By Philip J. Podrid M.D. (auth.), Robert E. Beamish, Vincenzo Panagia, Naranjan S. Dhalla (eds.)
The significance of center and artery illness as a explanation for loss of life and incapacity is hard to magnify: it reasons over half all deaths within the western international and now money owed for one-quarter of deaths within the complete international. This appalling prevalence persists regardless of commendable growth in remedy and prevention, fairly within the final or 3 a long time. Deaths from coronary affliction have lowered via a 3rd long ago two decades and stroke has reduced through a part within the similar interval. This extraordinary development, saving millions of lives in line with yr, has take place because of alterations in lifestyle (low fats nutrition, regulate of hypertension, much less smoking and extra workout) and development in remedy (more potent medications, coronary care devices, pacemakers, and cardiac surgery). growth in knowing the pathophysiologic and pharn,acologic mechanisms operative in center sickness were paramount within the improvement of extra rational and greater treatment. Dramatic and awesome surgical remedies have fired the general public mind's eye. pass surgical procedure is average and leads to whole or significant aid of indicators within the majority of sufferers operated upon.
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Extra info for Pharmacological Aspects of Heart Disease: Proceedings of an International Symposium on Heart Metabolism in Health and Disease and the Third Annual Cardiology Symposium of the University of Manitoba, July 8–11, 1986, Winnipeg, Canada
Sample text
Although sympathetic stimulation does not significantly affect conduction in ventricular muscle, it does shorten the effective refractory period (34). Dispersion of refractoriness may by caused by sympathetic stimulation to an area wi th an inhomogenous distribution of sympathetic nerves (34). If this should occur, a functional reentrant pathway might be established and reentry continued resulting in ventricular tachycardia (33). In this context, beta-blockers might work by decreasing inhomogeneous conduction.
6. Lindner, E. Arzneim. Forsch. 10: 569-573, 1960. Haas, H. and Hartfelder, G. Arzneim. Forsch. 12: 549-558, 1962. , Doring, H. J. Z. Kreislaufforsch. 56: 716-744, 839-853, 1967. Grun, G. and Fleckenstein, A. Arzneim. Forsch. 22: 334-344, 1972. O. Am. J. Cardiol. 46: 1047-1058, 1980. , Udvary, E. and-Vegh, A. Br. J. Pharmacol. 86: 341-350, 1985. 3 QUINIDINE REDUCES OUTWARD CURRENT IN SINGLE CANINE CARDIAC PURKINJE CELLS T. A. FOZZARD Cardiac Electrophysiology Labs, Departments of Medicine and the Pharmacological and Physiological Sciences, The University of Chicago, Chicago, 111,60637, USA INTRODUCTION The commonly used antiarrhythmic drug quinidine is a member of the local anesthetic class.
Am. J. Cardiol. 46: 1047-1058, 1980. , Udvary, E. and-Vegh, A. Br. J. Pharmacol. 86: 341-350, 1985. 3 QUINIDINE REDUCES OUTWARD CURRENT IN SINGLE CANINE CARDIAC PURKINJE CELLS T. A. FOZZARD Cardiac Electrophysiology Labs, Departments of Medicine and the Pharmacological and Physiological Sciences, The University of Chicago, Chicago, 111,60637, USA INTRODUCTION The commonly used antiarrhythmic drug quinidine is a member of the local anesthetic class. In cardiac muscle it reduces sodium (Na) current (1), thereby slowing the action potential (AP) upstroke (2), slowing conduction velocity, and reducing excitability.