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1972年,Vaterら1)によって開発された1,4-ジヒドロピリジン誘導体であるCa++拮抗物質Nifedipineは,その抗Ca++性血管拡張作用によって虚血性心疾患治療薬,降圧剤ならびに心不全時の左心室後負荷軽減薬としての有効性が種々報告されているが2〜17),心不全時における代謝,交感神経系およびgas分析に及ぼす影響に関してはきわめて報告が少ない18)。
以前,我々は重症心不全(NYHA分類IV°,10例)に対するNifedipine 10mg舌下投与の血行力学的効果を観察し,その最大効果時は投与後30分ないし2時間と報告した14,15)。
Simultaneous estimation of hemodynamics, catecholamine levels, metabolism and blood gas data were performed in 9 patients with severe heart failure before and 1 hr after administration of sublingual 10 mg Nifedipine.
CI increased from 2.58 L/min/M2 to 3.09 L/min/M2 (+ 25%, <0.01), SVI 32 ml/beat/M2 to 39 ml/beat/M2 (+ 20%, <0.02), Noradrenaline 0.59 ng/ml to 0.68 ng/ ml (+33%, <0.02), PCWP decreased from 22 mmHg to 17 mmHg (-23%, <0.001), PAm 29mmHg to 24mmHg (-19%, <0.001), RA 10 mmHg to 6 mmHg (-45%, <0.001), BPm 106 mmHg to 88 mmHg (-21%, <0.01), SVRI 3, 106 dynes・sec・cm-5. M2 to 2,160 dynes・sec・cm-5. M2 (-28%, <0.01), Double products 11,879 to 9,727 (-15%, <0.05), A-VO2 5.4 ml/dl to 4.7 ml/dl (-14%, <0.001), whereas there was no significant change in heart rate, Renin activity, Aldosterone, Adrenaline, Lactate/Pyruvate and blood gas (pH, P02, PCO2, BE). Therefore Nifedipine seemed to be a potent vasodilator with both acting as afterload and preload reduction and so to be useful for the treatment of severe heart failure as a deloading agent.
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