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Biomedical subjects

P Anversa

Publications and source records attributed to P Anversa.

At least 199 records · Page 11Linked to original sources
PubMed1984

Glomerular permeability in acute hypertension.

Acute hypertension induced by intravenous infusion of angiotensin II (AII) leads to enhanced transglomerular passage of albumin and IgG, as demonstrated by electronmicroscopic immunoperoxidase techniques. Although no morphological damage of the capillary wall was detected, significant amounts of macromolecules were present in the mesangial region. On a functional basis, a 42% decrease in glomerular filtration rate and a 63% decline in p-aminohippurate clearance were seen, resulting in a 54% increase in the filtration fraction. Quantitative measurements of albumin and IgG2a clearances showed a 90- and 15-fold increase, respectively. Similarly, the concentration of native ferritin particles in the glomerular basement membrane (GBM) increased 11-fold. On the other hand, the number of cationized ferritin particles and the staining properties of GBM to colloidal iron were not altered. These observations indicate that acute AII-induced hypertension affects glomerular permeability to proteins of different size and shape, possibly by increasing the pore size of the glomerular filter by either high intracapillary pressure and/or a direct action of AII on GBM constituents.

Albumins↗
PubMed1984

Morphometry of right and left ventricular myocardium after strenuous exercise in preconditioned rats.

Young male rats were exposed to a biphasic training program in which a 7-week preconditioning period of moderate treadmill exercise was followed by 8 weeks of strenuous endurance running. In comparison with sedentary control animals, the trained rats at 20 weeks of age had developed myocardial hypertrophy of the right ventricle (20%) and interventricular septum (23%), but there was no difference in the weight of the left ventricular free wall. Myocyte hypertrophy (26%) in the right ventricle was achieved through an increase in mean cell length (24%) and the addition of new sarcomere units in series. Exercise induced no acceleration of capillary growth in either ventricle, leading to significant decreases in the capillary luminal volume density (-21%) and surface density (-16%) in the right ventricle. Such alterations in the structural properties of the microvasculature implicated in oxygen availability and diffusion suggest that vigorous exercise, even after a preconditioning period, may still be detrimental to the myocardium. The techniques of myocardial morphometry were examined with respect to potential errors associated with oblique tissue sections and the use of light versus electron microscopy for cell counting. It was shown that the practical effects of obliquity are negligible and that electron microscopic resolution is essential.

Animals↗
PubMed1983

Morphometry of exercise-induced right ventricular hypertrophy in the rat.

In our morphometric study of the effects of exercise on the heart, male Wistar-Kyoto rats at 5 weeks of age were subjected daily to a moderate treadmill running program that lasted for 7 weeks. The heart responded to physical conditioning by different magnitudes of tissue growth of the right (22%) and left (7%) ventricular myocardium, the latter change not statistically significant. The increase in right ventricular volume was associated with a 25% enlargement of ventricular area, a 26% average lengthening of the myocytes, and no change in sarcomere length and in ventricular midwall thickness. Exercise produced significant alterations in the quantitative parameters of the microvasculature of the right ventricle, but no appreciable changes in the left ventricle. Right ventricular hypertrophy was characterized by an absolute 44% growth of the endothelial luminal surface brought about through a 16% increase in capillary numerical density, and a 41% augmentation of the total length of the capillary network. Maximum diffusion distance from the capillary wall to the mitochondria of myocytes decreased 10% as a result of capillary proliferation and the lack of lateral expansion of myocyte cross-sectional area. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria:myofibrils volume ratio, indicating a growth of these components proportional to each other and to the growth of the myocyte population as a whole. It was concluded that, as a result of running exercise, right ventricular growth is analogous to eccentric hypertrophy in which the structural adaptations of the capillary bed can be expected to improve the diffusion and transport of oxygen within the tissue.

Animals↗
PubMed1983

Morphometric measurement of cellular hypertrophy.

This study is a comparison of two morphometric methods for measuring mean cellular hypertrophy. One method, based on the relatively simple point-counting technique used to determine nuclear to cytoplasmic ratios, measures increases in mean cell volume per nuclear volume. The second method, involving nuclear profile counting in tissue sections of different known thicknesses, evaluates the increase in mean cell volume per nucleus. The latter method is considered more accurate because of the significantly greater amount of tissue sampling utilized. Furthermore, cellular hypertrophy is better defined by the increase in cell size per nucleus than by a change in the cell to nucleus volume ratio, values that can be numerically equal only if mean nuclear volume remains constant. Thus, comparison of these methods is a way to evaluate either the reliability of the point-counting technique or the equivalent hypothesis that mean nuclear volumes do not vary significantly during periods of growth. Cellular hypertrophy has been measured in 18 examples of normal tissue growth and 18 examples of induced growth. Five cell types are included: cardiac myocytes, aortic smooth muscle cells, capillary endothelium, and glomerular mesangial and epithelial cells. Little agreement was found between the two methods of measurement. Mean nuclear hypertrophy varied widely and unpredictably, more than +/- 20% in the majority of cell populations. It is concluded that the point-counting method alone is unreliable as a quantitative measure of cellular hypertrophy.

