Contractile State of Cardiac Muscle Obtained from Cats with Experimentally Produced Ventricular Hypertrophy and Heart Failure

The contractile state of papillary muscles from hypertrophied and from failing right ventricles of cats with pulmonary artery constriction was studied. In muscles from failing hearts, the maximum velocity of shortening, active length-tension curves, and maximum rate of tension development were decreased, while the passive length-tension curves and the time from stimulation to peak tension were normal. The augmentation of isometric tension achieved by paired electrical stimulation, increasing frequency of contraction, and strophanthidin was reduced. In muscle from hearts without failure but with ventricular hypertrophy, there were qualitatively similar depressions of contractile function, although of lesser magnitude. It is concluded that congestive heart failure is associated with extreme quantitative abnormalities of the intrinsic contractile state of each unit of heart muscle, which reflect a depression in the intensity of the active state. Further, ventricular hypertrophy in the absence of failure is associated with a depression of the contractility of each unit of myocardium, while cardiac compensation is maintained by the increase in muscle mass.

[1]  E. Braunwald,et al.  Myocardial High Energy Phosphate Stores in Cardiac Hypertrophy and Heart Failure , 1967, Circulation research.

[2]  E. Sonnenblick,et al.  Production of Right Ventricular Hypertrophy With and Without Congestive Heart Failure in the Gat , 1967, Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine.

[3]  R. Lee,et al.  Paired Electrical Stimulation and the Maximal Contractile Response of the Ventricle , 1967, Circulation research.

[4]  E. Sonnenblick,et al.  Active state in heart muscle. Its delayed onset and modification by inotropic agents. , 1967 .

[5]  E. Sonnenblick,et al.  Cardiac Norepinephrine Stores and the Contractile State of Heart Muscle , 1966, Circulation research.

[6]  H. Swan,et al.  Relation of Increase in Muscle Mass to Performance of Hypertrophied Right Ventricle in the Dog , 1966, Circulation research.

[7]  E. Braunwald,et al.  Reduction of the Cardiac Response to Postganglionic Sympathetic Nerve Stimulation in Experimental Heart Failure , 1966 .

[8]  E. Braunwald,et al.  Mechanism of Norepinephrine Depletion in Experimental Heart Failure Produced by Aortic Constriction in the Guinea Pig , 1965, Circulation research.

[9]  E. Braunwald,et al.  CATECHOLAMINE EXCRETION AND CARDIAC STORES OF NOREPINEPHRINE IN CONGESTIVE HEART FAILURE. , 1965, The American journal of medicine.

[10]  E. Braunwald,et al.  CARDIAC NOREPHINEPHRINE STORES IN EXPERIMENTAL HEART FAILURE IN THE DOG. , 1964, The Journal of clinical investigation.

[11]  E. Sonnenblick,et al.  Role of the Sarcomere in Ventricular Function and the Mechanism of Heart Failure , 1964, Circulation research.

[12]  A. Grimm,et al.  Properties of Myocardium in Cardiomegaly , 1963, Circulation research.

[13]  Sonnenblick Eh,et al.  Implications of muscle mechanics in the heart. , 1962, Federation proceedings.

[14]  E. Sonnenblick,et al.  Force-velocity relations in mammalian heart muscle. , 1962, The American journal of physiology.

[15]  N. Alexander,et al.  Cardiac Performance of Hypertensive Aorta‐Constricted Rabbits , 1962, Circulation research.

[16]  E. Sonnenblick Implications of muscle mechanics in the heart. , 1962, Federation proceedings.

[17]  R. J. Podolsky Mechanochemical basis of muscular contraction. , 1962, Federation proceedings.

[18]  M. Giambattista,et al.  Tension Developed by Papillary Muscles from Hypertrophied Rat Hearts , 1961, Circulation research.

[19]  A J LINZBACH,et al.  Heart failure from the point of view of quantitative anatomy. , 1960, The American journal of cardiology.

[20]  M. Beznák Cardiac Output in Rats During the Development of Cardiac Hypertrophy , 1958, Circulation research.