Abstract
Clinical studies have shown that spasms of the coronary arteries are fairly common and can cause myocardial ischaemia both in arteriosclerotic and in radio-graphically normal coronary arteries. Coronary spasms are not only the cause of Prinzmetal’s angina (variant angina), but are also important in typical angina pectoris and in myocardial infarction (Braunwald 1978; Hellström 1973; Hillis and Braunwald 1978; Maseri et al. 1975, 1978). The mechanisms which trigger coronary spasm are not understood. Experimental results suggest that possible causes are α-adrenergic transmitters, thromboxan A2 from platelets, and serotonin (Ellis et al. 1976; Hillis and Braunwald 1978; Holtz et al. 1978). Our own experimental and clinical studies suggest that the trace element nickel, which can cause vascular contraction and which is found in a higher concentration in the serum of patients, might also be an aetiological factor in coronary vascular spasm (Rubânyi 1981 ; Rubânyi et al. 1981).
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References
Bevan JA (1979) Some bases of differences in vascular response to sympathetic activity. Circ Res 45:161–171
Bohr DF (1973) Vascular smooth muscle updated. Circ Res 32: 665–672
Braunwald E (1978) Coronary spasm and acute myocardial infarction — new possibility for treatment and prevention. N Engl J Med 299:1301–1303
Ellis EF, Oelz O, Roberts LJ II, Payne NA, Sweetmann BJ, Nies AS, Oates JA (1976) Coronary arterial smooth muscle contraction by a substance released from platelets: evidence that it is thromboxane A2. Science 193:1135–1137
Fleckenstein A (1977) Specific pharmacology of calcium in myocardium, cardiac pacemakers and vascular smooth muscle. Ann Rev Pharmacol Toxicol 17:149–166
Fleckenstein A (1981) Pharmacology and electrophysiology of calcium antagonists. In: Zanchetti A, Kritzler DM (eds): Calcium antagonism in cardiovascular therapy: experience with verapamil. Excerpta Medica, Amsterdam Oxford Princeton, p. 10–29
Hellström HR (1973) Vasospasm in ischemic heart disease a hypothesis. Perspect Biol Med 16: 427–440
Hillis LD, Braunwald E (1978) Coronary-artery spasm. N Engl J Med 299: 695–702
Holtz J, Held W, Sommer O, Kühn G, Bassenge E (1982) Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: a-adrenoceptors are not involved. Basic Res Cardiol 77: 278–291
Kaufmann R, Fleckenstein A (1965) Ca++-kompetitive elektromechanische Entkoppelung durch Ni++- und Co++-Ionen am Warmblütermyokard. Pflügers Arch 282: 290–297
Kohlhardt M, Bauer B, Krause H, Fleckenstein A (1973) Selective inhibition of the transmembrane Ca conductivity of mammalian myocardial fibres by Ni, Co and Mn Ions. Pflügers Arch 338:115–123
Koller A, Rubányi G, Ligeti L, Kovách AGB (1982) Inhibition of myocardial reactive hyper-aemia but not of hypoxic coronary vasodilatation by constant verapamil infusion in the in situ dog heart. Acta Physiol Acad Sci Hung 59:187–195
Maseri A, Mimmo R, Chierchia S, Marchesi C, Pesola A, L’ Abbate A (1975) Coronary artery spasm as a cause of acute myocardial ischemia in man. Chest 68: 625–633
Maseri A, L’Abbate A, Baroldi G, Chierchia S, Marzili M, Ballestra AM, Severi S, Parodi O, Biagini A, Distante A, Pesola A (1978) Coronary vasospasm as a possible cause of myocardial infarction. N Engl J Med 229:1271–1277
Rubányi G (1981a) Control of coronary vascular tone in hemorrhagic shock. In: Biro Z, Kovách AGB, Spitzer JJ, Stoner HB (eds) Homeostasis and injury in shock. Adv Physiol Sci 26: 99–108
Rubányi G, Ligeti L, Koller A (1981b) Nickel is released from the ischemic myocardium and contracts coronary vessels by a Ca-dependent mechanism. J Mol Cell Cardiol 13:1023–1026
Singh BN, Ellrodt G, Peter CT (1978) Verapamil: a review of its pharmacological properties and therapeutic use. Drugs 15:169–197
Somlyo AP, Somlyo AV (1970) Vascular smooth muscle. II. Pharmacology of normal and hypertensive vessels. Pharmacol Rev 22: 249–353
Van Nueten JM, Van Beek J, Vanhoutte PM (1980) Inhibitory effect of lidoflazine on contractions of isolated canine coronary arteries caused by norepinephrine, 5-hydroxytryptamine, high potassium, anoxia and ergonovine maleate. J Pharmacol Exp Therap 213:179–187
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© 1984 Springer-Verlag Berlin Heidelberg
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Kovách, A.G.B., Ligeti, L., Bakos, M., Rubányi, G., Koller, A. (1984). Studies in Vitro and in Vivo on the Effect of Gallopamil on Coronary Vessels. In: Kaltenbach, M., Hopf, R. (eds) Gallopamil. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-07364-3_4
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DOI: https://doi.org/10.1007/978-3-662-07364-3_4
Publisher Name: Springer, Berlin, Heidelberg
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