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Biomedical subjects

P Anversa

Publications and source records attributed to P Anversa.

At least 181 records · Page 10Linked to original sources
PubMed1988

Cellular basis of wall remodeling in long-term pressure overload-induced right ventricular hypertrophy in rats.

To determine the effects of long-term pressure overload on the structural mechanisms implicated in wall remodeling of the right ventricle, a mild pulmonary artery banding was applied to rats approximately 2 months old, and the animals were killed 150 days later. The surgical procedure resulted in a 60% reduction in the cross-sectional area of the constricted vessel and a 52% increase in the weight of the right ventricle. The hypertrophic myocardial response was associated with an elevation in right ventricular systolic pressure (from 33 +/- 11 mm Hg to 71 +/- 12 mm Hg), right ventricular end-diastolic pressure (from 3 +/- 1 mm Hg to 10 +/- 3 mm Hg), and central venous pressure (from 2 +/- 0.2 mm Hg to 10 +/- 3 mm Hg). The 76% increase in wall thickness after pulmonary artery stenosis was the result of a 24% lateral expansion of cardiac muscle cells and a 44% increase in the number of myocytes across the ventricular wall. The intermyocyte distance was also increased by 22%. These cellular adaptations occurred with no alterations in total myocyte length, average sarcomere length, and volume composition of the myocardium. Ventricular wall area was decreased by 14%, which suggests a small reduction in chamber volume. Myocyte growth was accompanied by proportional expansions of mitochondrial and myofibrillar components, so that the ratio of mitochondria to myofibrils in the cytoplasm remained essentially constant. In conclusion, ventricular remodeling in this model of chronic pressure hypertrophy is characterized by increases in cellular diameter and number that would both tend to decrease the magnitude of systolic and diastolic stresses on a per cell basis and thus improve the myocardial response to a prolonged and sustained mechanical load.

Animals↗
PubMed1987

Coronary artery spasm: involvement of small intramyocardial branches.

A study was conducted to determine if the small (resistance) vessels of the coronary circulation could undergo spasm comparable to that of the major conductance (epicardial) arteries which in the rat measure 275-300 micron in diameter. This information may be relevant to the growing evidence of ischemic myocardial disease without significant coronary atherosclerosis or even spasm of the larger vessels. Vascular corrosion casts of the coronary circulation were prepared in the rat 20 min after intravenous injection of arginine vasopressin, a powerful coronary constrictor substance, under continuous electrocardiographic monitoring. Electrocardiographic changes observed consisted of S-T segment elevation and conduction disturbances, implying ischemic effects on the myocardium. Corrosion casts revealed spasm of smaller arteries only (50-150 micron diameter). Controls (vehicle-injected or untreated) showed no abnormalities of the coronary vasculature. These results suggest that myocardial vessels of this size are comparable in their potential for spasm to the large conductance arteries. Similar findings in patients involving smaller vessels could explain ischemic myocardial events in the absence of significant spasm, or organic stenosing pathology of major coronary arteries. As a corollary, it is suggested that the term "coronary artery spasm" could be enlarged in its definition to include other levels of the coronary circulation rather than that of the large conductance arteries alone.

Animals↗
PubMed1987

Increased incidence of isoproterenol-induced ventricular fibrillation in aging rats.

Prolonged beta-adrenergic stimulation obtained by subcutaneous injection of isoproterenol in unanesthetized, unrestrained rats elicited ventricular fibrillation in approximately 80% of animals at 10-12 months of age. Ventricular fibrillation failed to occur in 1-month-old rats and involved only 12% of rats at 2 months. Senescence appeared not to increase the frequency of ventricular fibrillation since a similar incidence was seen in rats at 10-12 and 19-21 months. In all instances, ventricular fibrillation was preceded by ECG changes consistent with acute subendocardial ischemia. To evaluate whether acute beta-adrenergic stimulation elicits comparable cardiovascular effects in animals of different age, a dose-response curve to intravenous injection of isoproterenol was performed in anesthetized rats. Changes in heart rate, systemic arterial pressure, left ventricular pressure, and dP/dt were not different among animal groups. It was concluded that the arrhythmogenic potential of isoproterenol may not be related to differences in cardiac beta-receptor sensitivity with age as suggested by the comparable changes in the inotropic and chronotropic actions of isoproterenol in the animal groups studied.

Aging↗
PubMed1987

Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic response was accompanied by a 41% increase in the total number of myocyte nuclei in the ventricle. Furthermore, average myocyte cell volume per nucleus increased by 28%. No changes in weight, myocyte size, and nuclear number were observed in the left ventricle. In conclusion, myocyte nuclear hyperplasia and cellular hypertrophy both participate to the adaptive response of the right ventricular myocardium in long-standing pressure overload cardiac hypertrophy.

