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Animal model of cor pulmonare: With special reference to monocrotaline injection method
J Mol
S-3-6
Cell
Cardiol
22 (Supplement
II)
(1990)
ANIMAL MODEL OF COR PULNONARE: WITH SPECIAL REFERWCE TO MONOCROTALINE INJECTION METHOD. H. Rajihera. Organizing Office for College of Medical Technology, Hiroshima University, Hiroshima, Japan There are a few animal models of car pulmonare. For example, rigation of pulmonary artery, A-V fistula formation and monocrotaline injection. However, experimental procedure of the first two is not so simple and the body of the experimental animals is severely injured. Moreover, pulmonary arterial pressure Is suddenly elevated in these animals. The sudden increase of pulmonary arterial pressure is etiologically very rare in the case of human car pulmonere. On the other hand, the method of monocrotaline injection is very simple and sure method for induction of car pulmonare. Pulmonary hypertension of these animals is caused by pulmonary vasculitis which is finally followed by diffuse interstitial fibrosis. Therefore, hemodynamic changes of these animals are quite similar to those of human car pulmonare, for example, Hmman-Rich syndrome, chronic pulmonary infection and diffuse emphysema. Nonocrotaline was first extracted in 1935 from seeds of "crotalaria spectabilis" by Neal and his co-workers and known as an alkaloid which induces pulmonary fibrosis. The lung of monocrotaline injected rats first shows perivascular and alveolar edema with slight inflammatory infiltration, and later interstitial fibrosis. Systolic pressure of the right ventricle is progressively elevated with development of pulmonary inflammation and can usually become up to 100 mmHg (normal; 50 mmHg). A right to left ventricular weight ratio (RV/LV ratio) is gradually increased and reaches up to 1.2 (normal; 0.35). In light microscopy, hypertrophy of the right ventricular myocardial cells becomes distinct at 18 to 20 days after monocrotaline injection. In electron microscopy, synthesis of myofilamants is already recognized after 8 to 9 days. All experimental animals show signs of congestive heart failure at the terminal stage of the experiment and the right ventricular hypertrophied myocardial cells undergo degeneration. These animals finally die of cardiac failure. As a result of these findings, car pulmonsre induced by injection of monocrotaline is available for investigation of human car pulmonare and of myocardial cell hypertrophy.
S.27
S-3-6
Cell
Cardiol
22 (Supplement
II)
(1990)
ANIMAL MODEL OF COR PULNONARE: WITH SPECIAL REFERWCE TO MONOCROTALINE INJECTION METHOD. H. Rajihera. Organizing Office for College of Medical Technology, Hiroshima University, Hiroshima, Japan There are a few animal models of car pulmonare. For example, rigation of pulmonary artery, A-V fistula formation and monocrotaline injection. However, experimental procedure of the first two is not so simple and the body of the experimental animals is severely injured. Moreover, pulmonary arterial pressure Is suddenly elevated in these animals. The sudden increase of pulmonary arterial pressure is etiologically very rare in the case of human car pulmonere. On the other hand, the method of monocrotaline injection is very simple and sure method for induction of car pulmonare. Pulmonary hypertension of these animals is caused by pulmonary vasculitis which is finally followed by diffuse interstitial fibrosis. Therefore, hemodynamic changes of these animals are quite similar to those of human car pulmonare, for example, Hmman-Rich syndrome, chronic pulmonary infection and diffuse emphysema. Nonocrotaline was first extracted in 1935 from seeds of "crotalaria spectabilis" by Neal and his co-workers and known as an alkaloid which induces pulmonary fibrosis. The lung of monocrotaline injected rats first shows perivascular and alveolar edema with slight inflammatory infiltration, and later interstitial fibrosis. Systolic pressure of the right ventricle is progressively elevated with development of pulmonary inflammation and can usually become up to 100 mmHg (normal; 50 mmHg). A right to left ventricular weight ratio (RV/LV ratio) is gradually increased and reaches up to 1.2 (normal; 0.35). In light microscopy, hypertrophy of the right ventricular myocardial cells becomes distinct at 18 to 20 days after monocrotaline injection. In electron microscopy, synthesis of myofilamants is already recognized after 8 to 9 days. All experimental animals show signs of congestive heart failure at the terminal stage of the experiment and the right ventricular hypertrophied myocardial cells undergo degeneration. These animals finally die of cardiac failure. As a result of these findings, car pulmonsre induced by injection of monocrotaline is available for investigation of human car pulmonare and of myocardial cell hypertrophy.
S.27