Myocyte morphology of free wall trabeculae in right ventricular pressure overload hypertrophy in rabbits

Hamrell, Burt B.; Roberts, Elizabeth T.; Carkin, Julie L.; Delaney, Carol

doi:10.1016/s0022-2828(86)80465-5

Cited by 17 publications

(8 citation statements)

References 37 publications

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“…The theoretical association between pressure overload and concentric hypertrophy (17,18,(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), with increased myocyte cross-sectional area as the predominant feature, has been supported by experimental data (19,33). In agreement with the aforementioned findings, the change in myocyte volume resulting from the left ventricular pressure overload induced in the present study was primarily due to increased cross-sectional area.…”

Section: Discussionsupporting

confidence: 89%

“…A shift to the right and minimal widening of the frequency distribution curve, based on myocyte width and volume, followed aortic constriction of two to three weeks duration produced in adult Sprague Dawley rats (22). A similar response, i.e., shift to the right and minimal widening of the frequency distribution based on cell width, was seen in right ventricular myocytes of rabbits two weeks after pulmonary artery constriction (19). In our investigation, the magnitude of the shift in size-frequency distribution to the fight and extent of the widening (indicating the heterogeneity of the myocyte population) were greater than the abovementioned reports.…”

Section: Discussionmentioning

confidence: 69%

“…Previous investigators have noted similar skewness toward higher values in size-frequency distributions based on cell volume, width, and cross-sectional area in various species, including man (5,15,19,32,36). Some investigators have attempted to define the changes in size-frequency distribution with cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 87%

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Change in cardiac myocyte size distribution in aortic-constricted neonatal rats

1989

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Regional changes in cardiac myocyte size and population distribution were examined in Sprague Dawley rats receiving an abdominal aortic constriction at five days of age. At specific time intervals post-constriction, hearts were recovered from constricted animals and weight-matched controls and isolated myocytes were obtained from right and left ventricles using retrograde coronary perfusion with collagenase. Cell volume and cardiac myocyte population distribution curves were determined using a Coulter Channelyzer system. Cell length was measured directly using a Bioquant Image Analysis system. Myocyte cross-sectional area was calculated from cell volume/length. By three months of age, heart weight and heart weight-body weight ratio in constricted animals had increased by approximately 115% (p less than 0.001) in females and 85% (p less than 0.001) in males compared to controls. Between 15 and 90 days of age, the growth response, as indicated by increased cell volume, was approximately 4x greater in constricted females and 2.5x greater in constricted males compared to corresponding controls. This increase was manifested by a shift in the mean size of the myocyte population to the right and a substantial widening of the distribution. Most of the enlargement was due to increased cross-sectional area, with only a moderate contribution from increased cell length. Significant increases in size were seen in both left and right ventricles. By three months of age, a significant interaction was apparent between aortic constriction and sex. The capacity for hypertrophy was greater in the smaller myocytes in female rats of similar age compared to males. The final degree of hypertrophy was similar for male and female rats, possibly indicating a critical upper limit in cell size for cardiac myocytes.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 69%

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Change in cardiac myocyte size distribution in aortic-constricted neonatal rats

1989

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“…In addition, possible differences in mechanical history between trabeculae or papillary muscles and myocardium in the heart wall could affect interpretation of mechanical perturbations in culture since the in vivo mechanical state forms the baseline for these perturbations. However, measurements of papillary muscle mechanics in situ show shortening patterns very similar to midwall circumferential shortening (20), and both papillary muscles (1) and trabeculae (9) have been shown to hypertrophy during in vivo hemodynamic overload.…”

Section: Discussionmentioning

confidence: 99%

Isometric contraction induces rapid myocyte remodeling in cultured rat right ventricular papillary muscles

