apoptotic effects, possibly by modulating the extracellular signal-regulated kinase, c-Jun N-terminal kinase/c-Jun and phosphoinositide 3-kinase/Akt pathways.
基金the National Natural Science Foundation of China,No.30801081, 30870691,30700303the New Teacher Foundation of Doctor Center of Ministry of Education of China,No. 200805581179
文摘BACKGROUND： Numerous studies have shown that magnetic resonance imaging （MRI） can detect survival and migration of super paramagnetic iron oxide-labeled stem cells in models of focal cerebral infarction. OBJECTIVE： To observe distribution of bone marrow mesenchymal stem cells （BMSCs） in a rat model of global brain ischemia following cardiac arrest and resuscitation, and to investigate the feasibility of tracing iron oxide-labeled BMSCs using non-invasive MRI. DESIGN, TIME AND SETTING： The randomized, controlled, molecular imaging study was performed at the Linbaixin Medical Research Center, Second Affiliated Hospital, Sun Yat-sen University, and the Institute of Cardiopulmonary Cerebral Resuscitation, Sun Yat-sen University, China from October 2006 to February 2009. MATERIALS： A total of 40 clean, Sprague Dawley rats, aged 6 weeks and of either gender, were supplied by the Experimental Animal Center, Sun Yat-sen University, China, for isolation of BMSCs. Feridex （iron oxide）, Gyroscan Inetra 1.5T MRI system, and cardiopulmonary resuscitation device were used in this study. METHODS： A total of 30 healthy, male Sprague Dawiey rats, aged 6 months, were used to induce ventricular fibrillation using alternating current. After 8 minutes, the rats underwent 6-minute chest compression and mechanical ventilation, followed by electric defibrillation, to establish rat models of global brain ischemia due to cardiac arrest and resuscitation. A total of 24 successful models were randomly assigned to Feridex-labeled and non-labeled groups （n = 12 for each group）. At 2 hours after resuscitation, 5 ×10^8 Feridex-labeled BMSCs, with protamine sulfate as a carrier, and 5 ×10^6 non-labeled BMSCs were respectively transplanted into both groups of rats through the right carotid artery （cells were harvested in 1 mL phosphate buffered saline）. MAIN OUTCOME MEASURES： Feridex-labeled BMSCs were observed by Prussian blue staining and electron microscopy. Signal intensity, celluar viability, and proliferative capacity of BMSCs were measured using MRI, Trypan blue test, and M-IT assay, respectively. Distribution of transplanted cells was observed in rats utilizing MRI and Prussian blue staining prior to and 1, 3, 7, and 14 days after transplantation. RESULTS： Prussian blue staining displayed many blue granules in the Feridex-labeled BMSCs. High density of iron granules was observed in the cytoplasm under electron microscopy. According to MRI results, and compared with the non-labeled group, the signal intensity was decreased in the Feridex-labeled group （P 〈 0.05）. The decrease was most significant in the 50 pg/mL Feridex-labeled group （P 〈 0.01）. There were no significant differences in celluar viability and proliferation of BMSCs between the Feridex-labeled and non-labeled groups after 1 week （P 〉 0.05）. Low-signal lesions were detected in the rat hippocampus and temporal cortex at 3 days after transplantation. The low-signal lesions were still detectable at 14 days, and positively stained cells were observed in the hippocampus and temporal cortex using Prussian blue staining. There were no significant differences in signal intensity in the non-labeled group. CONCLUSION： BMSC transplantation traversed the blood-brain barrier and distributed into vulnerable zones in a rat model of cardiac arrest-induced global brain ischemia. MRI provided a non-invasive method to in vivo dynamically and spatially trace Feridex-labeled BMSCs after transplantation.
