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.

Immunolocalization of microfibril and microfibril-associated proteins in the subendothelial matrix of the developing mouse aorta

1994 ◽  
Vol 107 (3) ◽  
pp. 727-736 ◽  
Author(s):  
E.C. Davis
Keyword(s):  
Endothelial Cell ◽  
Structural Integrity ◽  
Cell Layer ◽  
Endothelial Cell Layer ◽  
Associated Proteins ◽  
Subendothelial Matrix ◽  
Oriented Parallel ◽  
Mouse Aorta ◽  
Structural Entity ◽  
Elastic Lamina

In the developing aorta, endothelial cell connecting filaments extend from the abluminal surface of the endothelial cell to the subjacent elastic lamina. The connecting filaments are in alignment with intracellular stress fibers and are oriented parallel to the direction of blood flow. In the present study, the composition of the endothelial cell connecting filaments was investigated by indirect immunogold labeling with antibodies to the microfibril proteins, MP340 (fibrillin) and MAGP, and to fibronectin and heparan sulfate proteoglycan (HSPG). In the subendothelial matrix of both 15-day gestational and 5-day post-natal mouse aortae, the connecting filaments showed moderate immunoreactivity with anti-MP340; however, no significant immunoreaction was seen with anti-MAGP. Anti-fibronectin strongly labeled the connecting filaments and a weak immunoreaction was seen with anti-HSPG. In contrast, the adjacent ‘elastin-associated microfibrils’ showed a very strong immunoreaction with anti-MP340 and a moderate reaction with anti-MAGP. Little or no reaction was seen with anti-fibronectin or anti-HSPG. The filaments that connect endothelial cells to the subjacent elastic lamina during aortic development are thus microfibrillar in nature and related to elastin-associated microfibrils as evidenced by their positive immunoreaction with anti-MP340. The absence of labeling with anti-MAGP, however, suggests that either these fibrillin-containing filaments do not contain MAGP or that the immunoreactive epitopes are blocked by the proteins that coat the connecting filaments such as fibronectin. These results suggest that microfibrils not in association with elastin may play a role in cell anchorage and, more specifically, in the aorta may be involved in maintaining the structural integrity of the endothelial cell layer during early development of the vessel wall. Furthermore, the absence of immunoreactivity with anti-MAGP on the fibrillin-containing endothelial cell connecting filaments raises the possibility that microfibrils may consist of a family of related filaments rather than a single structural entity.

Thiouracil-Induced Elastic Tissue Degenerative Changes in Canine Arteries

1971 ◽  
Vol 29 ◽  
pp. 568-569
Author(s):  
Alberto Trillo
Keyword(s):  
Animal Species ◽  
Vascular Wall ◽  
Elastic Tissue ◽  
Cholesterol Feeding ◽  
Internal Elastic Lamina ◽  
Thyroid Activity ◽  
Common Procedure ◽  
Purina Chow ◽  
The Subject ◽  
Elastic Lamina

Unlike other animal species, the dog is relatively resistent to develop hypercholesterolemia and atheromatous lesions even after long periods of cholesterol feeding. This difficulty is, however, eliminated if the thyroid activity is suppressed surgically or pharmacologically. The most common procedure employed is thiouracil administration. During the course of our studies on the response of the vascular wall to various stimuli, it was of interest to assess the possible effects of thiouracil on the mural elements, since information on the subject is almost nonexistent. In this presentation reference will be made only to changes of the internal elastic lamina (IEL) observed in the carotid and femoral arteries of two mongrel young dogs fed purina chow supplemented by thiouracil (100/mg/kg/day) for 3 and 6 months respectively.The earliest change appeared to consist of an accentuation of the filamentous components of the IEL, formation of fissures or clefts partially filled with a fine fibrillar electron dense material (Fig. 1), and loose bundles of collagen fibrils (Fig. 2). At a later stage, large areas of IEL have a “spongy” appearance with numerous clefts and rarefied areas present.

