scholarly journals Dimensional changes associated with freeze-drying of the internal elastic lamina from cerebral arteries

Scanning ◽  
1983 ◽  
Vol 5 (3) ◽  
pp. 137-142 ◽  
Author(s):  
G. J. Campbell ◽  
M. R. Roach
Keyword(s):  
Freeze Drying ◽  
Cerebral Arteries ◽  
Internal Elastic Lamina ◽  
Dimensional Changes ◽  
Elastic Lamina

The effects of eazymetic digestion on the elastic properties of Isolated human cereberal arteries

1977 ◽  
Vol 55 (2) ◽  
pp. 161-169 ◽  
Author(s):  
Leslie C. Damude ◽  
David A. Cope ◽  
Margot R. Roach
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Cerebral Arteries ◽  
Age Group ◽  
Internal Elastic Lamina ◽  
Solution Ph ◽  
Medial Region ◽  
Histological Studies ◽  
Elastic Lamina ◽  
Scanning Electron

Measurement of volume, pressure, and length were made on eight segments of human cerebral arteries perfused with chymotrypsin (CT) (EC 3.4.21.1) solution (pH = 7.8) for no more than 19 h, and on nine arterial segments perfused with combined enzyme (CT, trypsin (EC 3.4.21.4), elastase (EC 3.4.21.11)) solutions (pH = 7.8) for no more than 4 h. Circumferential tension–strain (and absolute radius) curves were obtained through the Law of Laplace (tension = pressure × radius). Initial and final elastances (tension/strain) were calculated after 0, 0.5, 1.0, 2.0, and 4.0 h of perfusion under the combined enzyme category, and after 0, 0.5, 1.0, 2.0, 4.0, 6.0, and 19.0 h of perfusion with CT. The initial elastance showed a significant increase (0.02 < p < 0.05) after about 6 h of perfusion. Increases in the final elastance became significant only after prolonged periods of perfusion with CT. Histological studies using light and scanning electron microscopy confirmed the removal of the elastic lamina as well as portions of the medial region. Fragmentation of the internal elastic lamina did not appear to affect the distensibility of major cerebral arteries in the 50- to 80-year-old age group.

Abstract T P419: Pathological Arterial Wall Correlates of Lumen-based Remodeling: Results From the Brain Arterial Remodeling Study

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jose Gutierrez ◽  
Mitchell S Elkind ◽  
James Goldman ◽  
Lawrence Honig ◽  
Susan Morgello ◽  
...  
Keyword(s):  
Vascular Disease ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Internal Elastic Lamina ◽  
Cross Sectional ◽  
Luminal Stenosis ◽  
The Media ◽  
The Relationship ◽  
The Brain ◽  
Elastic Lamina

Background: There is paucity of data about arterial wall characteristics of the smallest and largest caliber cerebral vessels. Determining the relationship between the lumen and the wall might shed new insights into cerebral artery remodeling. Objective: To test the hypotheses that arteries with larger luminal diameters have a thinner wall and that arteries with the smallest lumina have thicker walls. Methods: Cross-sectional segments from large arteries (N=1392) were obtained from the circle of Willis in 196 autopsied brains (mean age 55 ± 17 yrs, 39% with hypertension, 15% with diabetes and 20% with dyslipidemia). Lumen diameter, stenosis percentage, and thicknesses of intima, media, and adventitia were calculated in digital microphotography after staining. Atheromas and internal elastic lamina (IEL) disruption were rated visually. Arteries were categorized into the top 5% (“dilated”) and bottom 5% (“narrowed”) of the luminal diameters, as well as an intermediate category (90% of sample as reference). We used logistic regression to obtain the odds of association (OR, 95% CI) after adjusting for demographic and vascular variables. Results: Narrowed arteries were more frequently found in men (OR 2.7, 95%CI 1.3-5.9) and with dyslipidemia (4.2, 1.6-11.1) while dilated arteries were more frequently found in women (5.6, 2.2-14.0), in smokers (2.6, 1.0-6.5) and those with prior MI (7.7, 1.2-48.7). Narrowed arteries were more likely to have atheromas (20.8, 4.8-90.3), greater luminal stenosis (per %, 1.1, 1.1-1.2), thicker vessel walls (1.3, 1.2-1.4), but thinner medias (0.9, 0.8-1.0). Conversely, larger arteries exhibited less IEL disruption (0.3, 0.1-0.9), atheromas (0.34, 0.1-0.9) and stenosis (0.8, 0.8-0.9), their walls were thinner (0.8, 0.8-0.9) but the media was thicker (1.1, 1.1-1.2). Conclusions: Narrowed cerebral arteries were more likely to have atheromas while dilated arteries had thinner walls and were more frequent in subjects with prior MI. These findings suggest that both extremes of the arterial spectrum might be differentially related with vascular disease, underscoring the need to revisit whether standard preventive measures for vascular disease are equally effective in patients harboring such disparate arterial phenotypes.

