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Biomedical subjects

P Anversa

Publications and source records attributed to P Anversa.

232 records · Page 13Linked to original sources
PubMedDate not supplied

Connective tissue accumulation in the left coronary artery of young SHR.

The left coronary artery of 21-, 28-, and 45-day-old spontaneously hypertensive rats and Wistar-Kyoto rats was analyzed morphometrically to evaluate the structural alterations of the vessel wall during the development of genetically determined hypertension. In 45-day-old rats, hypertension was associated with a significant expansion of the partial volume of collagen and ground substance (119%) within the arterial wall. This change exceeded the concurrent accumulation of elastin (77%) and smooth muscle cell mass (34%). The growth of the muscle compartment was also characterized by a marked increment of rough endoplasmic reticulum (103%). The increase in the mural concentration of fibrous proteins at this early age may be viewed as the initial adverse effect of hypertension on muscular arteries.

Aging↗
PubMedDate not supplied

Cardiomyocyte aging is gender-dependent: the local IGF-1-IGF-1R system.

To determine whether insulin-like growth factor 1 (IGF-1) and its receptor (IGF-1R) are implicated in the aging process of the heart, and if their impact differs in the two genders, the expression of IGF-1, and extracellular alpha-subunit and transmembrane beta-subunit of IGF-1R was measured in left ventricular myocytes isolated from male and female Fischer 344 rats at 3, 8, 12, 16, and 26 months after birth. Additionally, the extent of myocardial damage in both sexes was evaluated in rats at 3 and 26 months by confocal microscopy. Finally, ventricular hemodynamics was assessed in the closed-chest preparation. From 3 to 26 months, aging was characterized by an 83%, 84% decrease and disappearance in the quantity of IGF-1, IGF-1Ralpha and IGF-1Rbeta in male myocytes. Corresponding changes in female myocytes were 40%, 28% and 43%. These molecular modifications at the myocyte level were coupled with tissue injury, consisting of multiple foci of replacement fibrosis across the left ventricular wall. However, myocardial fibrosis in females was 76% and 77% significantly less than in the young and old male heart, respectively. These multiple age-associated events were accompanied by cardiac decompensation in the senescent male rat, while modest indices of ventricular dysfunction were detected in old female rats. In conclusion, the enhanced IGF-1-IGF-1R system in female myocytes may condition the favorable outcome of age in this gender.

Aging↗
PubMedDate not supplied

Coronary capillaries during normal and pathological growth.

The adaptive capacity of the myocardium with respect to its capillary concentration and distribution has been measured morphometrically during the hypertrophic growth occurring physologically after birth and as a result of induced overload in the adult. In particular, the growth of the capillary network of the left ventricle was examined in rats from one to 150 days of age and in rats with spontaneous hypertension, aortic stenosis, two-kidney one-clip renal hypertension and myocardial infarction. The following quantitative structural parameters of the capillary microvasculature were analyzed: 1. Capillary luminal volume density; 2. Capillary luminal surface density; 3. The average diffusion distance for oxygen; and 4. The aggregate capillary length in the whole ventricle. The major conclusions of the present study are: 1. The postnatal growth of the heart is characterized by lengthening of the whole capillary network that is linearly related to the aging process; 2. The rate of capillary proliferation, measured by changes in capillary density, is greater in the first month of age; 3. In contrast to postnatal development, lengthening of the capillary microvasculature is not a consistent adaptive mechanism of induced cardiac hypertrophy; 4. Capillary luminal volume and surface densities and the diffusion distance for oxygen are essentially maintained in spontaneous, mechanical and renal hypertension; and 5. Cardiac hypertrophy in acute and healed myocardial infarction results in alterations of the capillary properties implicated in tissue oxygenation that may constitute the morphological counterpart of the greater vulnerability to ischemic episodes of the hypertrophied myocardium after infarction.

Animals↗