Microvascular End-to-Side Arterial Anastomosis Using the Nd: YAG Laser

Neurosurgery ◽  
1989 ◽  
Vol 25 (4) ◽  
pp. 584-589 ◽  
Author(s):  
Scott Shapiro ◽  
Carl Sartorius ◽  
Steven Sanders ◽  
Steve Clark
Keyword(s):  
Histological Examination ◽  
Nd:Yag Laser ◽  
Carotid Arteries ◽  
Spot Size ◽  
Anastomotic Site ◽  
Internal Elastic Lamina ◽  
Time Intervals ◽  
Histological Assessment ◽  
Arterial Anastomosis ◽  
Elastic Lamina

Abstract End-to-side, laser-assisted vascular anastomosis (LAVA) using a Nd:YAG laser was successfully performed on rat carotid arteries. A midline neck incision allowed isolation and approximation of both carotid arteries in an end-to-side fashion using four 10-0 nylon stay sutures. The laser parameters used for vessel fusion were 0.3-second 5-W pulses at a spot size of 600 Mm. Anastomoses were analyzed at various time intervals from 1 day to 6 months by angiogram and histological examination. The anastomotic patency was 86%. Aneurysm formation occurred in 23%. Histological examination revealed an acute/subacute transmural injury both at the anastomotic site and several hundred microns away, with delayed re-endothelialization and some attempt at muscular and elastic regeneration. Histological assessment of the aneurysms demonstrated a total loss of the internal elastic lamina and muscularis. A brief discussion comparing Nd:YAG LAVA to other LAVA techniques follows.

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.

Functional medial thickening and folding of the internal elastic lamina in coronary spasm

2011 ◽  
Vol 300 (2) ◽  
pp. H423-H430 ◽  
Author(s):  
Yasumi Uchida ◽  
Yasuto Uchida ◽  
Akimasa Matsuyama ◽  
Atsushi Koga ◽  
Yuko Maezawa ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Structural Changes ◽  
Light And Electron Microscopy ◽  
Coronary Spasm ◽  
Cellular Level ◽  
Internal Elastic Lamina ◽  
Circular Smooth Muscle ◽  
The Media ◽  
Medial Thickening ◽  
Elastic Lamina

Although there are a number of studies on vasospastic angina, the structural changes at the cellular level that occur in the coronary arterial wall during spasm are not well known. Coronary spasm was induced by brushing the coronary adventitia in nine anesthetized beagles, and structural changes in the spastic coronary segments were examined by light and electron microscopy, making comparisons with the adjacent nonspastic segments. The % diameter stenosis of the spastic segments as measured angiographically was 79.4 ± 12% (mean ± SD). Light microscopic changes in the spastic and nonspastic segments were as follows: medial thickness 1,512 vs. 392 μm ( P < 0.0001) and % diameter and % area stenoses of spastic segment 81.0% and 96.5%, respectively, indicating that spasm was induced by medial thickening. Circular smooth muscle cells (SMCs) in the media were arranged in parallel with the internal (IEL) and external (EEL) elastic lamina in nonspastic segments but radially rearranged in spastic segments. SMCs were classified by their patterns of connection to IEL into six types by electron microscopy. Of these, three contracted and pulled the IEL toward the EEL, causing folding of the IEL and waving of EEL resulting in thickening of the media and narrowing of the lumen. We conclude that coronary spasm was elicited by radial rearrangement of the medial SMCs due to their own contraction and resultant medial thickening and folding of IEL, creating a piston effect to narrow the lumen, i.e., spasm.

Plasmin-induced reduction of heparan sulfate in cultured vascular endothelial cell layer

1994 ◽  
Vol 74 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Toshiyuki Kaji ◽  
Syouichi Hiraga ◽  
Noriyasu Fujii ◽  
Chika Yamamoto ◽  
Michiko Sakamoto ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Heparan Sulfate ◽  
Cell Layer ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Endothelial Cell Layer
Sign in / Sign up

Export Citation Format

Share Document