循環器疾患を中心に行つたロダン・スペース,細胞外液,ならびに,循環血量の吟味
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概要
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1) THS is not equivalent in meaning with ECF. Under conditions of the augmented permeability of the cellular membrane, THS increases apparently in its amount without any significant change of ECF. Such conditions can be observed in feverish patients. However THS, except for an apparent increase, fluctuates in the same direction with ECF. THS of hypertensive cardiac disease increases considerably even if neither edema nor fluid retention is determined. Such an augmented THS can not entirely be appreciated as an apparent increase. In some kinds of cardiac failure free from either edema or effusion in serous cavities there can be secured good evidence showing the retention of the large quantity of ECF. Therefore the augmentation of THS in the cases without edema or effusion- can be regarded as the increase of ECF, even if the augmented THS may partly contain an apparent increase. In essential hypertension without any complication, at least in the early stage, there is estimated no increase in ECF. The augmentation found in essential hypertension is chiefly caused by the cardio-renal complication. The correlation between THS and edema or effusion was investigated in renal diseases, anemic disorders and orthostatic edema etc. There can be obtained the result showing that THS reflects fairly the fluctuation of ECF. Generally speaking, while edema or effusion is often missed in patients with augmented THS less than 120 % of normal average, either edema or effusion is frequently found in patients with THS more than 120 % of normal average. Existence or degree of edema is not always paralell to the increase of THS. This fact suggests that the variation of the distribution of ECF is important as well as its quantitative change with respect to the relationship between edema and ECF. 2) The actual determinations of the circulating blood volume, except for some disagreement, mostly reveal a definite increase in patients with congestive heart failure.Its average increase in the circulating, blood volume is roughly paralell to prolongation in the circulation time and elevation of the venous pressure. Increase in plasma volume is due essentially to abnormal renal retention of sodium and water. If cardiac failure is related to a plus-decompensation, clinical improvement should correspond to a reduction of the circulating blood volume. The increase in plasma- and total blood-volume in heart failure is relatively small in comparison with the vast increase in ECF (plasma plus interstitial fluid) observed in patients with cardiac insufficiency, especially those with severe edema and effusion in the serous cavities. Plasma volume is often increased 10 to 20 % in moderately severe cases of heart failure, 30 to 50 % in very severe cases. On the other hand, ECF, chiefly interstitial fluid, may be increased 100 % or more. In cases of congestive heart failure there occurs often a reduction in the concentration of plasma protein, especially of the important albumin fraction. In general the reduction in blood proteins in most cases of heart failure is relatively small but occasionally it is pronounced, as in case of constrictive pericarditis. Therefore the lesser degree of hypoproteinemia often seen in patients with congestive heart failure is usually insufficient to produce edema and at most represent a minor accessory causative factor. The increase in plasma volume may diminish the concentration of albumin. Hypervolemia rerults the increase in the central venous reservoir which becomes one of the important factors in order to augment the inflow as well as the venous hypertension. But a clear distinction should be made between an increased venous return and an increased venous pressure. The venous return may be only augmented by increasing the circulating blood volume and at the same time by increasing the speed of the circulating blood.Thus the blood volume may be represented as a fundamental homeostatic mechanism for maintaining an adequate cardiac output within Starling's law. There are groups of cases with equivocal features of congestive heart failure in which the cardiac output is actually increased. This paradox is readily explained if one bears in mind that the physiologic definition of heart failure relates cardiac output to the needs of the tissue and not to some absolute normal. Severe anemia, hyperthyroidism, advanced pulmonary emphysema with arterial hypoxemia are conditions which are or may be associated with high cardiac output. In disease associated with high output (hyperthyroidism, severe anemia, etc.) as well as during marked fever, the circulation time is shortened. The venous return is augmented because ' of the increased speed of flow which outweighs any changes in circulating blood volume. With the occurrence of heart failure in these disorders, the speed of flow falls but the circulation time may still be normal or slightly diminished, therefore the circulating blood volume increases furthermore. In the early stage of the essential hypertension when there is no complication, the blood volume remains normal; the variation of the blood volume in this disorder can be seen in the existence of cardio-renal complication. The fluctuation of the blood volume in renal diseases is not uniform. In anemia the blood volume is as a rule maintained normally owing to the compensatory increase of the plasma volume against the reduction of the erythrocyte volume. However, the slight hypervolemia due to the extreme increase in plasma volume is not seldom found.
- 千葉大学の論文