The effects of aging and atherosclerosis on elastin of human aortas; quantitative analysis of elastin-content and SEM analysis of elastolysis

We have examined 24 human aortas aged 46 ~ 90 years obtained from autopsies. Most exhibited gross lesions of some degree on the lumenal surface. Using hot alkaline treatment (0.1 N NaOH) at 70 ~ 75degreeC for 5 hours, we extracted and quantitated elastin portions from the aortic wall in 3 different segments (UTA = upper thoracic aorta, LTA = lower thoracic aorta, AA = abdominal aorta). We have found UTA had 70.6% +/- 1.39 (SE), LTA 61.6% +/- 1.94 (SE), AA 49.2% +/- 1.84 (SE) elastin respectively based on wet weight. The differences between segments are statistically significant (p < 0.05, 0.025). However, there is no significant correlation between the age of the patients and the relative amounts of elastin in each segment. We have also observed the structure of elastin in the internal elastic lamina (IEL) and tunica media (TM) with SEM (scanning electron microscopy), and discovered that the IEL shows various forms of elastolysis-broken sheets, discontinuity, various sizes of lumps, vesicles, and possible newly formed elastin in the aortic lesions (Song and Roach submitted to YMJ). From these studies we conclude that elastin in the aortic wall remains well balanced quantitatively with age in spite of evidence suggesting vigorous degeneration and regeneration in the atherosclerotic lesions.

Surface features of human aortic atherosclerosis as seen with scanning electron microscopy

Using SEM, we have observed surface structures of atherosclerotic lesions of human aortas obtained from autopsies ranging from 59 to 84 years of age (5 males and 4 females). We have found four major interesting features on the lumenal surface of the aortas: 1) blood cells including leukocytes adhering to the endothelial surface, 2) a de-endothelialized surface showing both elastogenesis and elastolysis, 3) abundant cholesterol-ester crystals in extracellular spaces, and 4) cave-like structures possibly suggesting new capillarization in the thrombotic atherosclerotic plaques. We concluded that SEM has a great value in revealing more interesting surface structures if morphological studies are previously done in detail so that the characteristic shapes can be identified, and perhaps then meaningful interpretations can be made on the mechanism of human atherogenesis.

Morphological evidence of pulmonary vascular leakage through gaps observed with casting methods and S.E.M

We have used selective casting methods to separate pulmonary elastin from vascular elastin in the lungs of rabbits, dogs and pigs. The lungs are digested with 0.1 N NaOH at 75 degrees C for 24 approximately 48 hours with frequent turning as the lungs are filled with air to about 80% of the vital capacity prior to the casting which is done at pressure of 20 approximately 50 mmHg. After vascular injections, we saw many small globular bits of casting material well separated from cast vessels and lying in the pulmonary elastin. Surface forces should make the casting material creep along the vessels even if they are not completely filled, so that the spherical shape is the one expected if the case is extruded into the parenchymal space and the air space. We conclude that this suggests that the pulmonary circulation is partially and temporarily 'open' as seen in the spleen and some other organs, rather than a completely 'closed' one as is generally accepted. At least some of these extravasations may be associated with lymphatics, although we have not proved this.