| BackgroundPulmonary hypertension(PH) is the common pathology process of series of cardiopulmonary diseases, including congenital heart diseases, cardiomyopathy, other kinds of cardiovascular diseases and respiratory diseases. It is the pathophysiology basis of occurring, developing, and maintaining of cardiopulmonary diseases. More attention was usually put on mechanism cellular and molecular of congestive heart failure with diseases relating to left cardiac insufficiency, however, it was almost not recognized that the primary right ventricular functional abnormality may cause the secondary injury to the left cardiac function. Although it was proved recently by the clinical information and animal experiments that the abnormality of right ventricular function can also cause the changes of left ventricular function and morphology and finaly cause clinical abnormality of left ventricular functional abnormality the cellular and molecule mechanism is not as yet understood. Our teams investigated the application of the Doppler echocardiography on the clinical value on the left ventricular myocardial remodel and dysfunction in neonates with hypoxia-induced pulmonary hypertension, and observed the dynamics, structural and functional injury on left ventricular myocardium with pulmonary hypertension. The results demostrate that there were both the diameter of right ventricular increased and right ventricular myocardial remodel, and diastolic dysfunction of left ventricular decreased in PH. Objective:1. To prove the cytoskeleton protein abnormality mechanism of the intrinsic systolic and diastolic dysfunction with left ventricular function insufficiency by hypoxia-induced pulmonary hypertension.2.1n experiment on the relation among angotensin II in plasma and of myocardium, hemodynamics changes by hypoxia-induced pulmonary hypertension, mRNA of desmin and P-tubulin, and collagen volume fraction, the pathophysiologic mechanism of the secondary left ventricular function insufficiency caused by PH were clarified.Methods:1.The rabbit models of hypoxia pulmonary hypertension were made withventilutor.The myocardium were collected when the rabbits were killed afterthe hemodynamic parameters were tested.2.Six unexpected death neonates without cardiovascular diseases andrespiratory problems were studied as the control group, eight hypoxianeonates suffered from respiratory diseases without PH and fifteen hypoxianeonates suffered from respiratory diseases with PH were studied as theexperiment group.3.The Left ventricular myocardial pathologic alteration were observed byoptic microscope and electron microscope. The expression of protein andmRNA of Desmin and B-tubulin in left ventricular myocyte were detected byimmunohistochemistry and in situ hybridization respectively.4. The concentration of angotensin II in plasma and myocardium weredetected by radioimmunoassay.Results:1.The results of the rabbit models showed:(l)Compared with the control group, there was significantly increasedLVW/BW values, but no changes of LVSP MAP and +dp/dt max. there wassignificantly dcreased -dp/dtmax values, prolonged T values and elevatedLVEDP in the hypoxia rabbits group,(2)Severe lesions such as cloud swelling, hydropic degeneration, lyricnecrosis and interstitial edema were observed under optic microscopy. Thechondriosomes swelling, sarcoplas micreticula dilatation, myofibrillaesolution and edema of inside and outside of the celles, accumulation of Z-linematerial or hyperplasia of the mitochondria were shown under electronmicroscopy. These changes revealed that the cardie lesions of rabbits withhypoxia pulmonary hypertension were significant and severe.(3)Compared with the control group, the expression of desmin and P-tubulinand their mRNA in left ventricular myocardium with hypoxia-inducedpulmonary hyoertension were significantly up-regulated. In thehypoxia-induced PH rabbits left ventricular myocardium, there were both aloss of cross str...
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