Functional morphology of the pressure- and the volume-hypertrophied rat heart.

Lin, Hua; Katele, Kazimieras V.; Grimm, Arthur F.

doi:10.1161/01.res.41.6.830

Cited by 26 publications

(9 citation statements)

References 19 publications

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“…However, our work is in contrast to the results of Lin et al (1977) who have shown in the rat that apparently there are no regional dimensional differences 3 months after volume overloading by anemia. However, species differences, and the gradual onset of volume overload in this preparation, may account for this disparity.…”

Section: Discussioncontrasting

confidence: 99%

“…Fischl (1977) and Vokonas (1973) examined ventricular shape angiographically in patients with chronic aortic and mitral regurgitation and showed that eccentricity decreased compared to a control population, also suggesting a more globular heart with volume-overload lesions. In contrast, however, Lin et al (1977) demonstrated conflicting data in the volume-overloaded rat heart model produced by 3 months of a low iron diet resulting in significant anemia. They found essentially no difference in the ratio of the minor to major axis in volume-overloaded hearts compared to controls.…”

Section: Early Changes In Left Ventricular Regional Dimensions and Fumentioning

confidence: 99%

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Early changes in left ventricular regional dimensions and function during chronic volume overloading in the conscious dog.

Badke¹,

Covell²

1979

Circulation Research

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SUMMARY As the left ventricle dilates during chronic volume overloading, it assumes a more spherical configuration, suggesting a nonuniform regional myocardial response. Accordingly, we studied early alterations in left ventricular geometry and regional function induced by chronic volume overloading in the canine heart subjected to an aortocaval fistula. Nine mongrel dogs were instrumented with ultrasonic crystal pairs placed perpendicularly to the long axis to measure instantaneous segment lengths in the apical, midventricular, and basal portions of the left ventricle; another pair monitored an apical internal diameter. We obtained control measurements of end-diastolic dimensions and percent shortening in the conscious state. An aortocaval fistula was then constructed, resulting in an increase in resting end-diastolic pressure (EDP) from 11 ± 1 (SEM) to 22 ± 2 mm Hg and resting heart rate from 100 ± 4.9 to 131 ± S. O beats/min at 1 month (P < 0.01). At 10-20 days, mid-basal regional end-diastolic dimensions were significantly greater than control (8.8 ± 2.4% increase, P < 0.01), while there were no significant increases in apical dimensions when compared at the same EDP. However, by 20-40 days, all dimensions were significantly increased (11.4 ± 3.3% increase at the mid-base, P < 0.01), 7.8 ± 1.6% at the apex (P < 0.01), and 11.2 ± 4.5% at the diameter (P < 0.05). Regional function as measured by percent shortening at the same EDP exhibited early augmentation in all segments by 2 weeks compared to control (3.8 ± 1.3% increase at the diameter, 3.8 ± 1.9% at the base, 7.2 ± 2.2% at the middle, and 12.2 ± 4.7% at the apex, P < 0.05). Prom 4 to 6 weeks, however, function was not different from control, with a slight reduction in all regions from the peak values obtained at 2 weeks. We conclude that in the canine heart there are regional differences in the rate of left ventricular dilation to chronic volume overload, suggesting differential regional hypertrophy, with the earliest response at the mid-basal level. Furthermore, despite dilation, regional function is preserved or even augmented, although to varying degrees in each region. Circ Re* 45: 420-428, 1979 FOR many years, pathologists and clinicians have appreciated that the shape of the left ventricle is quite spherical late during the course of chronic volume overload (Kirch, 1920(Kirch, , 1930Grant, 1953). Since the normal heart is ellipsoidal in shape, this progressive change in geometry implies regional differences in the rate of left ventricular dilation and hypertrophy, the meaning and implications of which have been unclear. Since the geometry of the heart is an important determinant of ventricular wall stress, which in turn is an important determinant of ventricular performance and energy demands, such shape changes would appear to be key in the eventual adaptation of the heart to the volume overload. Attempts to quantify alterations in cardiac geometry have led to conflicting results, depending on the type of lesions and animal species examined. Ross ...

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Section: Discussioncontrasting

confidence: 99%

Section: Early Changes In Left Ventricular Regional Dimensions and Fumentioning

confidence: 99%

Early changes in left ventricular regional dimensions and function during chronic volume overloading in the conscious dog.

Badke¹,

Covell²

1979

Circulation Research

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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%

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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“…Though initially compensatory, this process may exhaust itself and consequently transition to a maladaptive course. magnetic resonance imaging; finite element modeling THE DISCRETE, PHYSIOLOGICAL states of hypertrophic remodeling (19,30) and congestive heart failure (13) have been well studied. The dynamic nature of the heart allows it the plasticity to progressively change structurally to accommodate an inciting stimulus in an attempt to maintain parameters, such as myocardial mass and cardiac output, within physiological ranges (3).…”

mentioning

confidence: 99%

Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation

Costandi¹,

Frank²,

McCulloch³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Although the physiological states of hypertrophic remodeling and congestive heart failure have been intensively studied, less is known about the transition from one to the other. The use of genetically engineered murine models of heart failure has proven valuable in characterizing the progression of remodeling and its ultimate decompensation to failure. Mice deficient in the cytoskeletal muscle LIM-only protein (MLP) are known to present with a clinical picture of dilated cardiomyopathy and transition to failure as adults. Longitudinal high-field magnetic resonance (MR) cardiac imaging provided a time course of remodeling where an improvement in ejection fraction and stroke volume (15- vs. 31-wk MLP(-/-) mice; P < 0.0001) was temporally concurrent with an abrupt phase of end-diastolic chamber dilatation. Hemodynamic analysis conducted throughout that dilatation phase showed improved ratio of maximum first derivative of pressure to end-diastolic pressure (dP/dt(max)/EDP; 15- vs. 31-wk MLP(-/-) mice; P < 0.0005), ratio of minimum first derivative of pressure to EDP (dP/dt(min)/EDP; 15- vs. 31-wk MLP(-/-) mice; P < 0.003), and developed pressure (15- vs. 31-wk MLP(-/-) mice; P < 0.0001) levels in the MLP(-/-) mice. Computational modeling techniques were used to estimate the EDP volume relationship, revealing that although MLP hearts possess a stiffer stress-strain relation, chamber compliance increased as a function of dilatation. This detailed physiological characterization during a phase of rapid anatomical remodeling suggests that systolic function in the MLP(-/-) mice may temporarily improve as a result of alterations in chamber compliance, which are mediated by dilatation. In turn, a balance may exist between exploiting the Frank-Starling mechanism and altering chamber compliance that maintains function in the absence of hypertrophic growth. Though initially compensatory, this process may exhaust itself and consequently transition to a maladaptive course.

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Functional morphology of the pressure- and the volume-hypertrophied rat heart.

Cited by 26 publications

References 19 publications

Early changes in left ventricular regional dimensions and function during chronic volume overloading in the conscious dog.

Early changes in left ventricular regional dimensions and function during chronic volume overloading in the conscious dog.

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

Role of diastolic properties in the transition to failure in a mouse model of the cardiac dilatation

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