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P Anversa

Publications and source records attributed to P Anversa.

10 recordsLinked to original sources
PubMed1978

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. I. Determination of myocyte size.

A method for determining the mean absolute volume of a specific population of cells within a tissue is described and applied to the measurement of endocardial and epicardial myocytes in the left ventricle of normal and hypertensive rats. The technique, based on nuclear counts per unit area in tissue slices of different known thicknesses, measures the mean cell volume per nucleus independent of previously unknown nuclear dimensions and systematic counting errors. Duplicate determinations, demonstrating reproducibility, were made in mutually perpendicular longitudinal and transverse sections of the myocardium. Combining these light microscopic measurements with electron microscopic data enabled the evaluation of the mean diameter and length of the cylindrical myocyte nuclei showing those in the epicardial cells to be significantly longer than the nuclei in endocardial cells. It was estimated that 2 to 4 per cent of ventricular myocytes are binucleate. After 1 to 4 weeks of hypertension, induced by constriction of the left renal artery, endocardial myocytes were enlarged 21 per cent, from 10,370 +/- 410 to 12,520 +/- 490 cu. micrometer., while epicardial myocytes showed a 37 per cent hypertrophy, from 12,600 +/- 1,600 to 17,300 +/- 1,100 cu. micrometer. The availability of a reliable determination of cell volume will make possible the interpretation of much biochemical, functional, and morphometric data at the whole cell level.

Animals↗
PubMed1978

Absolute morphometric study of myocardial hypertrophy in experimental hypertension. II. Ultrastructure of myocytes and interstitium.

The left ventricular myocardium of normal and hypertensive rats has been characterized morphometrically in the endocardial and epicardial zones. Compared to the epicardial regions, the normal endocardial regions contain 30 per cent more myocytes, 27 per cent less interstitial space, 48 per cent less capillary volume, 17 per cent less capillary surface, and the same capillary length per unit tissue volume. In terms of both the relative and absolute volumes and surface areas of their organelles, the cytoplasmic composition of normal endocardial and epicardial myocytes is nearly identical. After 14 weeks of hypertension, induced by constriction of the left renal artery, left ventricular weight is increased by 30 per cent, wall thickness by 42 per cent. The number of myocytes and the total length of capillaries remain constant. The epicardial region enlarged 37 per cent with proportional increases of myocyte and interstitial volumes. In contrast, the endocardial enlargement was only 26 per cent, comprised of 21 per cent hypertrophy of myocytes and a 55 per cent increase in interstitial components. Expansion of capillary lumina accounted for much of the interstitial enlargement throughout the myocardium. Hypertrophy of myocytes is 76 per cent greater in the epicardial region and is accompanied by a reduced mitochondria to myofibril ratio and disproportionately large increases (2- to 3-fold) in both smooth endoplasmic reticulum and T-system volume and surface area. On a cellular basis the absolute morphometric characteristics of myocytes from hypertensive rats are significantly different from normal, and significant differences occur between the inner and outer layers of the myocardium for practically every cytoplasmic component.

Animals↗
PubMed1977

Morphometry of the renal corpuscle during normal postnatal growth and compensatory hypertrophy. A light microscope study.

Renal corpuscles from the juxtamedullary and subcapsular regions of the renal cortex were morphometrically analyzed in young rats and in adult rats that had been unilaterally nephrectomized or sham-operated at an early age. Mean corpuscular volumes increased 4.5-fold during normal development, and 7.7-fold as a result of compensatory hypertrophy in both cortical regions. Relative and absolute volumes were determined for Bowman's space, the glomerular tuft, and five glomerular components: epithelial, endothelial, and mesangial cells, capillaries, and the filtration membrane. Normal and hypertrophic enlargement of Bowman's space was slightly greater than glomerular growth, and the growth response of subcapsular glomeruli was greater than that of juxtamedullary glomeruli. The ratio of mean glomerular volumes between outer and inner glomeruli was 1:2 in both adult groups. Both adult groups also developed nearly identical proportions of all glomerular component structures, representing a relative decrease of epithelial cells and increase of capillaries compared to the young animals. Normal and hypertrophic maturation involved absolute increases in all glomerular cell populations, the length of capillary loops and the surface area of the filtration membrane, all nearly in proportion to the respective four- and seven-fold increases in glomerular volume. Changes in the filtration surface area are consistent with published data for glomerular filtration rates in normal and hypertrophied kidneys. The mean cell size in epithelial and mesangial populations doubled during growth, but was not greater than normal in mononephrectomized rats. Hyperplasia among all populations of glomerular cells is indicated in normal growth, and to a greater extent in compensatory renal hypertrophy.

Aging↗
PubMed1976

Morphometry and autoradiography of early hypertrophic changes in the ventricular myocardium of adult rat: an electron microscopic study.

The ultrastructural composition of left ventricular myocardium and myocytes has been investigated at 20 hours after the surgical production of a subdiaphragmatic aortic stenosis in the adult rat. Morphometric analysis shows a 20% increase in the size of myocytes resulting principally from a 36% increase in mitochondrial volume and a 78% increase in the volumes occupied by smooth endoplasmic reticulum and matrix. Myofibrillar volume is increased only 4%. Measurements of the size and shape of individual mitochondria indicate that the augmentation of this compartment is wholly accountable by the enlargement of preexisting mitochondria. Quantitative autoradiographic analysis following a 2-hour pulse labeling with 3H-leucine shows that the rate of incorporation of newly synthesized proteins is practically uniform throughout all structural components of the sarcoplasm 18 to 20 hours after aortic banding. The conclusion is reached that this interval of hypertrophic response is a transition period characterized by an increasing rate of synthesis of contractile proteins overtaking a previously greater rate of mitochondrial synthesis.

Animals↗
PubMed1975

Morphometry and autoradiography of early hypertrophic changes in the ventricular myocardium of adult rat. A light microscopic study.

Quantitative autoradiographic localization of newly synthesized proteins was studied in the ventricular myocardium of adult rats 2 hours after the intravenous injection of 3H-leucine and 20 hours after the induction of hypertrophy by constriction of the abdominal aorta. Equal area samples of tissue from experimental and sham-operated controls were examined for differential grain counts and morphometric measurements by light microscopy. In comparison with control levels, the hypertrophic hearts show a 20 per cent increase in the average cross-sectional area of myocytes and a 43 per cent increase in the incorporation of amino acid into proteins. The higher concentration of labeled proteins is confined mainly to cardiac muscle cells, which show a 90 per cent increase in grain counts per cell cross-section, whereas no significant change is observed over the interstitium. A test of the specificity of the autoradiographic technique shows the expected reduction in tissue labeling following cycloheximide inhibition of protein synthesis, indicating that there is no significant amount of nonspecific binding of free amino acid during the paraformaldehyde-glutaraldehyde fixation procedure.

Amino Acids↗