scholarly journals Morphological Changes in the Smooth Muscle Cells of the Mouse Lower Oviduct during Pregnancy and Post-partum.

1995 ◽  
Vol 58 (3) ◽  
pp. 293-301 ◽  
Author(s):  
Maria-Simonetta FAUSSONE-PELLEGRINI ◽  
Patrizia MATINI ◽  
Gastone BANI
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Morphological Changes ◽  
Post Partum ◽  
Muscle Cells

An Arteriovenous Malformation Model for Stereotactic Radiosurgery Research

Neurosurgery ◽  
2007 ◽  
Vol 61 (1) ◽  
pp. 152-159 ◽  
Author(s):  
Reza Jahan ◽  
Timothy D. Solberg ◽  
Daniel Lee ◽  
Paul Medin ◽  
Satoshi Tateshima ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Arteriovenous Malformation ◽  
Smooth Muscle Cells ◽  
Stereotactic Radiosurgery ◽  
Intimal Hyperplasia ◽  
Morphological Changes ◽  
Muscle Cells ◽  
Collagen Type Iv ◽  
Internal Elastic Lamina ◽  
Type Iv

Abstract OBJECTIVE To introduce the utilization of a swine arteriovenous malformation (AVM) model for stereotactic radiosurgery research and to describe the morphological changes in the vessels after radiation. METHODS The model was created in six animals by creation of a right-sided carotid-jugular fistula. Pre- and postsurgical hemodynamic evaluation was performed. The left rete was radiated in four animals; two animals were not radiated. All animals were sacrificed 4 months after surgery, and the bilateral retia were obtained at autopsy. RESULTS There were no procedure-related complications. A pressure gradient of 20 mmHg across the nidus was obtained after surgery. The peak velocity in the arterial feeder increased from 18.5 to 83 cm/s. Microscopic examination of the control animals showed intimal hyperplasia and disrupted internal elastic lamina, similar to human AVMs. The radiated retia showed more prominent intimal hyperplasia. This was confirmed by histometric studies showing greater luminal occlusion in radiated specimens. Adventitial fibrosis was prominent in the radiated retia and was absent in the control animals. Immunohistochemical studies showed proliferating smooth muscle cells in the intima. The adventitial fibrosis consisted of smooth muscle cells surrounded by collagen Type IV extracellular matrix. CONCLUSION The nidus component and high-flow vasculopathy make this an attractive model for stereotactic radiosurgery research. Histology of the radiated models is similar to those described in radiated human AVMs. Further studies of the model are warranted to gain a better understanding of the cellular and molecular events in AVM vessels after stereotactic radiosurgery.

Structural alterations in fibronectin correlated with morphological changes in smooth muscle cells

1983 ◽  
Vol 97 (2) ◽  
pp. 391-397 ◽  
Author(s):  
Michael J. Brennan ◽  
Albert J.T. Millis ◽  
David Mann ◽  
Katherine E. Fritz
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Morphological Changes ◽  
Muscle Cells ◽  
Structural Alterations

Cerebral arterial pathology in experimental subarachnoid hemorrhage

1983 ◽  
Vol 58 (6) ◽  
pp. 843-850 ◽  
Author(s):  
Tetsumori Yamashima ◽  
Shinjiro Yamamoto
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Smooth Muscle Cells ◽  
Morphological Changes ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Internal Elastic Lamina ◽  
Content Type ◽  
Fine Print

✓ Pathological changes of the cerebral arteries were studied in 30 dogs after subarachnoid injections of saline, fresh autologous blood, epinephrine, blood plus epinephrine, norepinephrine, or blood plus norepinephrine. Macroscopically, the circle of Willis was maximally dilated after the injection of epinephrine and was constricted following administration of blood plus epinephrine. Microscopically, neither saline nor blood produced abnormalities, except for minor changes of the adventitia in the latter. Epinephrine produced frank necrosis of smooth-muscle cells, which was subsequently replaced by fibrosis in the media of larger subarachnoid arteries, and the leakage of necrotic material from the infarcted hypothalamus contributed to these lesions. Blood plus epinephrine produced marked changes in the internal elastic lamina and tortuosities of the nuclei of smooth-muscle cells, while norepinephrine and blood plus norepinephrine produced only minor changes. Previously reported findings of morphological changes due to vasospasm after subarachnoid hemorrhage were confirmed experimentally, but such changes were found only after application of epinephrine. It is suggested that epinephrine produced the most severe vasospasm among the five substances tested.

scholarly journals Morphological and Molecular-Biological Changes in the Coronary Arteries after Stenting

Kardiologiia ◽  
2021 ◽  
Vol 61 (7) ◽  
pp. 79-84
Author(s):  
S. S. Todorov ◽  
V. J. Deribas ◽  
A. S. Kazmin ◽  
S. S. Todorov (jr.)
Keyword(s):  
Extracellular Matrix ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Coronary Arteries ◽  
Morphological Changes ◽  
Muscle Cells ◽  
Vascular Wall ◽  
Autopsy Material ◽  
Intimal Injury ◽  
And Migration

This review addresses morphological changes in coronary arteries following stenting, which result from damage to the vascular wall. These changes include 1) formation of a thrombus in the site of intimal injury; 2) inflammation; 3) proliferation and migration of smooth muscle cells; 4) formation of extracellular matrix. Each of these pathological processes has specific morpho-biological features. The review shows the role of von Willebrand factor in development of early thrombosis after intimal injury, which provokes activation of the inflammatory response followed by proliferation of smooth muscle cell that synthetize the extracellular matrix. These cellular and intercellular changes are based on overexpression of TGF-β1 protein, which facilitates modulation of various types of smooth muscle cells, including contractile and secretory ones. Issues of fine regulation of cellular and intercellular interactions by apoptosis, activation of mTOR signaling molecules, and microRNA are still understudied. Dynamic changes in drug-coated stents during development of neoatherosclerosis and late thrombosis remain not elucidated. Current reports show that initial mechanisms triggering pathological regenerative and hyperplastic processes that result in coronary restenosis in the area of implanted stents may form early (first hours or days) after stenting. Most studies were performed on experimental rather than on autopsy material, which does not allow fully unbiased interpretation of obtained data. Studying dynamics of morphological and molecular changes in coronary arteries after stenting, including on autopsy material, will allow one to express an opinion on the risk of postoperative thrombosis and restenosis.

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