摘要:

The pathophysiological relationships of a myocardial depressant factor (MDF) present in the plasma of cats in hemorrhagic shock were studied. Aprotinin (Trasylol), an inhibitor of a variety of proteases including kallikrein and trypsin, prolonged survival of cats in postoligemic shock as well as prevented the appearance of MDF in the plasma. Trasylol did not alter the arterial blood pressure, venous pressure, or heart rate of these cats in shock, nor did it protect by exerting a positive inotropic effect. Trasylol was ineffective in preventing or reversing the negative inotropic effects of MDF in isolated cat papillary muscles. Column chromatography of plasma from control cats, from untreated shocked cats and from cats treated with Trasylol before shock showed six peptide peaks, designated A, B, C, D, E, and F in decreasing order of molecular weights. Peptides corresponding to peaks A, B, E, and F exhibited insignificant myocardial depressant activity. The peptide corresponding to peak C was present in control plasma and accounted for some of the small negative inotropic effect of control plasma. The peptide corresponding to peak D had a marked myocardial depressant effect which could account for all the activity of shock plasma. The molecular weight of this peptide was estimated to be 800 to 1000. This peptide is not bradykinin, but appears to be produced by a protease present in shock.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

Left ventricular dimensions from routine clinical one-plane cineangiograms were combined with left ventricular pressure measurements to permit calculation of left ventricular wall stresses. The 25 patients included 12 with normal left ventricular dynamics, 6 with volume overload, 3 with outflow obstruction, and 4 with cardiomyopathy. Average stresses calculated on the basis of an ellipsoid model agreed with average values obtained from the exact solution of a thick-walled elastic ellipsoidal shell. Peak values were 150 to 625 g/cm2in the circular direction and 75 to 365 g/cm2in the longitudinal direction. A fiber-corrected stress was defined which represents a force per muscle fiber. The variation in fiber-corrected stress during the cardiac cycle may be considerably different from the variation in simple stress.The force-velocity characteristics of circular fibers for the 25 patients are presented. The data on peak wall stress overlap in the four groups of patients. Peak velocity of circumferential fiber shortening varied from 0.44 to 0.63 lengths/sec in patients with myocardial weakness and varied from 0.74 to 2.56 lengths/sec in the other patients. Contractile element velocity was determined during ventricular ejection when the rate of force change equaled zero. Contractile element velocity of shortening was 0.22 to 0.32 lengths/sec in the cardiomyopathy group and 0.50 to 1.32 lengths/sec in the other patients.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

In the isolated, blood-perfused heart of the dog, left ventricular developed pressure and developed mean wall stress were observed while the ventricle contracted at a constant, nearly isovolumic afterload and while end-diastolic pressure was raised to levels exceeding 100 mm Hg. Coronary perfusion pressure was maintained at the level of the peak systolic pressure. Dilatation of the mitral ring and consequent mitral regurgitation were avoided by left atrial plication. Normalized graphs of percent of peak developed pressure against end-diastolic pressure showed that developed pressure rose abruptly with diastolic pressure, peaked at a diastolic pressure of approximately 30 mm Hg, and declined 14.7% (±0.9 SE) at an end-diastolic pressure of 100 mm Hg. Likewise, developed mean wall stress rose abruptly with diastolic pressure, peaked at a higher diastolic pressure of approximately 50 mm Hg, and declined only 7.5% (±0.8 SE) from this peak at an end-diastolic pressure of 100 mm Hg. Similar findings were observed in hearts acutely depressed with propranolol. Electron micrographs showed sarcomere length to average 2.275μ and 2.300μ in ventricles fixed in diastole while subjected to pressures of 61 and 100 mm Hg, respectively, after potassium arrest, confirming the findings illustrated by the normalized graphs. These observations imply that in the isolated heart of the dog there is no loss of ventricular performance attributable to a descending limb of the Frank-Starling mechanism until the end-diastolic pressure exceeds 60 mm Hg and that this loss is minimal at diastolic pressures as high as 100 mm Hg.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

Myocardial necrosis was produced in rats by administering isoproterenol, and the increase in hexosamine-containing materials in the injured myocardium was investigated. Total hexosamine, galactosamine, neutral sugars, and uronic acids were determined on various fractions isolated from the hearts. Mucopolysaccharides were precipitated as the cetyl pyridinium chloride complex and fractionated according to their solubility in NaCl solutions. Of the hexosamine in the heart, approximately 50% was retained after proteolytic digestion and dialysis. Approximately one-fourth to one-third of the nondialyzable hexosamine was in mucopolysaccharides. The hyaluronic acid fraction of the mucopolysaccharides increased during the early edematous reaction observed in the hearts. The chondroitin sulfate fraction increased in conjunction with the beginning fibrinogenic processes and remained elevated during repair. There was evidence that the glycoproteins may be involved in the myocardial necrosis and repair.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

摘要:

The use of maximum velocity of shortening (Vmax) as an index of contractility has been based on the assumption that Vmaxof muscle fibers is equivalent to Vmaxof the contractile element. It is shown here that such equivalence applies to the two-element model of skeletal muscle but not to three-element models of cardiac muscle. Analysis of published data in terms of the Voigt and Maxwell three-element models shows that the Vmaxof the contractile element, unlike that of the muscle fibers, is not independent of fiber length but increases at least 50% for a 25% increase of fiber length. Moreover, Vmaxof the contractile element is seen to be even more highly dependent on fiber length when correction is made for the nonuniform contribution of levels of active state to the force-velocity curves giving rise to Vmaxof the contractile element.It appears that in cardiac muscle an inotropic shift of Vmaxof the contractile element cannot be distinguished from a shift due to change in fiber length, thus invalidating it as an index of contractility.

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1970

数据来源: OVID