Aging changes of the angioarchitecture and arterial morphology of the spinal cord in rats.

BACKGROUND: It is well known that vascular myelopathy increases with age, however, there are no systematic reports on the quantitative capillary density in the spinal cord and no reports concerning the age-related changes of vascularity and capillary density of the spinal cord. OBJECTIVE: Age-related changes of vascularity and capillary density of the spinal cord and the morphology of the ventral spinal artery were observed and measured so as to provide reference to study the microcirculation of the spinal cord. METHODS: Three different age groups of Wistar rats (1-2, 6-7 and >22 months old) were studied by ink-gelatin injection, corrosion casts, biological stereological technique, image analysis and transmission electron microscope. RESULTS: The number of central arteries per centimeter of the spinal cord decreased significantly with age; the ventral spinal artery and central arteries often became tortuous in the >22 month group. Capillary density in the anterior horn was significantly higher than that in the posterior horn. Capillary density in the gray matter decreased significantly with age. These aging changes of the ventral spinal artery in the rat included that the folds of internal elastic membrane were reduced, the internal elastic membrane thinned and disrupted, the endothelial cells degenerated and broke away from the wall, and smooth muscle cells in the tunica media degenerated and protruded to the lumen. The relative content of the elastic fibers decreased significantly with age, while the relative content of the collagenic fibers and the ratio of the C/E increased significantly with age. CONCLUSIONS: The difference between capillary density in gray and white matter in the spinal cord has shown that the need of metabolization is adapted to the function of the neurons, and the anterior horn is more sensitive than the posterior horn to anoxia and is easily damaged during ischemia in the spinal cord. Aging changes of capillary density and arterial morphology of the spinal cord may be important contributory factors in vascular myelopathy.

Low shear stress regulates monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha dependent pathway.

In regions of a vessel that experience low shear stress and reversing flow patterns, early features in the pathogenesis of atherosclerosis include the accumulation of oxidized LDL (OxLDL) and adhesion of monocytes to endothelial cells (EC). Here we investigated the hypothesis that low shear stress (2 dyn/cm2) and OxLDL are synergistic for enhanced expression of vascular cell adhesion molecule (VCAM-1) and human aortic endothelial cell (HAEC)-monocyte adhesion. This study shows low shear stress can significantly reduce IkappaBalpha levels, activate NF-kappaB, increase the expression of VCAM-1 in HAEC and binding of monocytes. OxLDL itself cannot significantly increase the expression of VCAM-1 in HAEC and binding of monocytes, but through activation of NF-kappaB and degradation of IkappaBalpha induced by low shear stress it can significantly enhance VCAM-1 expression and monocyte adhesion, over that in unmodified LDL or control. These results suggest that low shear stress can regulate monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha-dependent pathway, and that low shear stress together with OxLDL may likely play an important role in atherogenesis.