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従来,心機能といえば、主に心筋の収縮能について論じられる傾向にあった。しかし,心筋は常に収縮と拡張をくりかえしており,拡張は次の収縮への準備状態として重要な要素を含んでいる。このような,心室の拡張機能を評価する1つの有用な手段として,古くから心室の内圧—内容積関係がとりあげられてきたが1)〜4),心室内容積を直接,測定することはきわめて困難であったため,内径を計測し,それから容積を算出する方法が一般に用いられてきた。しかし,正確に内径の変化を記録する方法には,なお,多くの問題を含んでいる。
そこで,著者らは、比較的簡単に,しかも連続的に心室内径を計測する装置を作製したので,その使用法を説明するとともに,これを用いて左心室の内圧—内径相関曲線を描かせ,循環動態の変化がこの曲線によってどのように表現されるかという点について,実験動物を用いて観察し,検討を行なった。
Continuous recording of instantaneous innerdiameter (D)-pressure (P) relationships of canineleft ventricle were obtained with a dimensiongauge newly deviced by the authors. Also, designand construction of the gauge for the directmeasurement of inner diameter of the beatingventricle were described in details. Using theD-P relating loop which was drawn on the twinbeam cathode ray oscilloscope. the changes of the dynamic functions of the left ventricle due to overtransfusion and hemorrhage, due to intra-venous administration of vasodilators and vaso-constrictors, myocardial stimulants and depressants were observed in this study.
When intravenous administration of a vaso-constrictor or overtransfusion was made, both the inner diameter and the pressure of the left ventricle were increased at the end-diastole. By intravenous administration of a vasodilator, the inner diameter of the left ventricle was decreased remarkably at the end-systole. In contrast with the concept generally agreed that ventricular contraction before ejection was isovolumetric, theinner diameter of the left ventricle consistently decreased during the pre-ejection phase of systole. Especially, when intraventricular volume was decreased by means of constriction of the pulmo-nary artery or by intravenous administration of a vasodilator, the inner diameter of the left ventricle decreased markedly before the ejection started. This shortening in diameter is probably due to bulging of mitral valve toward the atrium. The similar phenomenon was observed in early diastole. When a vasodilator was administered intravenously or the pulmonary artery was con-stricted temporarily, inner diameter of the ven-tricle increased markedly before the inflow of the blood to the left ventricle was started. It seems that the increase of the diameter in this case is due to recovery from bulging appeared on mitral valve by the contraction of the ventricle. Diastolic compliance of the left ventricle is calibrated with the stress-strain relationship of the muscle, but it could be inferred from the end-diastolic patterns of the D-P relating loop.
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