The Protective Effect Of PQDS On Ventricular Remodeling Rats

With the increasing of People's living standard and the average time of lifebecomes longer than before, the incidence, mutilation rate and fatality rate ofcardiovascular disease have been increasing all over the world year by year. Thereare many cardiovascular diseases progress into heart failure in clinic in the end.Cardiac ventricular remodeling is the most important risk factor to heart failure.Cardiac ventricular remodeling is a complex course. It makes the myocardialfunction, constitution and phenotype change through molecular and cellularmechanism. The hypertrophy and apoptosis of cardiac muscle cell, the re-expressof embryonic genes and its protein, and the hyperplasia of collagenoblast in thebase lead to that the ventricular wall becomes thick, the end-systolic volumeincreases, the ventricular chamber expands and even becomes spherical and theLVEF decreases. The heart failure occurs at last. The degree of cardiac ventricularremodeling has a great influence on the late prognosis of the congestive heartfailure patients. It is an independent risk factor of high disease incidence and highmortality of cardiovascular diseases. So exploiting a new, safe and effectiveanti-ventricular remodeling drug becomes an important topic of present medicalinvestigation. PQDS is 20s-diol saponin separated and purificated from panaxquinquefolium Linn. The chemical composition analysis indicates that the contentof PQDS in the leaf (9.05-10.45%) is apparently more than that in the root(3.89-6.49%). Therefore developing and exploiting PQDS is practically important.At present the exterior and interior scientists make many researches on thepharmacological activity of PQDS in many aspects. They find that PQDS has theeffect not only in anti-neoplasm, but also in anti-MI, even can decrease the MISobviously. PQDS may also reduce the number of cardiac cell apoptosis which isinducted by reperfusion injury. But now no literature reported that PQDS hadprotective effect to cardiac ventricular remodeling yet. So my research is toobserve how PQDS prevents the experimental rats from cardiac ventricularremodeling and its mechanism at the base of the cardiac ventricular remodelingresulted from over pressure load. The purpose is to research whether PQDS canreserve cardiac ventricular remodeling or protect the cardiac cell, and to find theway of protecting the IDEM and preventing and curing the cardiovascularremodeling, especially to research the effective component in potency and itsmechanism. This research has important significance in developing panax andpromoting Chinese crude drug modernization.Experimental procedure: Anesthetize the rats with pentobarbital sodium(30mg/kg) by intraperitoneal injection. Fix the rats on the operation tables insupine position. Open the abdominal cavity through the median incision of theepigastrium. Saperate the abdominal aorta which is over the left renal artery about1.0cm, and put a 0.63mm diameter smooth pinhead on the abdominal aorta, andligate the abdominal aorta and the pinhead with the thread. Then draw the pinheadout quickly. It leads to the abdominal arteriostenosis (65±7%). Inject PC into theabdominal cavity and close the abdominal cavity. Divide 60 Wistar rats into 5groups at random. 12 rats are in each one. The groups are respectively named withmodal group, positive control group (benazepril 10mg/kg/d), high dosage PQDSgroup (100mg/kg/d), low dosage PQDS group (50mg/kg/d) and pseudo operationgroup. All kinds of drugs we use are all dissolved in the distilled water for lavageto rats till 6 weeks after.After weigh the rats, anesthetize them with the 3% pentobarbital sodium(30mg/kg) by intraperitoneal injection, and then put the rats backs on theoperation tables, divide the right common carotid artery and put a 1mm diameterplastic tube in the left cardiac ventricle, and link the tube with the polygraph(RM-6000). After 20 minutes we measure the LVEDP, SBP and DBP to computethe MAP. The next we will get some blood from abdominal aorta and take a partof left ventricle into formaldehyde (12%). It will be a pathosample. Determine theMDA, SOD and NO according to the kit rule. Determine the AngⅡ, ET and thedensity of TXA2, PGI2 in the blood plasma. Determine the ET in the cardiacmuscle.Consequence:一. PQDS can inhibit cardiac muscle thicken, and improve the dropsy ofcardiac muscle. Furthermore it has the positive correlation with dosage.二. PQDS can obviate the cardiac ventricular remodeling to happen,it mayrealize through the mechanisms like these:1.PQDS can reduce the ET content of the blood plasma and cardiac muscleof the rat whose cardiac ventricle has remodeled, and can increase the BF ofcardiac muscle.2. High dose PQDS can reduce the MDA level in the cardiac ventricularremodeling rats blood serum. The activity of SOD obvious rising hints that PQDShas the effect on lipid peroxidation which is mediated by anti-free radical. PQDScan reinforce the anti-oxygen capability of experimental rats with cardiacventricular remodeling.3. PQDS can reduce the TXA2 level of cardiac ventricle, as well as canincrease the PGI2 level and the value of PGI2/TXA2. It hints that PQDS can holdthe balance of PGI2/TXA2 through increasing the level of PGI2.4. PQDS can both reduce the content of AngⅡ, and increase the content ofNO of the cardiac ventricle.Conclusion:PQDS have the reverse effect on cardiac ventricular remodeling obviously.The mechanism of PQDS is complement through increasing the haemodynamicsand improving myocardial metabolism and protecting cardio cell.But the precisemechanism of PQDS which protects cardiac ventricular remodeling and the reasonabledose to choose are waiting for advanced research.