Prevention of catecholamine-induced lesions of the endothelium of the rabbit aorta by alpha-and beta-adrenoreceptor antagonists and lithium hydroxybutyrate

1987 ◽  
Vol 103 (4) ◽  
pp. 449-452
Author(s):  
T. A. Voino-Yasenetskaya ◽  
L. N. Skuratovskaya ◽  
V. S. Repin ◽  
G. N. Kryzhanovskii
Keyword(s):  
Rabbit Aorta ◽  
Lithium Hydroxybutyrate

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.

A Cytochemical Study of Glucose-6-Phosphatase (G-6-PASE) in Cells Participating in Atherogenesis of Rabbit Aorta

1975 ◽  
Vol 33 ◽  
pp. 460-461
Author(s):  
Sidney D. Kobernick ◽  
Edna A. Elfont ◽  
Neddra L. Brooks
Keyword(s):  
Lipid Metabolism ◽  
New Zealand ◽  
Aortic Wall ◽  
Rabbit Aorta ◽  
Plaque Formation ◽  
Metabolic Changes ◽  
Atherosclerotic Plaques ◽  
Cytochemical Study ◽  
Cellular Alteration ◽  
New Zealand White Rabbits

This cytochemical study was designed to investigate early metabolic changes in the aortic wall that might lead to or accompany development of atherosclerotic plaques in rabbits. The hypothesis that the primary cellular alteration leading to plaque formation might be due to changes in either carbohydrate or lipid metabolism led to histochemical studies that showed elevation of G-6-Pase in atherosclerotic plaques of rabbit aorta. This observation initiated the present investigation to determine how early in plaque formation and in which cells this change could be observed.Male New Zealand white rabbits of approximately 2000 kg consumed normal diets or diets containing 0.25 or 1.0 gm of cholesterol per day for 10, 50 and 90 days. Aortas were injected jin situ with glutaraldehyde fixative and dissected out. The plaques were identified, isolated, minced and fixed for not more than 10 minutes. Incubation and postfixation proceeded as described by Leskes and co-workers.

Radiolabeled r-Hirudin as a Measure of Thrombin Activity at, or within, the Rabbit Aorta Wall In Vitro and In Vivo

1994 ◽  
Vol 71 (04) ◽  
pp. 499-506 ◽  
Author(s):  
Mark W C Hatton ◽  
Bonnie Ross-Ouellet
Keyword(s):  
Rabbit Aorta ◽  
Balloon Injury ◽  
Recombinant Hirudin ◽  
Aorta Wall ◽  
Thrombin Activity ◽  
Before And After ◽  
The Matrix

SummaryThe behavior of 125I-labeled recombinant hirudin towards the uninjured and de-endothelialized rabbit aorta wall has been studied in vitro and in vivo to determine its usefulness as an indicator of thrombin activity associated with the aorta wall. Thrombin adsorbed to either sulfopropyl-Sephadex or heparin-Sepharose bound >95% of 125I-r-hirudin and the complex remained bound to the matrix. Binding of 125I-r-hirudin to the exposed aorta subendothelium (intima-media) in vitro was increased substantially if the tissue was pre-treated with thrombin; the quantity of l25I-r-hirudin bound to the de-endothelialized intima-media (i.e. balloon-injured in vitro) correlated positively with the quantity of bound 131I-thrombin (p <0.01). Aortas balloon-injured in vivo were measured for thrombin release from, and binding of 125I-r-hirudin to, the de-endothelialized intimal surface in vitro; 125I-r-hirudin binding correlated with the amount of active thrombin released (p <0.001). Uptake of 125I-r-hirudin by the aorta wall in vivo was proportional to the uptake of 131I-fibrinogen (as an indicator of thrombin activity) before and after balloon injury. After 30 min in the circulation, specific 125I-r-hirudin binding to the uninjured and de-endo- thelialized (at 1.5 h after injury) aorta wall was equivalent to 3.4 (± 2.5) and 25.6 (±18.1) fmol of thrombin/cm2 of intima-media, respectively. Possibly, only hirudin-accessible, glycosaminoglycan-bound thrombin is measured in this way.

