title: Calcium antagonists and myocardial microperfusion.
abstract: Recent studies have improved our understanding of the beneficial actions of calcium antagonists on myocardial microcirculation and metabolism. The effect of calcium antagonists on the microcirculation of the left ventricular rat myocardium was studied using in vivo microscopic techniques. Intravenous verapamil 0.3 mg/kg and nifedipine 75 micrograms/kg produced a 15 to 18% increase in the diameter of larger A1 and A2 coronary arterioles (range 31 to 300 microns); diameters of terminal (A4) arterioles and capillaries did not change significantly. Furthermore, verapamil significantly (p less than 0.001) increased the ratio of capillaries filled with red cells to those containing plasma alone. Verapamil pretreatment produced a similarly selective dilatation of larger coronary arterioles and protected against the ischaemia-induced fall in capillary red cell content. Spectroscopic data show that verapamil also produces an increase in myocardial phosphocreatine and preservation of adenosine triphosphate (ATP) during ischaemia in the Langendorff-perfused heart. In patients with exercise-induced angina, gallopamil decreased global myocardial 201Tl and 123I phenylpentadecanoic acid (IPPA) uptake due to a reduction in myocardial oxygen consumption. Regional 201Tl and IPPA uptake as well as IPPA clearance in post-stenotic areas tended to rise after gallopamil treatment. Thus, the beneficial effects of calcium antagonists such as verapamil or gallopamil in patients with ischaemic heart disease may result from dilatation of predominantly larger arterioles. Consequently, there is an improvement in regional perfusion and free fatty acid utilisation in reversibly ischaemic regions.
authors.affiliation: Department of Internal Medicine-Cardiology, University of Giessen, Federal Republic of Germany.
authors.forename: H
authors.initials: H
authors.lastname: Tillmanns
authors.forename: F J
authors.initials: FJ
authors.lastname: Neumann
authors.forename: N
authors.initials: N
authors.lastname: Parekh
authors.forename: W
authors.initials: W
authors.lastname: Waas
authors.forename: P
authors.initials: P
authors.lastname: Möller
authors.forename: R
authors.initials: R
authors.lastname: Zimmermann
authors.forename: M
authors.initials: M
authors.lastname: Steinhausen
authors.forename: W
authors.initials: W
authors.lastname: Köbler
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology* / Q000627:therapeutic use; D003326:Coronary Circulation; D003327:Coronary Disease / Q000188:drug therapy; D005711:Gallopamil / Q000494:pharmacology; D006168:Guinea Pigs; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D016277:Ventricular Function, Left / Q000187:drug effects; D014700:Verapamil / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D005711:Gallopamil; D014700:Verapamil; D009543:Nifedipine