実験的心筋梗塞に対するnicardipineの効果

The effects of nicardipine on hemodynamics, regional myocardial function and myocardial metabolism in the dog with coronary artery occlusion

　nicardipineはnifedipineと化学構造上近似したdihydropyridine誘導体のCa拮抗薬の1つであり，血管，心筋の細胞膜においてCa^＋＋流入を阻害し，強力な血管拡張作用を発揮する^1〜6）。なかでも脳および冠血管での拡張作用は著明であり^1,2,6），心筋抑制作用は弱いと報告されている^3,6）。また，Ca拮抗薬には虚血心筋への直接保護作用もあり，nicardipineについても幾多の報告がある^5,7,8）。

　こうしたCa拮抗薬を心不全に対する血管拡張療法として用いることは合理的な治療法であり^9,10），なかでも心筋抑制の弱いnicardipineは使いやすいものといえる。急性心筋梗塞における左心不全に対して使用すれば，減負荷療法のみならず，虚血ら筋を保護し，梗塞量の縮小化をも期待できる^11）。本研究ではイヌにおいて実験的に心筋梗塞を作製して，nicardipineの血行動態および虚血，非虚血部の局所心筋機能，心筋エネルギー代謝に対する効果を検討した。

In order to study the effects of nicardipine on hemodynamics, regional myocardial function and myocardial metabolism in acute myocardial ischemia, nicardipine (30μg/kg) was administered intravenous-ly in the dog with left anterior descending coronary artery occlusion.

Maximum hemodynamic effects were observed 3 to 5 min after. Aortic systolic and diastolic pressures decreased by 18.7% (p<0.01, ^**) and 36.1% (^**), respectively. Stroke volume increased by 40.9% (^**), cardiac output increased by 27.3% (^**), SVR de-creased by 42.0% (^**), and pressure-time index decreased by 23.7% (^**). Peak negative dp/dt decreased by 25.2% (^**), and time constant of left ventricular pressure fall in isovolumic relaxation phase lengthened by 10. 1% (p<0.05, ^*). Though systolic shortening during ejection phase increasedby 49.4% (^*) in the non-ischemic segment, it did not change significantly in the ischemic segment. End-diastolic length did not change significantly in every segment. Coronary arteriovenous differences of O₂ content and pH, lactate extraction ratio did not change significantly in both ischemic and non-ischemic regions.

These observations indicate that nicardipine im-prove left ventricular performance in the ischemic heart by the vasodilating action without deteriora-tion of regional myocardial function and myocardial energy metabolism in the ischemic myocardium.