| Japanese |
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| Title | 麻酔薬とCa++拮抗薬の心機能における相互作用 -摘出筋, 心臓- |
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| Subtitle | 特集 |
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| Authors | 仲田房蔵*, 横田祥*, 劔物修* |
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| Organization | *北海道大学医学部麻酔学講座 |
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| Journal | 循環制御 |
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| Volume | 11 |
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| Number | 4 |
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| Page | 463-470 |
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| Year/Month | 1990/ |
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| Article | 報告 |
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| Publisher | 日本循環制御医学会 |
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| Abstract | 「I はじめに」近年, カルシウム拮抗薬は, 術前の虚血性心疾患や高血圧治療の目的で長期連用されていたり, 術中の心筋虚血, 高血圧, 不整脈に対して投与される機会が多い. カルシウム拮抗薬は細胞膜におけるカルシウムチャンネルを介するカルシウムの細胞内への流入を阻害して, 心筋収縮性, 洞結節での興奮自動能や房室伝導を抑制する. したがって, 臨床麻酔で多用され, 心筋細胞への作用機序や作用部位が重複する吸入麻酔薬を同時使用する場合の相互作用を把握する意義は大きい1)2). 本稿では, 著者らが報告してきた各種吸入麻酔薬とカルシウム拮抗薬の心筋収縮性と房室伝導に及ぼす相互作用の結果を比較検討し4)〜8), 文献的考察を行いたい. 「II 方法」「(1)心筋収縮性に及ぼす相互作用4)〜6)」雑種成犬をペントバルビタール25mg/kgの静脈内投与で麻酔後, 心臓を速やかに取り出して右室摘出心筋標本を作成した. 摘出心筋は95%O2-5%CO2混合ガスで通気され36℃に保持されているKrebs-Henseleit溶液中で, 一方を等張性収縮トランスデューサに連結している等張性バーに, 他方を張力トランスデューサにそれぞれ接続し懸垂固定した. 刺激電極装置を用い, 白金電極により毎分12回の頻度で, 持続時間5msecの矩形波を域値よりも20%高い電位で刺激した. |
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| Practice | 基礎医学・関連科学 |
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| English |
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| Title | Interactions between inhalation anesthetics and calcium channel blockers on myocardial contractility and AV nodal function |
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| Authors | Fusazo Nakata, Show Yokota, Osamu Kemmotsu |
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| Organization | Department of Anesthesiology Hokkaido University School of Medicine |
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| Journal | Circulation Control |
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| Volume | 11 |
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| Number | 4 |
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| Page | 463-470 |
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| Year/Month | 1990/ |
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| Article | Report |
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| Publisher | Japan Society of Circulation Control |
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| Abstract | Combined effects of inhalation anesthetics and calcium channel blockers on were evaluated utilizing dog preparations. 1. Dose-dependented decerases in maximal velocity of shortening (Vmax), maximal developed isometric force (Fm) and maximal dF/dt by verapamil, diltiazem, nifedipine and nicardipine were obtained either with or without volantile anesthetics：halthane, enflurane, or isoflurane. 2. When anesthetic depressed values for Vmax, Fm and maximal dF/dt were used for the control in groups with halothane and enflurane, there were additive effects with verapamil or diltiazem. However, the negative inotropic effect of verapamil, ditiazem and nifedipine were potentiated by isoflurane. 3. Prolongations of atrium-His intervals and functional refractory period of the atrio-ventricular node induced by verapamil or diltiazem were augmented by additional administration of halothane. Comparing effects of verapamil, ditiazem and nifedipine with and without halothane, there were additive effects of halothane with verapamil or diltiazem were obtained. And nifedipine had little effect on electrophysiological changes. 4. Halothane and enflurane depressed AV nodal function as compared with isoflurane and sevoflurane. These effects were potentiated by verapamil. |
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| Practice | Basic medicine |
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