文摘Aim: To observe the effect of electroacupuncture (EA) on acute myocardial ischemia (AMI) induced changes of cardiac sympathetic discharges and the effects of some related receptors in the spinal cord. Methods: A total of 53 rabbits anesthetized with mixture solution of 25% urethane (420 mg/kg) and 1.5% chloralose (50 mg/kg) were used in this study. AMI was induced by occlusion of the ventricular branch of the left coronary artery. Discharges of the left cardiac sympathetic nerve were recorded by using a bipolar platinum electrode. Bilateral "Ximen"(PC 40) and "Kongzhui"(LU 6) were stimulated electrically by using an EA therapeutic apparatus or an electrical stimulator. DPDPE δ opiate receptor agonist, 20 nmol, 10 μL, n=8), Naltrindole Hydrochloride (δ opiate receptor antagonist, 20 nmol, 10 μL, n=8), DAP5 (NMDA receptor antagonist, 5 nmol, 10 μL, n=9) and CNQX (non NMDA receptor antagonist, 5 nmol, 10 μL, n=8) were respectively injected into the thoracic subarachnoid space of the spinal cord in different groups, followed by observing their effects on changes of sympathetic activity evoked by EA of the abovementioned acupoints. Results: ① After AMI, sympathetic discharges increased (200.56±79.89%) in 10 cases and decreased (-59.34 ±7.06%) in other 9 cases in comparison with their individual basal values. After EA of "Ximen" (PC 4) and "Kongzhui"(LU 6), AMI induced increase and decrease changes of the sympathetic activity were suppressed significantly, but the effect of EA of LU 6 was weaker than that of EA of PC 4. ② Following EA of PC 4 and LU 6, sympathetic discharges increased significantly in 2 and 4 cases, decreased apparently in 7 and 3 cases, and had no striking changes in 1 and 3 cases respectively. The mean reaction threshold of sympathetic activity after EA of PC 4 and LU 6 were 2.1±0.65 mA and 3.28±1.13 mA separately. ③ After pre treatment with DPDPE, the reaction threshold of the cardiac sympathetic activity to EA of PC 4 elevated significantly (35.89±6.12%); while after pre treatment with Naltrindole, this reaction threshold decreased considerably (84.88±26.58%). Following intrathecal injection of DAP5 (n=9) and CNQX (n=9) , the reaction thresholds of the cardiac sympathetic activity to EA of PC 4 increased obviously (142.06±60.27% and 112.54±28.58% separately). It suggests that spinal δ opioid receptor, NMDA and non NMDA receptors are involved in EA induced changes of sympathetic activity. Conclusion: ① EA could regulate AMI induced changes of cardiac sympathetic activity; and ② spinal δ opioid receptors, NMDA and non NMDA receptors participate in the effect of EA on the cardiac sympathetic activity.
文摘The effect of ischemia like solution and high concentration of isoprenaline and Phenylephrine in that solution on normal pacemaker current If of sheep cardiac Puekinje fibres were observed After perfusing the preparations with “ischemia” solution 15, 30, and 60 min, the amplitude of If current at all measured membrane potentials (from -60 to -120 mV) decreased (n=7,p<0.05)and the activation curve of If current shiftea to left side,E0.5 changed from control value -85.0±3.7 mV to -91.7±4.1 mV at 30 min. Isoprenaline 1×10-6mol/L could increase the amplitude of If current in “ischemia” solution (n= 10, P<0.05) and shift the activation curve of If current back to right side, but it could not completely reverse the inhibitory effect of“ ischemia“. In the presence of propranolol 5 ×10-7 mol/L, 5×10-5 mol/L phenylephrine decreased the amplitude of If current further in “ischemia” solution (n= 7, P<0.05-0.01), the activatior curve of If current shifted to left side further. The above results indicate that the normal pacemaker current was inhibited in “ischemia” condition even in the presence of high concentration of beta and alpha adrenoceptor agonists so the genesis of ischemic ventricular arrhythmia is hardly due to the abnormal enhancement of normal ventricular pacemaker activity.
基金supported by a grant from the National Natural Sciences Foundation of China (No. 30670856)
文摘Our previous studies demonstrated that CD151 gene promoted neovascularization in ischemic heart model.To improve the delivery efficacy and target specificity of CD151 gene to ischemic heart,we generated an adeno-associated virus（AAV） vector in which CD151 expression was controlled by the myosin light chain（MLC-2v） promoter to achieve the cardiac-specific expression of CD151 gene in ischemic myocardium and to limit unwanted CD151 expression in extracardiac organs.The function of this vector was examined in rat ischemic myocardium model.The protein expression of CD151 in the ischemic myocardium areas,liver and kidney was confirmed by using Western blot,while the microvessels within ischemic myocardium areas were detected by using immunohistochemistry.The results showed that MLC-2v significantly enhanced the expression of CD151 in ischemic myocardium,but attenuated its expression in other organs.The forced CD151 expression could increase the number of microvessels in the ischemic myocardium.This study demonstrates the AAV-mediated and MLC-2v regulated CD151 gene is highly expressed in the ischemic myocardium and cardiac-specific delivery that is more efficiently targets CD151 to the ischemia myocardium after myocardial infarction.
