Effects Of KNHX-Ⅱ On MMPS And CGRP After AMI In The Rats

In order to study the mechanism and curative effectiveness of the KangNingHuXin(KNHX-II) on the AMI.we established on rats the acute myocardial infarction models to study the change of the activity of MMP9 in the necrosis zone and the levels of CGRP in the plasma of AMI rats . adult wistar rats were ligated the left descinding coronary artery, then being devided randomly into six groups: sham-operation; saline; aspirin-Kaptopril; low-dosage, normal-dosage,high-dosage group.The quantity of each group is ten. After the operation was finished,Two hours later, taking the blood in the artery to measure the CGRP. The contents of CGRP in the plasma of rats (50 AMI and 10 sham-operaton rats )were masured by the methods of radioimmunoassay. Parts of the necrosis zone in rats heart were selected for HE and immunohistochemical staining .Some of the specimens in necrosis zone of AMI rats were stained with HE to identify the ischemic or necrosis degree. Immunohistochemical method was used to measure the secretion of MMP9.we learned the results by measuring the contents of CGRP and MMP9.The results demonstrated that normal-dosage of KNHX-II,high-dosage of KNHX-II can increase the contents of CGRPand decrease the concentration of MMP9,singnificantly,the effects were enhanced with the increasing of the drugs' concentration.The favourable regulation of plasma CGRP and MMP9 in necrosis zone is possibly one of mechanisms for KNHX-II preventing and treating AMI. As is well known to all .the ability of the heart to continue functioning as a pump relates directly tothe extent of myocardial damage. AMI is usually accompanied with coronary spasm .The mechanism of therapeutic actions of KNHX-II may be explained by its ability to increase the contents of CGRP .CGRP can relax vascular smooth muscle and cause coronary arterial dilatation, consequently ,reduce cardial preload and afterload ,reduce the work of the heart.The activity of MMP9 in the necrosis zone showed an obvious increase . The latent MMP9 were activated after infarction ,which resulted in the damage of the fibrillar network and dalitation of the left ventricle and ventricle remodeling . KNHX-II not only attenuates the activity of MMP9 but also prevents collagen synthesis, decreases the total collagon in the necrosis zone at the stage after infarction .Thus regressing the progress dysfunction of the infarction heart and protecting the ischemic myocardium.Conclusions : the KNHX-II can alleviate coronaryspasm and prevent ventricle remodeling and avoid the occurance of re-infarction after AMI. .