Further Evidence that Glycoprotein IIb-IIIa Mediates Platelet Spreading on Subendothelium

1991 ◽  
Vol 65 (02) ◽  
pp. 202-205 ◽  
Author(s):  
Harvey J Weiss ◽  
Vincet T Turitto ◽  
Hans R Baumgartner
Keyword(s):  
Platelet Adhesion ◽  
Surface Coverage ◽  
Rabbit Aorta ◽  
Conclusive Evidence ◽  
Initial Contact ◽  
Single Exposure ◽  
Vessel Segment ◽  
Multiple Exposures ◽  
Wall Interaction ◽  
Platelet Spreading

SummaryIn order to explore further the mechanism by which glycoprotein GPIIb-IIIa promotes platelet vessel wall interaction, platelet adhesion to subendothelium was studied in an annular chamber in which subendothelium from rabbit aorta was exposed at a shear rate of 2,600 s−1 to blood from patients with thrombasthenia. Perfusions were conducted for each of 5 exposure times (1 ,2,3, 5 and 10 min), and the percent surface coverage of the vessel segment with platelets in the contact (C) and spread (S) stage was determined. Increased values of platelet contact (C) were obtained in thrombasthenia at all exposure times; this finding is consistent with a defect in platelet spreadirg, based on a previously described kinetic model of platelet attachment to subendothelium. According to this model of attachment, increased values of platelet contact (C) at a single exposure time may be indicative of either a defect in spreading (S) or initial contact (C), but multiple exposures will result in increased contact only for defects which are related to defectiye platelet spreading (s).The results obtained over a broad range of exposure times provide more conclusive evidence that GPIIb-IIIa mediates platelet spreading than those previously obtained at single exposure times.

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.

Synthesis and biological activity of new metallocenic angiotensin II analogs

1988 ◽  
Vol 53 (11) ◽  
pp. 2914-2919 ◽  
Author(s):  
Pierrette Maes ◽  
Annie Ricouart ◽  
Emmanuel Escher ◽  
André Tartar ◽  
Christian Sergheraert
Keyword(s):  
Amino Acids ◽  
Biological Activity ◽  
Angiotensin Ii ◽  
Solid Phase ◽  
Rabbit Aorta ◽  
Phase Method ◽  
Solid Phase Method

Analogs of angiotensin II in which phenylalanine in position 8 was replaced with cymantrenylalanine or with its triphenylphosphine photosubstitution product were synthesized by the solid-phase method. On rabbit aorta strips, these peptides were found to be pure antagonists of angiotensin II. Their relative affinities are higher than most other analogs substituted in position 8 with bulky amino-acids.

Effects of Injury on ApoB Kinetics and Concentration in Rabbit Aorta

1995 ◽  
Vol 15 (7) ◽  
pp. 930-936 ◽  
Author(s):  
Gun Olsson ◽  
Olov Wiklund ◽  
Göran Bondjers
Keyword(s):  
Rabbit Aorta

Lysophosphatidylcholine Inhibits Receptor-Mediated Ca 2+ Mobilization in Intact Endothelial Cells of Rabbit Aorta

1997 ◽  
Vol 17 (8) ◽  
pp. 1561-1567 ◽  
Author(s):  
Yoichi Miwa ◽  
Ken-ichi Hirata ◽  
Seinosuke Kawashima ◽  
Hozuka Akita ◽  
Mitsuhiro Yokoyama
Keyword(s):  
Endothelial Cells ◽  
Rabbit Aorta

Familial And Constitutional Moderate Bleeding Disorder Associated With Defective Platelet Cyclo-Oxygenase

1981 ◽  
Author(s):  
C Lecrubier ◽  
F Fouque ◽  
M Chignard ◽  
M H Horellou ◽  
J Conard ◽  
...  
Keyword(s):  
Autosomal Dominant ◽  
Atp Release ◽  
Rabbit Aorta ◽  
Total Radioactivity ◽  
Bleeding Disorder ◽  
Similar Extent ◽  
Synthetase Deficiency ◽  
Successive Generations ◽  
Second Wave ◽  
Rule Out

Three family members from two successive generations showed a moderate bleeding disorder. The bleeding times (Duke and Ivy-Borchgrevink) were both constantly prolonged. Platelet aggregation induced by ADP and adrenaline showed no second wave; collagen at low to moderate concentrations failed to aggregate and release ATP whereas higher amounts aggregated and released. Aggregation and release due to thrombin, ristocetin and synthetic epoxy derivatives (U 44069 and U 46619) were normal. Arachidonate (A.A.) was inactive and was not converted into thromboxane (TX) A2 activity evaluated on the rabbit aorta strip. The patient’s platelets did not respond to A.A. when PRP from an aspirin treated control was added. Platelet phospholipids (PL) were labelled by 14C - A.A. before stimulation by thrombin (T). Radioactivity of the PL of the propositus' platelets was affected with T to a similar extent as 5 laboratory controls, indicating that the phospholipase activity was not impaired. In contrast, no TXB2 was found: 0.9 p. cent as compared to 6 p. cent of total radioactivity in controls.Our data suggest a deficit in cyclo-oxygenase particularly since the levels of PGE2, PGF2a and PGD2 were within the limits of detection. These results seem to rule out the possibility of a TX-synthetase deficiency with excessive production of anti-aggregating PGs. This study suggests that transmission is autosomal dominant and confirms that cyclo-oxygenase is not needed for aggregation and ATP-release by high amounts of collagen.

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