Inhibition of Intimal Proliferation of Rabbit Aorta by Ticlopidine

1979 ◽  
Author(s):  
A. H. Reece ◽  
P.L. Walton
Keyword(s):  
Smooth Muscle ◽  
Cell Injury ◽  
Balloon Catheter ◽  
Rabbit Aorta ◽  
Endothelial Cell Injury ◽  
Intimal Proliferation ◽  
Image Analyser ◽  
Effect Of Treatment ◽  
C 30 ◽  
C 50

Proliferation of smooth muscle cells in the intima of arteries at sites adjacent to damaged endothelium may be stimulated by growth factors released from platelets. We have studied the effect of treatment with two inhibitors of platelet function, Ticlopidine and Sulphlnpyrazone, on the rate and extent of intimal proliferation In rabbit abdominal aorta following endarterectomy using a balloon catheter. Aortas were removed at Intervals after surgery, fixed, sectioned and the extent of intimal proliferation was measured using an Image analyser (Quantlmet 720). The arc a of Intimal growth as a percentage of total area of aorta was 42.4±2.8,22.3±1.2 and 50.9±2.0, 33.9±2.0 in control and Ticlopidine treated animals 30 and 60 days after endarterectomy, respectively. Thus treatment with Ticlopidine (50mg/kg/day P. O.) produced a highly significant (p<.001) reduction In the extent of intimai growth In these animals (c 50%), where as Sulphlnpyrazone (50mg/kg/day P. O.) had no effect. ADP Induced platelet aggregation was reduced (c 30%) during the treatment with Ticlopidine but not during treatment with Sulphlnpyrazone.These findings indicate that Ticlopidine treatment limits intimai proliferation In rabbits following endothelial cell Injury and may be of value in limiting this process In man.

Medial Smooth Muscle Cell Proliferation in the Balloon Injured Rabbit Aorta: Effect of a Thiazole Compound with Platelet Inhibitory Activity

1984 ◽  
Vol 51 (01) ◽  
pp. 075-078 ◽  
Author(s):  
R G Schaub ◽  
C A Simmons
Keyword(s):  
Smooth Muscle ◽  
Platelet Aggregation ◽  
Balloon Catheter ◽  
Rabbit Aorta ◽  
Surface Characteristics ◽  
Inhibitory Effect ◽  
Lesion Size ◽  
Blue Staining ◽  
Morphologic Characteristics ◽  
Time Period

SummaryTwenty-seven adult male New Zealand rabbits (3–4 kgs) were used in this study. Six rabbits received vehicle, 3 groups of 6 each received doses of 4,5-bis(p-methoxyphenyl)-2-(trifluoromethyl)- thiazole, (U-53,059), at 0.3 mg/kg, 3.0 mg/kg and 30.0 mg/kg/day respectively. Drug and vehicle doses were given orally each day starting 3 days before balloon injury and continuing for the entire 2 week time period. Three rabbits were used as nontreated sham controls. In the vehicle and U-53,059 treated groups aortae were denuded of endothelial cells by balloon catheter injury. Two weeks after injury platelet aggregation to collagen was measured and the aortae removed for analysis of surface characteristics by scanning electron microscopy and lesion size by morphometry. All doses of U-53,059 inhibited platelet aggregation. The 3.0 and 30.0 mg/kg groups had the greatest inhibitory effect. All balloon injured aortae had the same morphologic characteristics. All vessels had similar extent and intensity of Evan’s blue staining, similar areas of leukocyte/platelet adhesion, and a myointimal cell cover of transformed smooth muscle cells. The myointimal proliferative response was not inhibited at any of the drug doses studied.

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.

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.

Qualitative and Quantitative Characteristics of Rat Aortic Intimal Response to Endothelial Cell Injury

1982 ◽  
Vol 40 ◽  
pp. 342-343
Author(s):  
G. E. Visscher ◽  
R. L. Robison ◽  
C. W. Billings
Keyword(s):  
Animal Model ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Baseline Data ◽  
Endothelial Cell Injury ◽  
Qualitative And Quantitative ◽  
Intimal Proliferation ◽  
Morphometric Methods ◽  
Quantitative Characteristics ◽  
Qualitative And Quantitative Characteristics

It was our goal to characterize, qualitatively and quantitatively, the changes associated with arterial intimal proliferation after endothelial cell injury in rats. The work which is presented here was performed to establish semi-automated morphometric methods and baseline data for this animal model upon which further experiments could be based.

