Lining cell and intimal smooth muscle cell response and Evans blue staining in abdominal aorta of young swine after denudation by balloon catheter

1980 ◽  
Vol 33 (2) ◽  
pp. 185-202 ◽  
Author(s):  
R.F. Scott ◽  
H. Imai ◽  
T. Makita ◽  
W.A. Thomas ◽  
J.M. Reiner
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Abdominal Aorta ◽  
Evans Blue ◽  
Cell Response ◽  
Balloon Catheter ◽  
Blue Staining

Quantitation of Platelet Adherence to Rabbit Aortae and Platelet Survival After two Injuries with a Balloon Catheter

1979 ◽  
Author(s):  
R.L. Kinlough-Rathbone ◽  
H.M. Groves ◽  
S. Maric ◽  
M.A. Packham ◽  
J.F. Mustard
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Balloon Catheter ◽  
Rabbit Aorta ◽  
Platelet Adherence ◽  
Platelet Survival ◽  
Single Balloon

Following a single balloon catheter injury to a rabbit aorta (INJ 1) a monolayer of platelets covers the subendothelium within 10 min, the surface becomes relatively non-reactive to further platelet accumulation and platelet survival is not altered. We have now studied whether a second similar injury (INJ 2) of the non-reactive, smooth muscle cell-rich neointima 7 days after INJ 1 makes the surface of the neointima reactive to platelets or alters platelet survival. 51Cr-platelet adherence to the neointima of aortae subjected to INJ 2 in vitro 7 days after an initial in vivo injury was not significantly different from the adherence following a single in vitro injury (16,600 ± 3100 platelets/mm2 and 27,600 ± 4000 respectively, ρ > 0.2). In vivo adherence of 51Cr-platelets to the surface of rabbit aortae was similar following INJ 1 (0.084 ± 0.009% of the circulate, platelets) and INJ 2 (0.130 ± 0.03%, p > 0.2). Platelet survival after injury to the neointima was not significantly different in animals with an undamaged aortic endothelium (74.6 ± 5.9 hr and 80.2 ± 4.3 hr respectively, ρ > 0.5). Thus, a second injury involving the smooth’ muscle cell-rich neointima that forms after removal of the endothelium with a balloon catheter does not cause more platelets to accumulate than the initial injury, nor shorten platelet survival.

scholarly journals Integrin-Linked Kinase in the Vascular Smooth Muscle Cell Response to Injury

2008 ◽  
Vol 173 (1) ◽  
pp. 278-288 ◽  
Author(s):  
Bernard Ho ◽  
Guangpei Hou ◽  
J. Geoffrey Pickering ◽  
Gregory Hannigan ◽  
B. Lowell Langille ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Response ◽  
Integrin Linked Kinase

Tempol therapy attenuates medial smooth muscle cell apoptosis and neointima formation after balloon catheter injury in carotid artery of diabetic rats

2005 ◽  
Vol 289 (3) ◽  
pp. H1047-H1053 ◽  
Author(s):  
D. K. Jagadeesha ◽  
Timothy E. Lindley ◽  
Jason DeLeon ◽  
Ram V. Sharma ◽  
Francis Miller ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Injury ◽  
Critical Role ◽  
Balloon Catheter ◽  
Vascular Complications ◽  
Diabetic Rats ◽  
Neointima Formation ◽  
Muscle Cell Apoptosis

Accumulating data support the hypothesis that reactive oxygen species (ROS) play a critical role in the vascular complications observed in diabetes. However, the mechanisms of ROS-mediated vascular complications in diabetes are not clear. We tested the hypothesis that ROS-mediated increase in proapoptotic factor Bax expression leads to medial smooth muscle cell (SMC) apoptosis that is associated with neointima formation. We used a fructose-rich diet for 4 wk to model Type 2 diabetes in rats. SOD mimetic membrane-permeable 4-hydroxy-2,2,6,6,-tetramethylpiperidine-1-oxyl (Tempol, 1 mM) was administered in drinking water to scavenge superoxide starting 1 day before surgery and continued during the duration of the experiment. Vascular injury resulted in a significant increase in medial SMC apoptosis that was associated with neointima formation. The number of medial SMC positive for Bax immunostaining significantly increased in injured arteries compared with uninjured arteries. Superoxide scavenging by Tempol treatment inhibited both the Bax-positive index as well as the apoptotic index of medial SMC in response to vascular injury. Tempol treatment inhibited apoptotic loss of medial SMC, thus increasing their density in the injured arteries. These alterations in the media were associated with a marked decrease in neointima formation in injured arteries. We conclude that Bax expression may play an important role in vascular SMC apoptosis and, finally, that this regulatory mechanism is redox sensitive.

Evaluation of Smooth Muscle Cell Response Using Two Types of Porous Polylactide Scaffolds with Differing Pore Topography

2004 ◽  
Vol 10 (3-4) ◽  
pp. 505-514 ◽  
Author(s):  
Jonathan B. McGlohorn ◽  
Walter D. Holder ◽  
Larry W. Grimes ◽  
Chuck B. Thomas ◽  
Karen J.L. Burg
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Cell Response

Quantitation of Platelet Adherence to Rabbit Aortae and Platelet Survival After Two Injuries With a Balloon Catheter

1979 ◽  
Author(s):  
R Kinlough-Rathbone ◽  
H Groves ◽  
S Maric ◽  
M Packham ◽  
J Mustard
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Balloon Catheter ◽  
Rabbit Aorta ◽  
Platelet Adherence ◽  
Platelet Survival ◽  
Single Balloon

Following a single balloon catheter injury to a rabbit aorta (INJ 1) a monolayer of platelets covers the subendothelium within 10 min, the surface becomes relatively nonreactive to further platelet accumulation and platelet survival is not altered. We have now studied whether a second similar injury (INJ 2) of the non-reactive, smooth muscle cell-rich neointima 7 days after INJ 1 makes the surface of the neointima reactive to platelets or alters platelet survival. 51Cr-platelet adherence to the neointima of aortae subjected to INJ 2 in vitro 7 days after an initial in vivo injury was not significantly different from the adherence following a single in vitro injury (16,600 ± 3100 platelets/mm2 and 27,600 ± 4000 respectively, p > 0.2). In vivo adherence of 51Cr-platelets to the surface of rabbit aortae was similar following INJ 1 (0.084 ± 0.009% of the circulating platelets) and INJ 2 (0.130 ± 0.03%, p > 0.2). Platelet survival after injury to the neointima was not significantly different in animals with an undamaged aortic endothelium (74.6 ±5.9 hr and 80.2 ± 4.3 hr respectively, p > 0.5). Thus, a second injury involving the smooth muscle cell-rich neointima that forms after removal of the endothelium with a balloon catheter does not cause more platelets to accumulate than the initial injury, nor shorten platelet survival.

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