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うっ血性心不全においては末梢血管抵抗の増加がみられるが,これには2つの因子が関与している1〜3)。1つは交感神経緊張や血中カテコラミンの増加に基づく末梢血管の収縮であり,他は血管壁Na含量の増加によるvas—cular stiffnessの増加である。容量血管においても同様の機序が想定されているが4),この中で交感神経緊張による血管収縮因子の役割は比較的小さいとされている5)。すなわちZelisら5)によれば.心不全患者の静脈コンプライアンスは低く,これにphentolamineを投与しても,静脈の拡張性は完全に正常化しないことから,神経性血管収縮以外の因子の関与が大きいことを報告している。
さらに最近Magriniら6,7)は,高度の末梢浮腫を有するうっ血性心不全患者における静脈コンプライアンスの低下には,浮腫による血管外圧の影響が大で,これは利尿剤の投与により改善されることを報告している。
It has been accepted that peripheral vasomotor tone is increased in patients with congestive heart failure (CHF) probably due to two basic mechanisms ; incre-ased sympatho-adrenergic activity and increased vascular stiffness. Although these two mechanisms has their roles on increased venous tone in CHF, an important role of peripheral edema has recently been suggested. Therefore, we measured central and peripheral hemodynamics using Swan-Ganz catheter and occlusion plethysmogra-phy in 17 patients before and after treatment of their CHF, which were classified into two groups ; acute left heart failure (n=8) and chronic bilateral heart failure (n=9). Venous tone was represented by VV30, the increase in calf volume at occlusion pressure of 30mmHg, as well as slope (b) and intercept (a) obtained from exponential approximation of venous pressure-volume relationship.
When peripheral hemodynamic parameters were com-pared with central hemodynamics, calf blood flow (CBF) and calf vascular resistance (CVR) significantly correlated with cardiac index and total systemic resi-stance, respectively. VV30 and intercept (a) correlated with right atrial pressure r=-0.80 and 0.80, respectively), indicating that peripheral venous tone is largely dependent on venous pressure itself. After treat-ment of CHF, filling pressure of right and left ventricle decreased, VV30 increased and intercept (a) decreasedsignificantly; the extent of those peripheral hemody-namic changes were more in bilateral heart failure compared to acute left heart failure. VV30 also signi-ficantly correlated with the decrease in body weight and sum of water balance during the treatment of CHF.
These results indicate that peripheral edema plays an important role in the genesis of increased venous tone in congestive heart failure.
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