IN VIVO POTENCY OF HEPARIN AND HEPARINOIDS TO INHIBIT RAT SMOOTH MUSCLE CELL PROLIFERATION

1987 ◽  
Author(s):  
Maciej Dryjski ◽  
Eileen Mikat ◽  
Thorir D Bjornsson
Keyword(s):  
Smooth Muscle ◽  
Endothelial Cell ◽  
Cell Injury ◽  
Response Curves ◽  
Endothelial Cell Injury ◽  
Antiproliferative Effects ◽  
Transmission Electron ◽  
Isolated Segment

The final response of endothelial cell injury in the arterial wall is characterized by proliferation of smooth muscle cells (SMC) in the intima to form a fibro-musculo-elastic plaque. Recent in vivo and in vitro studies have shown that heparin can inhibit proliferation of SMC. These studies, however, have not elucidated the relationships between heparin dose or concentration and its in vivo antiproliferative response. In the present study, we investigated the potency of standard heparin (SH), low molecular weight heparin (LMWH) and a mixture of sulfated glycosaminoglycans (Organon 10172) with respect to the in vivo inhibition of SMC proliferation after endothelial cell injury. The injury was achieved by a short infusion of air into an isolated segment of the rat carotid artery. The drugs were administered by the AlzetR miniosmotic pumps for two weeks, at which time the animals were sacrificed and both carotid arteries were fixed in situ for light and transmission electron microscopy. The index of the intimal SMC proliferation was the maximum intima to media area (I/M) ratio. The control animals developed a marked intimal thickening (I/M: 0.97). The animals treated with 50 units/kg/hr of SH exhibited significantly less intimal hyperplasia (I/M: 0.10). With decreasing SH doses, there were increases in the I/M ratio (5 units/kg/hr, I/M: 0.44; 0.5 units/kg/hr, I/M: 0.75, and 0.05 units/kg/hr, I/M: 0.84). LMWH in doses of 50 units/kg/hr inhibited SMC proliferation as effectively as SH (I/M: 0.10), however, at doses of 15 units/kg/hr the I/M ratio was 0.55. The effect of Organon 10172 was significant at doses of 50 units/kg/hr (I/M: 0.04), but limited at doses of 15 units/kg/hr (I/M: 0.61). The APTT and anti-Xa levels were only slightly increased in the animals treated with 50 units/kg/hr of LMWH and Organon 10172, but unchanged in the animals receiving SH and the lower doses of LMWH and Organon 10172. It is concluded that SH, LMWH and Organon 10172 have significant antiproliferative effects upon SMC. The differences in the dose-response curves suggests more than one mechanism of action.

The Cellular Origin in Atheromatous Lesion

1970 ◽  
Vol 28 ◽  
pp. 202-203
Author(s):  
T. M. Murad ◽  
H. A. I. Newman ◽  
K. F. Kern
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Rabbit Aorta ◽  
Mixed Population ◽  
The Other ◽  
Cellular Origin ◽  
Ultrastructural Studies ◽  
Atherosclerotic Lesions ◽  
Show Evidence ◽  
Early Lesion

The origin of lipid containing cells in atheromatous lesion has been disputed. Geer in his study on atheromatous lesions of rabbit aorta, suggested that the early lesion is composed mainly of lipid-laden macrophages and the later lesion has a mixed population of macrophages and smooth muscle cells. Parker on the other hand, was able to show evidence that the rabbit lesion is primarily composed of lipid-laden cells of smooth muscle origin. The above studies and many others were done on an intact lesion without any attempt of cellular isolation previous to their ultrastructural studies. Cell isolation procedures have been established for atherosclerotic lesions through collagenase and elastase digestion Therefore this procedure can be utilized to identify the cells involved in rabbit atheroma.

507-P: Changes of miR-223-3p May Play an Important Role in Renal Endothelial Cell Injury of Diabetes Kidney Disease (DKD)

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 507-P
Author(s):  
RONG LI ◽  
LIN JIE ◽  
JINGMEI LUO ◽  
ZHONGCE YANG ◽  
LIHUA ZHANG
Keyword(s):  
Endothelial Cell ◽  
Kidney Disease ◽  
Cell Injury ◽  
Endothelial Cell Injury
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