At approximately half the normal life span of a number of mammals, including man, we have demonstrated an altered histochemistry of the media of the arteriolar wall; we have termed these """"""""old"""""""" arterioles. However, in old animals with revascularized tissue due to injury, the newly formed arterioles are """"""""young"""""""" but age subsequently.
The aims of this proposal are: (1) to define and quantitate the chemical (histochemical) and morphological changes in the smallest arteries and arterioles which occur simultaneously in aging; (2) to determine the time course (weeks/months) of the conversion of """"""""young' arterioles to """"""""old"""""""" arterioles in the revascularized tissue of injury of old animals """"""""accelerated aging""""""""; (3) to evaluate the relative roles of local environmental (tissue fluid) factors and/or genetic factors in the development of microvascular aging in such revascularized tissues; and (4) to quantify similarly the basal lamina thickening of capillaries and altered adjacent interstitium which are part of the microvascular aging complex. Tissues from various organs will be analyzed to obtain the necessary data from the various ages spanning the natural lifetime of the inbred albino rat. Studies of the revascularized (injured by incision) skin tissue will be in both the (old) donor and (young) recipient animal and the converse. The methods to be used are morphologic and physiologic: the former include histological, histochemical and electron microscopical, and employ quantitative analytic methods to obtain the various data by image scopical, and employ quantitative analytic methods to obtain the various data by image analysis techniques; the latter include microhemodynamics, capillary permeability and vasoactive responses. From these studies it is anticipated that this knowledge of the aging of the microvasculature may lead to further understanding of the alterations in blood flow, diffusion and exchange which may occur in aging. These studies should also provide a precisely defined control model for future research in microvascular aging.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
5R01HL042073-05
Application #
3360058
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1988-07-01
Project End
1991-06-30
Budget Start
1989-07-01
Budget End
1990-06-30
Support Year
5
Fiscal Year
1989
Total Cost
Indirect Cost
Name
Los Angeles County-University of S Cal Medical Center
Department
Type
DUNS #
City
Los Angeles
State
CA
Country
United States
Zip Code
90033
Sobin, S S; Bernick, S; Ballard, K W (1992) Acute wound repair in an aged animal: a model for accelerated aging of the microvasculature? J Gerontol 47:B121-5
Jiang, H X; Chen, P C; Sobin, S S et al. (1992) Age related alterations in the response of the pial arterioles to adenosine in the rat. Mech Ageing Dev 65:257-76
Sobin, S S; Bernick, S; Ballard, K W (1992) Histochemical characterization of the aging microvasculature in the human and other mammalian and non-mammalian vertebrates by the periodic acid-Schiff reaction. Mech Ageing Dev 63:183-92
Netto, D J; Chen, P C; Sobin, S S et al. (1991) Demonstration of uniform capillary basal lamina thickness by computer technology. Ann Biomed Eng 19:209-17