Normal Contractile State of Hypertrophied Myocardium after Pulmonary Artery Constriction in the Cat

A B S T R A C T To determine the effect of prolonged digitoxin administration on contractile function of nonfailing myocardium, right ventricular papillary muscle mechanics were examined after 6 or 24 wk of glycoside administration to control and pulmonary artery banded cats. Resting length-tension relations were not affected by digitoxin; however, isometrically developed force and the maximal rate of force development at the peak of the length-tension curve were increased in all treated groups.In untreated animals, banding resulted in a 28% incidence of deaths from heart failure. 6 wk after constriction, contractile function was depressed whereas normal function was observed 24 wk after banding. Digitoxin significantly reduced mortality from heart failure and enhanced the recovery of contractile function; contractile function in the 6 wk banded treated group approached that of untreated control and 24-wk banded groups. The long-term effects of digitoxin on contractile function were not importantly related to the temporal association between banding and institution of glycoside administration. Development of myocardial hypertrophy was comparable in treated and untreated banded groups.These results demonstrate that a significant positive inotropic effect persists in both normal and nonfailing hypertrophied myocardium during chronic digitoxin administration.

Section: Resultssupporting

confidence: 76%

Section: Discussionsupporting

confidence: 71%

The effect of chronic digitoxin administration on the contractile state of normal and nonfailing hypertrophied myocardium.

Williams¹,

Potter²

1975

“…At 2 wk dense fibrosis was found around the band and we suspect that an inflammatory reaction reduced pulmonary artery diameter more quickly than anticipated. Nevertheless, both the load and hypertrophy occurred more slowly in this model than in a banded adult cat model used previously in our laboratory (17). We examined seven additional kittens 1 wk after banding in a similar manner and found the RV systolic pressure averaged 40±4.0 mm Hg and the RV/LV ratio 0.38±0.03, whereas in six adult cats 1 wk after banding in the more standard manner (17) RV systolic pressure and RV/LV averaged 48±4 mm Hg and 0.49±0.02, respectively, both values being significantly greater (P < 0.05) than their respective values in kittens banded for 1 wk.…”

Section: Discussionmentioning

confidence: 54%

Hydroxyproline and passive stiffness of pressure-induced hypertrophied kitten myocardium.

Williams¹,

Potter²,

Hern³

et al. 1982

A B S T R A C T Passive stiffness and hydroxyproline content of myocardium hypertrophied by pressureloading were determined in kittens 2, 8-16, and 24-52 wk after pulmonary artery banding, which initially elevated right ventricular systolic pressure by 10-15 mm Hg. Right ventricular mass increased by -75%, three-quarters of which occurred during the first 2 wk after banding. Passive stiffness was assessed from resting length-tension relations of isometrically contracting isolated right ventricular papillary muscles. Stiffness constants, a and B were determined from the relationship a = a(ee -1) where a = stress and e = Lagrangian strain. Elastic stiffness (dl/dE) was derived from: da/de = f#a + ,3a. Right ventricular hydroxyproline increased in proportion to muscle mass so that hydroxyproline concentration remained unchanged after banding. Both a, f, and elastic stiffnessstress relations were similar to values in nonbanded controls. Thus, we did not observe an increase in passive stiffness or hydroxyproline concentration of pressure-induced hypertrophied myocardium in contrast to most previous studies.

“…This preparation does not permit sampling of the venous effluent from the hypertrophied right ventricle, thus direct measurements of right ventricular oxygen consumption are not possible. However, heart rate, ventricular wall tension, contractility, and afterload (19,20) or no change (1,(21)(22)(23) in contractile activity of the hypertrophied heart. Because the observed increases in blood flow are specific to the right ventricle,' it is likely that a major determinant of this increased blood flow is the increased external work that must be performed by the right ventricle to maintain function in the face of the pressure overload.…”

Section: Methodsmentioning

confidence: 99%

Effects of exerimental right ventricular hypertrophy on myocardial blood flow in conscious dogs.

Murray¹,

Baig²,

Fishbein³

et al. 1979

A B S T R A C T The effects of right ventricular hypertrophy on the overall and regional distribution of myocardial blood flow in the absence of an elevated coronary arterial driving pressure were evaluated in 18 conscious dogs subjected to a chronic pressure overload of the right ventricle induced by pulmonary artery constriction. The sustained pressure overload for duration of4-6 wk or 4-5 mo resulted in significant increases in right ventricular mass (45 and 110%, respectively) and right ventricular fiber diameter (22 and 60%, respectively). Moreover, the presence *tmoderate and severe hypertrophy was associated with marked increases in transmural blood flow per gram to the right ventricle proportional to the observed increases in mass, i.e., of 36 and 109%, respectively, from a normal value of 0.67+0.04 ml/min per g, whereas left ventricular blood flow remained unaltered from a normal value of 1.00±0.06 ml/min per g. Despite the large increases in blood flow per gram to moderately and severely hypertrophied right ventricle, no significant changes in the ratio of capillary:muscle fiber number were observed. These data suggest that the development of right ventricular hypertrophy is characterized by a sustained compensatory response of the coronary circulation to the augmented work load and mass, and that it is not associated with a proliferative response of the vasculature supplying the enlarged ventricle.