Physiologic or pathologic hypertrophy

Krayenbuehl, H. P.; Om, Hess; Schneider, Jakob; Turina, Marko

doi:10.1093/eurheartj/4.suppl_a.29

Cited by 46 publications

(10 citation statements)

References 4 publications

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“…This suggests the influence of other factors, including sarcoplasmic reticulum, calcium movements, and sensitivity of myofilaments or sarcolemma to calcium, in the regulation of cardiac contractility. 7 This discrepancy is still much more evident in humans, where a drop in shortening velocity 45 was not accompanied by any detectable changes in myosin. 8 One of the goals of this work was to detect, by amplification of the enzymatic reaction, a change in myosin ATPase activity in hypertrophied human hearts that was caused by an unknown isomyosin or to a posttranscriptional modification of the molecule.…”

Section: Discussionmentioning

confidence: 98%

ATPase activity of the cross-linked complex between cardiac myosin subfragment 1 and actin in several models of chronic overloading. A new approach to the biochemistry of contractility.

Lauer

Thiem

Swynghedauw

1989

Circulation Research

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Myosin ATPase activity is usually considered to reflect the contractile capacity of a given muscle since it correlates with the maximum initial speed of shortening of the unloaded muscle (V max). There are several exceptions to this scheme, and it was the goal of this study to determine if the Mg 2+-ATPase activity of the covalently bound actomyosin SI is a more physiological index of contractility. On polyacrylamide gels, the complex obtained after condensation of fast skeletal myosin SI to skeletal actin is identical to that obtained with myosin SI from the ventricles of different species, including rat, guinea pig, and human, cross-linked to cardiac or skeletal actin. In every condition, the ATPase activity of the complex is 700-fold higher than that of myosin SI. It correlates linearly with the V mra both in phylogeny and in conditions in which an isomyosin shift has been reported, such as hypothyroidism and chronic cardiac overload. Such a relation indicates that, in species that already have a low V raax , a small change in myosin ATPase may induce dramatic consequences in the shortening velocity. Cardiac hypertrophy in humans, where the drop in V raax is not associated with a myosin change, does not fit into this scheme. The enzymatic activity of the complex is also unmodified in this condition, which shows that, in humans, the myosin ATPase is not a determinant of \ mm and suggests that other mechanisms may be involved. Measurement of this type of ATPase activity provides a new tool to explore contractility biochemically, which is more reproducible and, from a technical point of view, easier to perform than a kinetic assay. It also correlates better with mechanical data obtained with skinned fibers than with those measured on fresh papillary muscles. (Circulation Research 1989;64:1106-1115) I t is now well established that the maximum shortening velocity of an unloaded skeletal 1 or cardiac 2 muscle (V max) correlates linearly to both Ca 2+-activated and actin-activated myosin ATPase activity measured in the steady state 12 and also to the activity measured during the initial phosphate burst. 3 This relation is one of the basics of muscle physiology and pathology since, in response to chronic overload in some animal species such as rats, it has been shown that the drop in V m ax correlates with a diminution in myosin ATPase and to a corresponding isomyosin shift from the fast isoform V, to the slow isoform V 3. 4-7 From INSERM, Hdpital Lariboisiere,

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Section: Discussionmentioning

confidence: 98%

ATPase activity of the cross-linked complex between cardiac myosin subfragment 1 and actin in several models of chronic overloading. A new approach to the biochemistry of contractility.

Lauer

Thiem

Swynghedauw

1989

Circulation Research

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“…Abnormalities of diastolic relaxation may be related to the presence of chronic ischemic damage and/or fibrosis (Bailey et al, 1977;Lund et al, 1979;Yonekura et al, 1985) or to systolic myocardial failure which may supervene during advanced cardiac hypertrophy (Sordahl et al, 1973;Krayenbuehl et al, 1983;Grossman and Lorell, 1983). It is unlikely that the differences in diastolic Lorell et al /Hypertrophy and Hypoxic Contracture behavior seen during hypoxia in the two groups in this study were related to overt end-stage heart failure or chronic ischemia in the hypertensive rats.…”

Section: Limitations Of the Experimental Modelmentioning

confidence: 99%

The influence of pressure overload left ventricular hypertrophy on diastolic properties during hypoxia in isovolumically contracting rat hearts.

Lorell¹,

Wexler²,

Momomura³

et al. 1986

Circulation Research

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SUMMARY. We tested the hypothesis that there is an enhanced susceptibility in hypertrophied cardiac muscle to develop decreased diastolic distensibility of the left ventricle in response to hypoxia. The effects of brief hypoxia (3 minutes) were studied in rats with and without chronic left ventricular pressure overload hypertrophy using an isolated buffer-perfused and isovolumic (balloon-in-left ventricle) heart preparation with excised pericardium and vented right ventricle. We compared hypertrophied hearts from hearts from hypertensive uninephrectomized WistarKyoto rats (» = 12) with normotensive uninephrectomized age-matched controls (n = 13). Coronary flow was held constant and adjusted so that an identical flow per gram left ventricular weight was achieved in both groups. The left ventricular balloon volume was adjusted to produce an initial left ventricular end-diastolic pressure of 10 mm Hg in both groups and was held constant thereafter so that changes in left ventricular end-diastolic pressure during hypoxia represented changes in diastolic chamber distensibility. Under aerobic conditions, left ventricular systolic pressure was 66% higher in the hypertrophied hearts than in the controls, but there was no difference in the rate or extent of left ventricular relaxation as estimated by the exponential time constant of pressure decay and the asymptote to which pressure decayed. In response to hypoxia, left ventricular end-diastolic pressure was significantly higher in the hypertrophied hearts than in the controls (37 ± 5 vs. 22 ± 5 mm Hg, P < 0.001). In response to hypoxia, the rate of left ventricular relaxation was depressed to a comparable degree in both groups, but there was a greater upward shift in the asymptote to which pressure decayed in the hypertrophied hearts. Hypoxia-induced coronary vasodilation as assessed by the change in coronary vascular resistance was similar in the hypertrophied and control hearts (2.9 ± 0.5 vs. CARDIAC hypertrophy is a compensatory response to chronic pressure or volume overload of the heart. However, adaptive cardiac hypertrophy may result in an enhanced vulnerability to ischemia or hypoxia,* as manifested by a decrease in diastolic distensibility. Bache et al. (1984a) have shown that pacing tachycardia in dogs with chronic left ventricular (LV) hypertrophy without coronary stenoses produces myocardial ischemia associated with a substantial increase in left ventricular end-diastolic pressure. A similar dramatic and reversible decrease in left ventricular diastolic distensibility has been * In this paper, hypoxia will be used to indicate an abnormally low level of tissue oxygenation due to hypoxemia, an abnormally low arterial oxygen content. Ischemia will mean an abnormally low level of myocardial perfusion.

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“…However, growth of the coronary microcirculation is not proportional to the increase in the cardiac mass, with an increased minimum coronary vascular resistance and decreased blood flow to the endocardium being observed. In addition, interstitial fibrosis and vascular media hypertrophy also contribute to the reduction of vasodilation capacity 28,29 . Comparatively, in diseases such as idiopathic dilated cardiomyopathy 30 or in chronic aortic regurgitation 31 , both with eccentric hypertrophy, a reduction in CFR is observed, and its presence characterizes a subgroup of patients with increased mortality, regardless of the degree of left ventricular dysfunction 30 .…”

Section: Discussionmentioning

confidence: 99%