Cardiovascular Function in Experimental Chronic Mitral Insufficiency in Dogs

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  • PRASAD Kailash
    Department of Physiology, College of Medicine, University of Saskatchewan Cardiovascular Surgery, College of Medicine, University of Saskatchewan
  • KHATTER Jagdish C.
    Department of Physiology, College of Medicine, University of Saskatchewan Cardiovascular Surgery, College of Medicine, University of Saskatchewan
  • BHARADWAJ Baikunth
    Department of Physiology, College of Medicine, University of Saskatchewan Cardiovascular Surgery, College of Medicine, University of Saskatchewan

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  • Cardiovascular Function in Experimental

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Various cardiovascular parameters (blood pressure, pressures in the 4 chambers of the heart, cardiac output, cardiac index, dp/dt and (dp/dt)/IIP of left and right ventricular pressures, heart rate, total peripheral resistance, left ventricular work index, roentgenogram, electrocardiogram) were assessed before and after various intervals of mitral insufficiency in 45 dogs produced by detaching 2 or 3 chordae tendineae from one papillary muscle through left atrial route to raise the left atrial pressure up to 2.5 to 3 times the normal. Fourteen of 45 dogs that died within 2 weeks had left atrial pressure more than 60mmHg. The present method of production of mitral insufficiency was compatible with prolonged survival (11 months). Systolic thrills, cine-angiocardiography, and left atrial expansion during systole prior to sacrifice documented the presence of mitral insufficiency. Roentgenograms, hemodynamic measurements and necropsy data documented the presence of left ventricular hypertrophy and failure. Hemodynamic measurements performed just prior to sacrifice showed that there was an increase in the left ventricular function during the early stage of ventricular adjustments to a chronically increased volume overload. Later on as hypertrophy progressed, cardiac function became depressed and left ventricular failure subsequently developed. The hemodynamic and autopsy data indicated that the right ventricle and right atrium were not affected initially. Later on because of the back pressure, the right side of the heart also began to show the effect of back pressure. There was an increase in the blood pressure and total peripheral resistance. The present results provide an experimental model of chronic cardiac hypertrophy and failure to study the pathophysiology of heart failure due to mitral insufficiency.

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