Influence of Contractility on Myocardial Ultrasonic Integrated Backscatter and Cyclic Variation in Integrated Backscatter

To evaluate the effects of left ventricular contractility on the changes of aver age image intensity (AII) of the myocardial integrated backscatter (IB) and cyclic variation in IB (CVIB), 7 adult mongrel dogs were studied. The magnitude of AII and CVIB were measured from myocardial IB carves before and after dobuta mine or propranolol infusion. Dobutamine or propranolol did not affect the magnitude of AII (13.8±0.7 vs 14.7±0.5, P >0.05 or 14.3±0.5 vs 14.2±0.4, P >0.05). However, dobutamine produced a significant increase in the magnitude of CVIB (6.8±0.3 vs 9.5±0.6, P <0.001) and propranolol induced significant decrease in the magnitude of CVIB (7.1±0.2 vs 5.2±0.3, P <0.001). The changes of the magnitude of AII and CVIB in the myocardium have been demonstrated to reflect different myocardial physiological and pathological changes respectively. The alteration of contractility did not affect the magnitude of AII but induced significant change in CVIB. The increase of left ventricular contractility res ulted in a significant rise of the magnitude of CVIB and the decrease of left ventricular contractility resulted in a significant fall of the magnitude of CVIB.

Assessment of Contractility for Fontan Connections

This study is performed to investigate the effect of Fontan operations on cardiac contractility. Investigation of articles about the contractility in Fontan published in PubMed up to now revealed that the measurement of contractility values did not include the rudimentary ventricle. Connections between right atrium and right ventricle as well as right atrium and pulmonary artery were studied in the same group as well. In our opinion, for the single ventricular physiology, the RA-RV and RA-PA connected patients’ preload and afterload values cannot be calculated in the same group since volume of rudimentary ventricles must be considered from this point of view as well.

Coronary microembolization induced myocardial contractile dysfunction through a p38 mapk pathway

Background Cathepsin S and its endogenous inhibitor cystatin C are implicated in the pathogenesis of atherosclerosis,especially in the plaque destabilization and rupture leading to acute coronary syndrome.However, whether circulating cathepsin S and cystatin C also change in association with coronary plaque morphology is unknown yet. Methods Sprague-Dawley rats were randomly divided into three groups;Sham group,CME group and SB203580 group (n=10 per group).CME rats were produced by injection of 42μm microspheres into the left ventricle with occlusion of the ascending aorta.SB203580,a p38 MAPK inhibitor,was injected into femoral vein after finishing the injection of microspheres in SB203580 group.Left ventricular Ejection Fraction was determined by echocardiography.The level of phosphorylated and total P38 MAPK in myocardium was assessed by Western Blot.Results Left ventricular(LV) Ejection Fraction was depressed at 3 hours and until up to 12 hours in CME group.The increased p38 MAPK activation was observed in CME group.The administration of SB203580 partly inhibited the p38 MAPK activity and preserved cardiac contractile function.Conclusions p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly preserve cardiac contractile function.