A novel positive inotropic substance enhances contractility without increasing the Ca2+ transient in rat myocardium.

[1]  E. Lakatta,et al.  Simultaneous measurement of Ca2+, contraction, and potential in cardiac myocytes. , 1990, The American journal of physiology.

[2]  R. Jonas,et al.  Imidazopyridines: roles of pyridine nitrogen position and methylsulfinyl oxygen for in vitro positive inotropic mechanism and chronotropic activity. , 1989, Journal of cardiovascular pharmacology.

[3]  H. Spurgeon,et al.  Milrinone enhances cytosolic calcium transient and contraction in rat cardiac myocytes during beta-adrenergic stimulation. , 1989, International journal of cardiology.

[4]  N. Sperelakis,et al.  Differential effects of d- and l-pimobendan on cardiac myofilament calcium sensitivity. , 1988, The Journal of pharmacology and experimental therapeutics.

[5]  N. Sperelakis,et al.  Sensitization of Dog and Guinea Pig Heart Myofilaments to Ca2+Activation and the Inotropic Effect of Pimobendan: Comparison With Milrinone , 1988, Circulation research.

[6]  J. Harting,et al.  Effect of isomazole on the responsiveness to calcium of the contractile elements in skinned cardiac muscle fibres of various species. , 1988, European journal of pharmacology.

[7]  E. Lakatta,et al.  Spontaneous Ca2+ release from the sarcoplasmic reticulum limits Ca2+- dependent twitch potentiation in individual cardiac myocytes. A mechanism for maximum inotropy in the myocardium , 1988, The Journal of general physiology.

[8]  W Grossman,et al.  Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. , 1987, Circulation research.

[9]  J. C. A. Meel Effects of some cardiotonic agents on contractility of skinned fibers from mammalian heart. , 1987 .

[10]  F. Schoen,et al.  Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure. , 1987, Circulation.

[11]  E. Lakatta,et al.  Single adult rabbit and rat cardiac myocytes retain the Ca2+- and species-dependent systolic and diastolic contractile properties of intact muscle , 1986, The Journal of general physiology.

[12]  Rüegg Jc Effects of new inotropic agents on Ca++ sensitivity of contractile proteins. , 1986 .

[13]  T. Yanagisawa,et al.  Effects of new inotropic agents on cyclic nucleotide metabolism and calcium transients in canine ventricular muscle. , 1986, Circulation.

[14]  J. R. Blinks,et al.  Modification of myofibrillar responsiveness to Ca++ as an inotropic mechanism. , 1986, Circulation.

[15]  H. Scholz,et al.  Phosphodiesterase-inhibiting properties of newer inotropic agents. , 1986, Circulation.

[16]  G. Stankus,et al.  Characterization of the Cardiotonic Effects of Milrinone, a New and Potent Cardiac Bipyridine, on Isolated Tissues from Several Animal Species , 1983, Journal of cardiovascular pharmacology.

[17]  D C Harrison,et al.  Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. , 1982, The New England journal of medicine.

[18]  G. Ferrier The Effects of Tension on Acetylstrophanthidin‐Induced Transient Depolarizations and Aftercontractions in Canine Myocardial and Purkinje Tissues , 1976, Circulation research.

[19]  B. Hoffman,et al.  Toxic effects of ouabain on Purkinje fibers and ventricular muscle fibers. , 1962, The American journal of physiology.