The organic diseases of the heart and great vessels, e.g. valvular regurgitation and/or stenosis, anomalous shunt between right and left side of the heart and so on, may produce disorder of blood stream and result in turbulance or impact of accerelated blood flow, which cause "organic heart murmur". The murmur is important for diagnosis of these cardiac abnormalities. "Functional cardiac murmur" is defined as a bruit which is produced only by functional exaggeration of blood flow velocity, and never based on any structural cardiovascular anomalies. The differentiation between these two different type of murmur, therefore, is very important and not always easy to achieve. There have been several reports concerning to the differentiation between two types of murmur, some of these include murmur caused by secondary hypertrophy of crardiac chamber in the category of "functional murmur" and some are inclined to exclude these type of murmur. So far the pathogenesis of functional murmur is persumed to be based on increased blood flow velocity. It is described that functional murmur is usually ejection type systolic murmur arising in the outflow tract of the right ventricle or across pulmonic valve. MACHII has presumed the mechanisrn as eddy current effects right behind the "trigonoidation" of pulmomic valves. The data obtained by intracardiac phonocardiography and direct surface phonocardiography, which indicate that main pulmonary artery is the point of maximal intensity in all of the cases, strongly suports the above conclusion. GROOM has demonstrated consistent occurrence of ejection type systolic murmur in all of the healthy materials regard-less sex or age using high gain high frequency phonocardiography in "sound proof room". So-called "functional murmur" s, i therefore, thought to be exaggeration of above mentioned bruit. Hyperthyroidism and anemia have been named as most typical exaggeration. Disappearance or diminution of functional murmur in these diseases after improvement of the conditions have been reported. The author has experimentally induced anemia in dogs by exchanging blood with Moriamin-P at a dosis of 20 cc per Kilogram bodyweight within 10 minutes. This procedure was repeated 4 times in succession. All of the animals have presented systolic murmur at the end of the experiment. Moramin-P has lower viscosity than that of blood. The same experiment using 2.5% gelatin solution, which has same viscosity as blood, instead of Moriamin-P has resulted systolic murmur in none of the animals. Another attempt to induce experimental hemolytic anemia was made by subcutaneous injection of phenylhydrazin in dosis of 10 mg pro die. 15 days after the first injection, hematocrit level has declined down to 15% and all of the animals have presented systolic anemic murmur. Hematocrit level reached down to its lowest level around 10 days after the first injection, when II-I time shortened to its minimal level, and the maximal intensity of the murmur and maximal increase in the area of the cardiac silhouette were observed 2 or 3 days later the time of minimal hematocrit.
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