Animals↗
PubMed1982

Endothelial morphology and plasma total and high density lipoprotein cholesterol changes in hypothalamically stimulated squirrel monkeys fed a modified atherogenic diet.

Experimental animals fed atherogenic diets show endothelial damage, impairment of endothelial regeneration and plasma lipid changes characterized by elevation of LDL and decrease of HDL cholesterol concentrations. Previous studies in this laboratory disclosed that chronic electrical stimulation of the lateral hypothalamus was associated with electron-microscopic evidence of endothelial injury in rats and squirrel monkeys maintained on basal (low fat/cholesterol-free) diets. In the present investigation squirrel monkeys fed similar diets supplemented with "modest" amounts of caloric fat and cholesterol were subjected to chronic lateral hypothalamic stimulation for periods as long as 20 months with the expectation that endothelial injury would be greater than in the absence of the supplements. The expectations were not substantiated. Endothelium was found to be surprisingly intact by electron microscopy and similar to that of implanted nonstimulated controls. A further observation of interest was the cholesterolemic response, notably in the HDL fraction, observed in both groups, but more striking in experimental animals. The data suggest that an interaction between a modified lipid/cholesterol diet and hypothalamic stimulation may lead to elevation of plasma HDL cholesterol concentration and preservation of endothelial integrity. Further investigation is required to determine whether these two events are causally related.

Animals↗
PubMed1982

Morphometry of right ventricular hypertrophy induced by strenuous exercise in rat.

Effects on the myocardium, particularly those structural properties of the capillary network relevant to tissue oxygenation, were studied morphometrically in rats subjected to a severe running program. Physical conditioning produced a 31% increase in right ventricular weight and only a 12% increase in the weight of the left ventricle. Quantitative analysis of right ventricular myocardium demonstrated relative decreases in capillary luminal volume density (-27%) and capillary luminal surface density (-20%) and an increase in the average maximum distance from the capillary wall to the mitochondria of myocytes (14%). In contrast, the contractile mass expanded in proportion to the growth of the ventricle through augmentation of the cross-sectional area (17%) and length (19%) of the average myocyte. Evaluation of the subcellular constituents of myocytes showed no change in the mitochondria-to-myofibril volume ratio. In conclusion, the capillary bed controlling oxygen availability, diffusion, and transport suggests that excessive physical activity may be detrimental to the myocardium.

Animals↗
PubMed1982

Quantitative structural changes of the rat thoracic aorta in early spontaneous hypertension. Tissue composition, and hypertrophy and hyperplasia of smooth muscle cells.

The thoracic aorta of 21-, 28-, 35-, and 45-day-old spontaneously hypertensive (SH) and Wistar Kyoto (WK) rats was analyzed morphometrically to evaluate the cellular hypertrophy and proliferation of medial smooth muscle cells during the development of genetically determined hypertension. The absolute increase in volume of collagen and ground substance, and elastic tissue was also measured. In SH animals, cellular hypertrophy was found to be the dominant mechanism of muscle growth in the 21- to 28-day and 35- to 45-day intervals, resulting in an overall 68% enlargement of the mean cell volume from 21 to 45 days. The total number of smooth muscle cells increased only 21% (not statistically significant) and the tendency toward hyperplasia was restricted to the 28- to 35-day period. Normotensive controls showed cell proliferation mainly from 21 to 28 days and cellular hypertrophy from 35 to 45 days with an absolute 33% increase in the number of cells and a 26% larger volume of the mean smooth muscle cell at 45 days of age. from 21 to 45 days, the above changes in cell size and number provoked an overall 104% and 67% growth of the muscle mass in SH and WK rats, respectively. The initial response phase of spontaneous hypertension was also characterized by an increase of collagen and ground substance, 184%, which was slightly greater than that of the elastic component, 168%. Changes in mural concentration of fibrous proteins that were similar to but of less magnitude than those of controls, were seen. These results demonstrate that short-term spontaneous hypertension determines a simultaneous growth adaptation in every component structure of the media of the thoracic aorta leading to a disproportionate accumulation of scleroproteins that markedly exceeds that of the contractile component of the vessel wall. At a cellular level, smooth muscle cell hypertrophy is the prevailing process that underlies the tissue response of the aorta in early hypertension.

Aging↗
PubMed1981

Effect of hypothalamic stimulation on the endothelial morphology of the aorta in the conscious squirrel monkey.

The role of neurogenic factors in the development of atherosclerosis has not previously been studied in detail. In recent years evidence has accumulated to implicate endothelial injury as a primary stimulus for the proliferation of myo-intimal cells resulting in the formation of the early morphologic lesion. In the present investigation, the effect on aortic endothelial morphology of repetitive electrical stimulation of the lateral hypothalamus in the conscious, unrestrained squirrel monkey, maintained on a cholesterol-free low-fat diet, has been studied. Stimulation was performed with a self-powered, miniaturized electronic stimulator connected to indwelling electrodes. Implanted nonstimulated animals served as controls. Endothelial injury in the form of cell degeneration, denudation, with plasma insudation and partial junctional separation were observed electron-microscopically in stimulated animals compared with controls. These alterations were found to be independent of hypercholesterolemia and/or hypertension. Possible pathways for the induction of injury in this neurogenic model are: (1) direct, through neural circuits from the brain to the vessel wall, and (2) indirect, by elaboration of angiopathic substances inside or outside of the CNS, released into the circulation and transported to the vessel wall where they exert their effects. Reversibility of the endothelial injury progression to established lesions and mechanisms involved remain to be determined in further investigations.

