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The impairment of cardiac function resulted from acute pulmonary embolization (PE) is very important to the determination of the patient s treatment and prognosis. But, the current state of knowledge of it s mechanism is obscure. The purpose of this study is to obtain the information on the mechanism of irreversible cardiac failure and the augmentation of coronary blood flow by acute PE. Changes of ventricular function of the both ventricles and left and right coronary blood flow were observed under right ventricular loading from the normal up to possible maximum strain. Materials and Methods Thirty-three anesthetized (pentobarbital soda 30 mg/kg) adult mongrel dogs, weighing 12 to 28 kirograms, were used. A bilateral thoractomy was performed in the fourth intercostal space under positive pressure air ventilation and the heart was suspended in a pericardial cradle. Aortic pressure (AoP) (via the right carotid artery), main pulmonary arterial pressure (PAP) (via the pulmonary arteria trunk), right ventricular pressure (RVP) (via the free wall) and left ventricular pressure (LVP) (via the apex) were measured through short polyethylene catheters connected directly to the pressure transducers (Nihon Kohden MPU 0.5). The zero level of the pressures were determined at the midpoint of the right auricle. The first derivatives of the ventricular pressures (dp/dt) were obtained by using matched RC differentiating circuits. Aortic blood flow (AF), left circumflex coronary blood flow (LCF) and right coronary blood flow (RCF) were measured with electromagnetic flowmeters (Nihon Kohden) placed around the vessles.
Kazuo Tomita (Wed,) studied this question.