Animals↗
PubMed1987

Effects of exercise on the capillary vasculature of the rat heart.

Effects on the myocardium, particularly those structural properties of the capillary network relevant to tissue oxygenation, were studied morphometrically in rats subjected to moderate exercise, strenuous exercise, and strenuous exercise preceded by a preconditioning period of moderate exercise. These different modalities of exercise were used to test the hypothesis that endurance training leads to capillary proliferation in the heart. The findings indicate that treadmill running produces right ventricular hypertrophy exclusively, which is accompanied by lengthening of the myocytes. Furthermore, a moderate running program results in an increase in the numerical density, luminal surface, and total length of capillaries in the right ventricle. In contrast, strenuous exercise with or without a preconditioning period produces a relative decrease in capillary luminal volume, surface, and numerical density. In the former case the diffusion distance for oxygen is decreased and in the latter it is increased. These data suggest that moderate exercise affects the microvasculature in ways that improve the efficiency of tissue oxygenation in the myocardium, whereas strenuous exercise has the opposite effect.

Adaptation, Physiological↗
PubMed1987

Spasm of small coronary arteries and ischemic myocardial injury induced by hypothalamic stimulation in the rat.

Electrical stimulation of the lateral hypothalamus resulted in electrocardiographic evidence of acute myocardial ischemia in 35% of normal adult rats under anesthesia. Mean arterial blood pressure was also elevated. Study of vascular corrosion casts disclosed that spasm of smaller branches of the coronary circulation, rather than the major epicardial arteries, was the main cause of the ischemic response. The histologic changes of the same experimental treatment in a separate group of animals revealed multiple focal areas of tissue damage throughout the myocardium, which were quantitatively assessed. The results may be relevant for the clinical problem of various forms of ischemic heart disease in which little evidence is found for organic (atherosclerosis) or dynamic (spasm) stenosis involving the major coronary arteries.

Animals↗
PubMed1986

Quantitative structural analysis of the myocardium during physiologic growth and induced cardiac hypertrophy: a review.

The quantitative structural properties of the ventricular myocardium during postnatal physiologic growth are compared with those accompanying an increased load in the adult rat heart to determine whether induced cardiac hypertrophy is a pathologic condition or simply a form of well compensated accelerated growth. The expansion of the ventricular myocardium during maturation shows a remarkable degree of well balanced compensatory response, because the capillary microvasculature, parenchymal cells and subcellular components of myocytes all grow in proportion to the increase in cardiac mass. In contrast, the increases in myocyte diameter and length caused by pressure hypertrophy, volume hypertrophy and infarction-induced hypertrophy are consistent with concentric, eccentric and a combination of concentric and eccentric hypertrophic growth of the whole ventricle, respectively. These cellular shape changes may represent a compensatory response of the myocardium at the cellular level of organization that tends to minimize the effects of an increased pressure or volume load, or both, on the heart. Cardiac hypertrophy, however, may also show alterations affecting capillary luminal volume and surface and the mitochondrial to myofibril volume ratio, which indicate an inadequate growth adaptation of the component structures responsible for tissue oxygenation and energy production. Thus, hypertrophy of the adult heart differs from that during physiologic growth, and the hypertrophied myocardium may exhibit structural abnormalities that can be expected to increase its vulnerability to ischemia.

Blood Pressure↗
PubMed1986

Myocyte cell loss and myocyte hypertrophy in the aging rat heart.

To determine the effects of age on the myocardium, the functional and structural characteristics of the heart were studied in rats at 3, 10 to 12 and 19 to 21 months of age. Systemic arterial pressure, left ventricular pressure and its first derivative (dP/dt) and heart rate were comparable in the three animal groups. In the interval between 3 and 10 to 12 months, mean myocyte cell volume per nucleus increased 53 and 26% in the left and the right ventricle, respectively. The total number of myocyte nuclei remained constant in either ventricle. In the following period, between 10 to 12 and 19 to 21 months, a 39% further cellular hypertrophy on the left side of the heart was found in association with an 18% loss of cells in the ventricle. Cell loss was accompanied by discrete areas of interstitial and replacement fibrosis in the subendocardium. In contrast, no myocardial damage was observed in the right ventricle, and the measured 35% additional enlargement of myocytes occurred without a change in cell number. Thus, the aging left ventricle is composed of a smaller number of hypertrophied cells. Cellular hypertrophy may explain the unaltered cardiac function of the aged myocardium.

Aging↗
PubMed1986

Myocardial infarction in rats. Infarct size, myocyte hypertrophy, and capillary growth.