Guterl¹,

Haggart²,

Janssen³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Guterl KA, Haggart CR, Janssen PM, Holmes JW. Isometric contraction induces rapid myocyte remodeling in cultured rat right ventricular papillary muscles. Am J Physiol Heart Circ Physiol 293: H3707-H3712, 2007. First published October 5, 2007; doi:10.1152/ajpheart.00296.2007.-The hypothesis that elevated systolic stress induces myocyte thickening has been difficult to test directly. We tested this hypothesis in working rat right ventricular papillary muscles using a recently developed technique for long-term muscle culture. Muscles were cultured for 36 h either isometrically at different levels of systolic stress or at physiological amounts and rates of shortening. Isometric contraction induced rapid increases in myocyte diameter regardless of the level of systolic stress, whereas control myocyte dimensions were maintained if physiological amounts and rates of systolic shortening were imposed. Myocyte thickening was accompanied by a significant decrease in cell length and number of sarcomeres in series along the long axis of the myocyte, suggesting that thickening may have occurred in part by rearrangement of existing sarcomeres. We conclude that the pattern of systolic shortening and/or diastolic lengthening regulates myocyte shape in working rat right ventricular papillary muscles, whereas systolic stress plays little or no role. hypertrophy; pressure overload; volume overload; myocyte size; myocyte shape THIRTY YEARS AGO, Grossman et al. (8) articulated the hypothesis that systolic stress regulates parallel addition of sarcomeres in ventricular myocytes. In that study, Grossman et al. found that, in patients with long-standing hypertension, left ventricular wall thickness increased just enough to balance the elevated ventricular pressure and produce normal calculated systolic wall stress values. They proposed that elevated systolic wall stress might drive a parallel addition of sarcomeres, leading to myocyte and wall thickening that reduced wall stress in a classic negative feedback loop (8).Although this elegant and attractive hypothesis has been widely accepted, it has proved remarkably difficult to test directly. In vitro stretching of cultured myocytes has produced a wealth of information on the molecular pathways involved in cardiac hypertrophy (3,21,22,24), but the relatively unphysiological nature of this preparation has limited its value for exploration of the role of specific mechanical signals in regulating hypertrophy. In vivo models of hemodynamic overload alter not only mechanics but also the levels of hormones such as norepinephrine and angiotensin that can independently stimulate hypertrophy. Attempts to separate hormonal from mechanical effects using pharmacological blockers have produced mixed results (18). Finally, many of the mechanical signals that have been proposed as stimuli for hypertrophy covary in vivo. For example, pressure overload not only increases wall stress but also decreases stroke volume and related variables such as the amount and rate of systolic shortening (10).We used a...

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“…In the presence of heart disease, myocardial fibers grow in width and length as sarcomeres and other cell constituents accrue in parallel and series, respectively (10). During hypertrophic growth the connective tissue network surrounding bundles of myocytes and the network's lateral connections with myocardial fibers thicken (4,5,21) and fiber orientation differs from normal (19).…”

Section: Discussionmentioning

confidence: 99%

Isotonic muscle and sarcomere shortening in rabbit right ventricular preparations

Hamrell

Hultgren

1989

Basic Res Cardiol

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Cardiac muscle fibers are suspended within and attached to an elaborate connective tissue matrix that includes numerous compliant interconnections. Myocardial muscle fibers are not branched, but connect at small angles to each other to form a branched array. Therefore, fiber shortening occurs as a vector within a connective tissue framework and individual fiber work may exceed external muscle work. To evaluate the latter we measured isotonic muscle shortening simultaneous with sarcomere shortening. The hearts were obtained from rabbits (n = 4) anesthetized with intravenous pentobarbital sodium. We isolated right ventricular trabeculae or free wall papillary muscles in Krebs-Ringer's solution (2.5 mM Ca2+, 28 degrees C). Cross-sectional area was 0.038 +/- 0.003 mm2 (+/- SE throughout) and resting sarcomere length was 2.33 +/- 0.12 microns. Sarcomere length was measured with laser diffraction (He-Ne, lambda = 632.8 nm) during force clamps in single- and paired-stimulation twitches. Relative sarcomere shortening (delta SL) was isotonic sarcomere shortening divided by sarcomere length at the onset of isotonic shortening. Relative muscle shortening (delta ML) was isotonic muscle shortening divided by muscle length at zero load; the latter was estimated from the stress-strain relation of elastic recoil at the onset of load clamps. Average delta SL/delta ML at peak shortening was 3.38 +/- 0.16 and was independent of stimulus pattern, isotonic load, amount of shortening, time during a twitch or laser beam position along a muscle. Therefore, the ratio greater than 1 was neither a function of activation nor heterogeneous sarcomere length change.(ABSTRACT TRUNCATED AT 250 WORDS)

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Myocyte morphology of free wall trabeculae in right ventricular pressure overload hypertrophy in rabbits

Cited by 17 publications

References 37 publications

Change in cardiac myocyte size distribution in aortic-constricted neonatal rats

Change in cardiac myocyte size distribution in aortic-constricted neonatal rats

Isometric contraction induces rapid myocyte remodeling in cultured rat right ventricular papillary muscles

Isotonic muscle and sarcomere shortening in rabbit right ventricular preparations

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