Acute myocardial ischemia was induced by intravenous injection of pituitrin, and electroacupuncture (EA) was applied at the Heart and Lung Meridians (HM and LM), 3 points on each meridian. The changes in the left ... Acute myocardial ischemia was induced by intravenous injection of pituitrin, and electroacupuncture (EA) was applied at the Heart and Lung Meridians (HM and LM), 3 points on each meridian. The changes in the left intraventricular pressure (LVP), the maximum rise rate of intraventricular pressure (LVP dp/dtmax), the area of cardiac force loop (ACFL), and the maximum shortening velocity of myocardial contractile element (Vmax) were observed. As a result, there were significant differences in the improvement of LVP, LVP dp/dtmax, ACFL and Vmax between EA at HM and LM. The regulatory action of EA at HM on the myocardial contractile function was significantly better than that of EA at LM, indicating that HM has a close relationship with the myocardial contractile function.……展开更多
Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused b...Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases （MAPK） in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown. Methods Sprague-Dawley rats were randomly divided into three groups： Sham group, coronary microembolization （CME） group and SB203580 group （n=-10 per group）. CME rats were produced by injection of 42 pm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction （LVEF） was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor （TNF）-a was assessed by the technique of semi-quantitative polymerase chain reaction amplification. Results LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-a mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function. Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-a expression and preserve cardiac contractile function.展开更多
The left ventricular apical systolic dysfunction syndrome was a rare acute cardiac syndrome.Its clinical presentation and electrocardiography were similar to acute myocardial infarction.The syndrome was characterized ...The left ventricular apical systolic dysfunction syndrome was a rare acute cardiac syndrome.Its clinical presentation and electrocardiography were similar to acute myocardial infarction.The syndrome was characterized by transient ventricular wall-motion abnormalities involving the left ventricular apex and mid-ventricle in the absence of obstructive epicardial coronary disease.Cardiac enzyme was normal or minor elevation.At present,the cause of the syndrome is unknown.In this paper,we describe a 56-year-old female patient.She was admitted in hospital for acute appendititis and the transient left ventricular apical ballooning syndrome.She developed acute heart failure and septic shock in the hospital.The drainage of the appendiceal abscess was done and the heart failure and septic shock recovered completely in a few days.展开更多
文摘 Acute myocardial ischemia was induced by intravenous injection of pituitrin, and electroacupuncture (EA) was applied at the Heart and Lung Meridians (HM and LM), 3 points on each meridian. The changes in the left intraventricular pressure (LVP), the maximum rise rate of intraventricular pressure (LVP dp/dtmax), the area of cardiac force loop (ACFL), and the maximum shortening velocity of myocardial contractile element (Vmax) were observed. As a result, there were significant differences in the improvement of LVP, LVP dp/dtmax, ACFL and Vmax between EA at HM and LM. The regulatory action of EA at HM on the myocardial contractile function was significantly better than that of EA at LM, indicating that HM has a close relationship with the myocardial contractile function.……
文摘Background The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases （MAPK） in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown. Methods Sprague-Dawley rats were randomly divided into three groups： Sham group, coronary microembolization （CME） group and SB203580 group （n=-10 per group）. CME rats were produced by injection of 42 pm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction （LVEF） was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor （TNF）-a was assessed by the technique of semi-quantitative polymerase chain reaction amplification. Results LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-a mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function. Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-a expression and preserve cardiac contractile function.
文摘The left ventricular apical systolic dysfunction syndrome was a rare acute cardiac syndrome.Its clinical presentation and electrocardiography were similar to acute myocardial infarction.The syndrome was characterized by transient ventricular wall-motion abnormalities involving the left ventricular apex and mid-ventricle in the absence of obstructive epicardial coronary disease.Cardiac enzyme was normal or minor elevation.At present,the cause of the syndrome is unknown.In this paper,we describe a 56-year-old female patient.She was admitted in hospital for acute appendititis and the transient left ventricular apical ballooning syndrome.She developed acute heart failure and septic shock in the hospital.The drainage of the appendiceal abscess was done and the heart failure and septic shock recovered completely in a few days.