To determine the compensatory reserve capacity of the ventricular myocardium following infarction, the left coronary artery in rats was ligated, and the animals were killed 40 days later. Infarcts affecting an average 23% of the left ventricle were characterized by a 27% hypertrophic growth of the remaining myocardium that produced a complete replacement of the necrotic tissue. In contrast, infarcts with an average 50% loss of mass resulted in 83% expansion of the spared myocardium that was inadequate for a complete restoration of ventricular tissue. Myocyte hypertrophy was 26% and 78% in small and large infarcts, respectively. Cellular hypertrophy in both cases involved significant increases in myocyte transverse area and myocyte length. After large infarcts, there was an 18% reduction in capillary surface and a 16% increase in the diffusion distance. Corresponding values for small infarcts were -10% and 9%. These alterations combined with the deficient reconstitution of myocardial mass following large infarcts resulted in 25%, 29%, and 30% deficits in the absolute amounts of capillary lumen, surface, and length per ventricle respectively. Even with small infarcts, a deficit was seen in capillary luminal surface (-16%), and length (-19%). In conclusion, we have demonstrated that cardiac hypertrophy following myocardial infarction is consistent with cellular shape changes characteristic of a combination of concentric and eccentric hypertrophic growth. However, cardiac muscle cells appear to be unable to compensate for the loss of mass induced by a 50% infarct. The inadequate adaptation of the capillary vasculature in the infarcted hearts suggests that the injured ventricle is more vulnerable to additional ischemic episodes.

Animals↗
PubMed1986

Response of the border zone to myocardial infarction in rats.

The response of the surviving myocardium 30 days after coronary artery occlusion was measured morphometrically in the regions bordering and remote from infarcts of different sizes. Mean cell volume per nucleus increased with infarct size in both zones, but the rate of change was greater in the border than in the remote portion of the unaffected myocardium. Capillary numerical density within the uninjured tissue progressively decreased with infarct size leading to an increased diffusion distance for oxygen. Although the magnitude of changes in capillary density was similar in the two regions of the ventricle, the analysis of the individual values in each heart showed that in infarcts comprising more than 11% of the ventricular wall capillary concentration and the path length for oxygen supply to the myocytes were affected more in the border zone than in the myocardium remote from the scar. In conclusion, the border zone participates in the hypertrophic recovery process after infarction, but the inadequate growth of the capillary microvasculature suggests that this region is more susceptible to additional ischemic episodes.

Animals↗
PubMed1985

Effects of strenuous exercise on the quantitative morphology of left ventricular myocardium in the rat.

The adaptation of the structural components in the myocardium of the left ventricle to strenuous exercise was studied morphometrically in rats following a treadmill running program. The response of the left ventricle was evaluated separately in the interventricular septum and in the left ventricular free wall. Exercise produced a 24% growth of the septum without altering free wall volume. The hypertrophic expansion of the septum was characterized by a decrease in the volume fraction of capillary lumen in the myocardium (-20%), a reduction in the capillary luminal surface per unit volume of myocytes (-17%) and by an increase in the maximum distance from the capillary wall to the mitochondria of myocytes (9%). Although none of these changes were demonstrable on a statistical basis in the left ventricular free wall, similar results were obtained in the whole left ventricle by combining the data from the septum and free wall. Since the septum constitutes a functional unit with the free wall, it was concluded that the effect of excessive physical activity on the capillary parameters responsible for oxygen availability and diffusion could lead to a local reduction in the oxygenation potential of ventricular myocardium.

Animals↗
PubMed1985

Left ventricular failure induced by myocardial infarction. I. Myocyte hypertrophy.

To determine whether left ventricular failure after acute myocardial infarction is associated with a growth response of the myocytes that tends to compensate for the loss of muscle mass and function, the left coronary artery in rats was ligated near its origin, and the animals were killed 3 days later. Elevated left ventricular end-diastolic pressure and decreased first derivative of left ventricular pressure and systolic arterial pressure indicated significant impairment of ventricular function. Absolute infarct size, determined morphometrically by measurement of the fraction of myocyte nuclei lost, averaged 57%. Hypertrophy of surviving left ventricular myocytes was 28%, involving a 14% increase in cell length and a 6% increase in diameter. Right ventricular myocyte volume per nucleus increased 21% by a 10% enlargement of cellular diameter with no change in length. These results show on a cellular basis that myocardial hypertrophy in the left ventricle is accomplished by cellular shape changes characteristic of a combination of pressure and volume overload hypertrophy, whereas cellular growth in the right ventricle is consistent with pressure overload hypertrophy.

Animals↗
PubMed1985

Left ventricular failure induced by myocardial infarction. II. Tissue morphometry.