Anchoring Fibrils in Arterial Endothelium

1969 ◽  
Vol 27 ◽  
pp. 274-275
Author(s):  
A. Trillo
Keyword(s):  
Carotid Arteries ◽  
Animal Species ◽  
Cell Layer ◽  
Present Communication ◽  
Internal Elastic Lamina ◽  
Endothelial Cell Layer ◽  
Structural Details ◽  
Rats And Mice ◽  
Arterial Endothelium ◽  
Elastic Lamina

There are conflicting reports regarding some fine structural details of arteries from several animal species. Buck denied the existence of a sub-endothelial space, while Karrer and Keech described a space of variable width which separates the endothelium from the underlying internal elastic lamina in aortas of aging rats and mice respectively.The present communication deals with the ultrastrueture of the interface between the endothelial cell layer and the internal elastic lamina as observed in carotid arteries from rabbits of varying ages.

scholarly journals Elastic Fibers of the Internal Elastic Lamina Are Unraveled But Not Created With Expanding Arterial Diameter in Arteriogenesis

2020 ◽  
Vol 1 ◽  
pp. 247
Author(s):  
Derek Afflu ◽  
Dylan D. McCreary ◽  
Nolan Skirtich ◽  
Kathy Gonzalez ◽  
Edith Tzeng ◽  
...  
Keyword(s):  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Arterial Diameter ◽  
Elastic Lamina

The Psychiatric Aspects of Temporal Arteritis

1952 ◽  
Vol 98 (411) ◽  
pp. 280-286 ◽  
Author(s):  
R. Vereker
Keyword(s):  
Virus Infection ◽  
Giant Cell Arteritis ◽  
Temporal Arteritis ◽  
Giant Cells ◽  
Low Grade ◽  
Internal Elastic Lamina ◽  
Temporal Arteries ◽  
The Media ◽  
Cranial Arteries ◽  
Elastic Lamina

Temporal arteritis, also called giant cell arteritis, or cranial arteritis, was first described in 1932 by Horton and Magath. This syndrome is caused by a reversible inflammation of the cranial arteries, especially the temporal arteries (which are visibly inflamed), causing headache, mental and neurological disturbances as well as general toxic signs, and almost always occurring after the age of fifty-five years.Pathology.—In the arteries involved there is a subacute inflammation of the adventitia and media with focal necrosis of the media, fragmentation and destruction of the internal elastic lamina with gross hypertrophy of the intima, often leading to occlusion of the vessel. In many cases giant cells are found in the media. Besides the cranial arteries other vessels are sometimes involved, e.g., the carotids (Scott and Maxwell 1941; Gilmour 1941), subclavian, coronary and femoral arteries (Cookeet al., 1946), post-auricular (Dick and Freeman 1940).Aetiologyis unknown. There is no evidence of tuberculosis or syphilis. A low-grade bacterial or virus infection of the arteries has been postulated, but repeated bacteriological examinations of the biopsied arteries have failed to isolate any organisms. The predilection which the condition shows for the temporal and cranial arteries is unexplained.

Abstract W P73: Inside Intramural Thrombus Formation with Inflammatory Reactions Is Relevant to the Rupture of Cerebral Aneurysms

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yusuke Shimoda ◽  
Naoki Nakayama ◽  
Masaaki Hokari ◽  
Takeo Abumiya ◽  
Hideo Shichinohe ◽  
...  
Keyword(s):  
Thrombus Formation ◽  
Cerebral Aneurysms ◽  
Histopathological Finding ◽  
Internal Elastic Lamina ◽  
Electron Microscopic ◽  
Inflammatory Reactions ◽  
Aneurysmal Wall ◽  
The Common ◽  
Collagen Layer ◽  
Elastic Lamina

Background and Purpose: Although recent researches on cerebral aneurysms (CAs) have been performed with the hydrodynamic or the molecular biological technique, the mechanisms of rupture are not fully understood. The aim of this study is to assess the mechanism by a comparison between ruptured and un-ruptured CAs with histopathological and electron-microscopic analysis. Methods: We analyzed 33 CAs (24 ruptured, 9 un-ruptured) collected surgically after neck clipping. As for the ruptured CAs, we operated them within 24 hours from the onset. HE staining, Elastica Masson staining, PTAH staining, and CD68 immunohistochemical staining were performed with paraffin sections. Morphological analysis with Scanning Electron Microscopy (SEM) was performed with 6 CAs (3 ruptured, 3 un-ruptured). Results: The common histopathological finding in both ruptured and un-ruptured CAs was that the aneurysmal wall consisted mostly of thick collagen layer without normal internal elastic lamina and media. The characteristic histopathological finding in ruptured CAs was inside intramural thrombus formation with infiltration of CD68 positive cells at the rupture point. The common SEM finding in both ruptured and un-ruptured CAs was the denudation of endothelial cells and the exposure of a subendothelial amorphous or a fibrous surface. The characteristic SEM finding in ruptured CAs was the cluster formation of thick fibrin fibers with incorporation of macrophages and platelets. Conclusions: While the endothelial denudation, the disappearance of internal elastic lamina and media, and the predominance of collagen layer in the aneurysmal wall were common in both ruptured and un-ruptured CAs, inside intramural thrombus formation with inflammatory reactions was characteristic only in ruptured CAs. This result suggests that thrombo-inflammatory reactions in CAs may act as a trigger for ruptures.

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