Afterload reduction therapy in congestive heart failure

AFTERLOAD REDUCTION THERAPY IN CONGESTIVE HEART FAILURE. D. T. Mason. Cardiovascular Medicine, University of California, School of Medicine, Davis, California, U.S.A. While digitalis and diuretics constitute conventional therapy of congestive heart failure, systemic vasodilators offer an innovative approach in acute and chronic heart failure of + elevated left ventricular (LV) systolic wall tension (LV afterload) by J aortic impedance and/or by + cardiac venous return. Thus vasodilators 4 cardiac output (CO) by + peripheral vascular resistance (PVR) and/or 4 increased LV end-diastolic pressure (LVEDP) (LV preload) by + venous tone. Concomitantly there is + of myocardial oxygen demand thereby limiting infarct size and ischemia, and J of angina pectoris in coronary disease. The vasodilators produce disparate modifications of cardiac function depending upon their differing alterations of preload versus impedance: nitrates principally cause venodilation (+ LVEDP); nitroprusside, phentolamine, trimethaphan, and prazosin produce balanced arterial and venous dilation (+ LVEDP and + CO); while hydralazine predominantly effects arteriolar dilation (4 CO). With depressed CO plus highly elevated LVEDP and elevated PVR, nitrates also achieve some + of CO by C PVR. Combined nitroprusside and dopamine synergistically enhance CO and decrease LVEDP. Mechanical counterpulsation aids nitroprusside in acute myocardial infarction. Ambulatory oral vasodilator therapy is provided by long-acting nitrates (C pulmonary congestion), hydralazine (+ fatigue), and prazosin alone or combined nitratehydralazine (C both dyspnea and fatigue).

CAVEOLAR INVAGINATIONS IN SINUS NODE RABBIT HEART CELLS. M. Masson-Pevet, D. Gras*, C.E. Besselsen and L.N. Bouman. Department of Physiology, University of Amsterdam, le Const. Huygensstraat 20, Amsterdam, The *Laboratory of Zoology and Cellular Biology, 40 Av. du Netherlands. Recteur Pineau, Poitiers 86022, France. Caveolar invaginations were examined on electron micrographs obtained from thin sectioned fixed preparations and from freeze-cleaved replicas of myocardial cells from the sinus node. Preliminary measurements on 2 sarcolemmal replicas gave a mean value of 20 caveolar necks per !.m of made on caveolar apparent external sarcolemmal surface area. Measurements profiles in thin sections gave a value of 0.092 2 0.003 m for the diameter of the circle equivalent to the non-circular profile of the caveolae. It is clear from the micrographs that the number of caveolae/ caveolae neck was >l, situated between 1 and 2. Calculations based on these data suggest that the apparent surface area of the external sarcolemma would be increased by at least 53% or 106% if the number of caveolae per neck is 1 and 2 respectively. The increment in membrane area due to caveolae is thus much more in rabbit sinus node cells than in rabbit papillary muscle described by Levin and Page (J. Cell Biol. 75: present on PF and EF fracture Mu276, 1977). The numbers of particles faces of the external sarcolemma and of the caveolar invaginations have been counted and compared. It has been found that these particles are about 4 times less numerous in caveolae than on the external sarcolemma both on PF and EF fracture faces.