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.

Adenosine Triphosphate↗
PubMed1985

Myocardial response to infarction in the rat. Morphometric measurement of infarct size and myocyte cellular hypertrophy.

For determination of the effects of myocardial infarction on the recovery potential of muscle mass in the surviving tissue, ligation of the left coronary artery was performed in 3-month-old rats, and the infarcted ventricles were analyzed morphometrically a month after surgery. Comparisons were made with 4-month-old control rats that underwent sham operations and with 3-month-old control rats that were not operated upon for evaluation of the magnitude of infarct size and discrimination of the relative contribution of tissue growth that occurred in the surviving myocardium solely as a result of the change in age, from 3 to 4 months (postoperative tissue growth, or POTG), from the additional growth induced by infarction (hypertrophic growth, or HG). Coronary occlusion induced a 276-cu mm loss of ventricular tissue volume that corresponded to 43% of the total left ventricular mass, 648 cu mm. Over a 30-day period the remaining 372 cu mm of viable tissue expanded by 90% with an overall volume gain of 334 cu mm. This tissue augmentation consisted of 20% POTG, 67 cu mm, and 80% HG, 267 cu mm. Total myocyte volume increased 89%, from 302 cu mm to 571 cu mm, and average myocyte cell volume per nucleus increased 92%, from 16,500 cu mu to 31,600 cu mu. The expansion of the myocyte mass was the result of a 21% POTG and a 79% HG. Corresponding values for the myocyte population were 19% and 81%.

Age Factors↗
PubMed1984

Coronary artery spasm in the rat induced by hypothalamic stimulation.

Anesthetized rats were sterotaxically implanted with electrodes and electrically stimulated in the lateral hypothalamus. During elevation of the S-T segment on simultaneous precordial electrocardiograms, the heart was perfused with glutaraldehyde-paraformaldehyde fixative and the major coronary arteries prepared for morphometry of luminal dimensions. A similar procedure was performed in a second group receiving intravenous arginine vasopressin (AVP) in place of hypothalamic stimulation. Elevation of the S-T segment was present in these animals as well. Control animals were implanted, not stimulated and otherwise treated in the same way. Morphometry showed that reductions of mean luminal diameter and cross-sectional area of statistical significance occurred in the two experimental groups compared to controls, suggesting that coronary spasm was the cause of the elevated S-T segments. Pooled plasma from separate groups of implanted control and hypothalamically-stimulated animals revealed substantial elevation of AVP levels in the latter raising the possibility that the neuroendocrine was involved in eliciting coronary artery spasm.

Animals↗
PubMed1984

Structural compensatory mechanisms in rat heart in early spontaneous hypertension.

The response of the left ventricle (LV) during the development of spontaneous hypertension (SH) in rats was studied morphometrically at 21, 28, 35, and 45 days after birth and compared with that of normotensive (WK) controls. LV hypertrophy, varying from 24 to 27%, was characterized by the preservation of the volume fraction of capillary lumen and capillary luminal surface in the myocardium, as a result of capillary proliferation. From 21 to 45 days the number of capillaries per unit area of myocardium increased 68% in SH rats by the insertion in parallel of new capillary elements among the myocytes. This estimation was obtained by correcting the value of capillary density at 45 days for the amount of spreading produced by myocyte growth during this interval. On a similar basis capillary proliferation was only 24% in WK rats. Myocyte growth in experimental animals (151%) was achieved by a 77% enlargement in myocyte cross-sectional area (MCSA) and by a 42% lengthening of the cells. In controls myocyte expansion (124%) was the result of comparable increments in MCSA (47%) and myocyte length (53%).

Aging↗
PubMed1984

Morphometry of right ventricular hypertrophy induced by myocardial infarction in the rat.

The growth response of the right ventricle was studied in rats following ligation of the left coronary artery, which produced infarcts comprising approximately 40% of the left ventricle. A month after surgery the weight of the right ventricle was increased 30%, and this hypertrophic change was characterized by a 17% wall thickening, consistent with the 13% greater diameter of myocytes. Myocardial hypertrophy was accompanied by an inadequate growth of the microvasculature that supports tissue oxygenation. This was seen by relative decreases in capillary luminal volume density (-27%) and capillary luminal surface density (-21%) and by an increase in the average maximum distance from the capillary wall to the mitochondria of myocytes (19%). In contrast, measurements of the mean myocyte volume per nucleus showed a proportional enlargement of these cells (32%), from 16,300 cu mu in control animals to 21,500 cu mu in experimental rats. Quantitative analysis of the right coronary artery revealed a 33% increase in its luminal area, commensurate with the magnitude of ventricular hypertrophy.

Animals↗