Animals↗
PubMed1981

Postnatal development of the M-band in rat cardiac myofibrils.

Cardiac muscle fibers in rats at 1 and 5 days after birth showed little evidence of M-bands. An ultrastructural analysis of myofibrils failed to demonstrate dense M-band material in longitudinal sections or M-bridges in transverse sections of sarcomeres. M-bands began to increase in number after 5 days of postnatal life and were present in 60% of all sarcomeres at 11 days of age. Polypeptides with molecular weights of 190,000 (Ma) and 175,000 (Mb) were obtained by polyacrylamide-sodium dodecyl sulfate (SDS) gel electrophoresis of myofibril preparations. These two proteins were found in both 1- and 11-day-old rats and were considered to be specific components of the M-band. The densitometric analysis demonstrated that Ma and mb polypeptides increased approximately 2-fold during the interval from 1 to 11 days after birth. These structural and biochemical changes of the M-band material in myocytes appear to be related to the maturation of contractile function in the young heart.

Animals↗
PubMed1980

Morphometry of the renal corpuscle during postnatal growth and compensatory hypertrophy.

Morphometry was used to measure the growth changes in renal corpuscle and glomerular size and composition in outer, middle, and inner cortical layers during postnatal development in normal and mononephrectomized rats. Glomerular growth was 4.16-fold in normal rats and 6.12-fold after nephrectomy. The cell populations in glomeruli showed distinctly different growth patterns. Cellular hypertrophy and hyperplasia during normal growth were 2.72 and 1.52 for epithelial cells, 0.93 and 3.70 for endothelial cells, and 1.28 and 2.65 for mesangial cells; corresponding values during stimulated growth were 2.75 and 1.92, 1.19 and 4.11, and 1.65 and 3.09. A linear transcortical gradient of corpuscle diameters was found in young animals and normal adults, with the mean volume of juxtamedullary renal corpuscles two times greater than that of subcapsular corpuscles in all animal groups. Despite their size variation, a striking transcortical uniformity was evident in the composition of glomeruli in each group with respect to the volume fractions and mean cell volume in each cell population, the volume and surface density of basement membrane, the volume and length density of capillary loops, the volume fraction of mesangial matrix, and the division of basement membrane into peripheral and axial portions.

Animals↗
PubMed1980

Morphometric study of early postnatal development of the thoracic aorta in the rat.

Tissue, cellular, and subcellular morphometry of the thoracic aorta in 1-, 5- and 11-day-old rats was used to quantify the cellular hypertrophy and proliferation of smooth muscle cells and the absolute increases in volume of elastic laminase and collagen during the early postnatal period. In the 1- to 5-day interval, total wall volume increased 2.9-fold, wall thickness and the number of smooth muscle cells doubled, mean cell volume increased by 40%, and the volumes of elastic laminae and collagen increased 3.7- and 3.3-fold, respectively. From 5 to 11 days, circumferential growth of the aortic wall, without further thickening, produced smaller and unequal growth increments of each of its component structures, with increases in collagen (3.2-fold) > elastic laminae (2.3-fold) > muscle cells (1.6-fold). In the overall growth of smooth muscle cells (4.6-fold) from 1 to 11 days, only the cytoplasmic volume fractions of glycogen aggregates and rough endoplasmic reticulum were altered significantly (-76%, +32%). Certain aspects of normal postnatal aortic growth paralleled the response of adult aorta to experimentally induced hypertension.

Animals↗
PubMed1980

Morphometry of medial hypertrophy in the rat thoracic aorta.

Surgical constriction of the subdiaphragmatic aorta in young adult male rats induced a 54 per cent hypertrophy (39 per cent thickening) of the wall of the thoracic aorta in 8 days, with no increase in the number of elastic lamellae. Morphometric analysis of the aorta wall showed volume increases of its component smooth muscle cells (57 per cent) elastic laminae (30 per cent), collagen (136 per cent), and endothelium plus subendothelial space (40 per cent). Mean cell volume of smooth muscle cells increased 55 per cent from 272 +/- 11 to 421 +/- 21 cu. mum. (p less than 0.005). The number of smooth muscle cells per centimeter of length of thoracic aorta was 4.2 +/- 0.3 x 10(6) in both control and experimental animals. Thus, aortic medial hypertrophy following aortic stenosis included enlargement but no proliferation of smooth muscle cells. Absolute volume increases in the average smooth muscle cell included the nucleus (27 per cent), myofilaments (47 per cent), mitochondria (62 per cent), rough endoplasmic reticulum (246 per cent), smooth endoplasmic reticulum (23 per cent), and caveolae (37 per cent).

Animals↗