scholarly journals An Aorta Intima Inhibitor of Platelet Aggregation

1977 ◽  
Author(s):  
A.duP. Heyns ◽  
C.J. Badenhorst ◽  
F.P. Retief
Keyword(s):  
Platelet Aggregation ◽  
High Voltage ◽  
Vessel Wall ◽  
Prostaglandin Synthesis ◽  
Human Aorta ◽  
Intravascular Thrombosis ◽  
Wall Interaction ◽  
High Voltage Electrophoresis

The interaction of platelets and the vessel wall is of importance in the pathogenesis of intravascular thrombosis and atherosclerosis. We have previously described the presence of an inhibitor of platelet aggregation and a low Km ADPase in aorta intima extracts. The inhibitor was further characterized.Human aorta intimas were homogenized, centrifuged and supernatants used. Platelet aggregation was measured in a aggregometer.ADPase activity was measured by incubating 14C-ADP with intima, separating metabolites by high voltage electrophoresis and quantitated.Aggregation induced by ADP, collagen, Ristocetin and polylysine was inhibited by the intima extract. The inhibition was still evident in aspirin treated platelets. The inhibitor is present in the supernatant of 100 000g centrifuged extracts. This inhibitor appears not to be ADPase or the recently described prostacyclin (PGX) :- it is stable and not destroyed by incubation at 37°C, blocking of prostaglandin synthesis by pre-incubation of the intima with indomethacin has no effect on inhibitor activity.ADPase is inactivated by KCN whereas the inhibitor is not.The inhibitor of platelet aggregation and to a lesser extent ADPase, in the intima may be important regulators of platelet-vessel wall interaction.

Effect of Sulphinpyrazone (SP) Aspirin (ASA) and Dipyridamole (DP) on Plateletvessel Wall Interaction after Oral Administration to Rabbits

1979 ◽  
Author(s):  
J.A. Davies ◽  
V.C. Menys
Keyword(s):  
Clinical Trials ◽  
Platelet Aggregation ◽  
Vessel Wall ◽  
Platelet Adhesion ◽  
Ex Vivo ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Human Dose ◽  
Wall Interaction ◽  
Adhesion Of Platelets

Clinical trials of anti-platelet drugs have suggested that they may be useful in the prevention of thrombotic disease. While such drugs inhibit platelet function, those which act on cyclooxygenase also reduce PGI2 synthesis and may interfere with tne natural antithrombotic properties of the vessel wall. We studied the effects of SP, ASA and OP ex vivo on the platelet-vessel wall interaction. Rabbits were dosed by mouth with drug (at about twice the weight-adjusted human dose) or placebo for 5 days, then exsanguinated and aortas removed. Washed platelets prepared from the blood were labelled with 51Cr. and their adhesion to everted aortapr epared from treated or control rabbits was measured in a perfusion device. PGI2-like activity in aortic rings was assayed by its inhibitory effect on platelet aggregation to ADP. Adhesion of platelets to aort as from SP- treated rabbits was i ncreased (p < 0.025), PGI2 - like activity was partially inhibited, but over all adhesion of SP-treated platelets to aor tas f rom SP-treated animals reduced by 30% (p < 0.02). Adhesion to aortas of ASA- treated rabbits was sliahtly inc r ea=-.ed (p > 0 . 1) , PGI 2 - l ike act ivi ty abolished , and no overall reduc tion in platelet adhesion seen. DP had no effecton adhesion or PGI-like activity. These results support the evidence that cyclo-oxygenase inhibitors reduce the inherent resistance of the vessel wall to platelet adhesion. However with SP, inhibitory effects on platelets appear to be more important.

Platelet-Vessel Wall Interactions In Experimentally Induced Hypercholesterolemia

1981 ◽  
Author(s):  
E Tremoli ◽  
E Aqradi ◽  
A Socini ◽  
A Petroni ◽  
C Galli
Keyword(s):  
Platelet Aggregation ◽  
Vessel Wall ◽  
Aortic Wall ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Lower Sensitivity ◽  
High Cholesterol ◽  
Simple Method ◽  
Wall Interaction ◽  
Wall Interactions

A simple method was developed to study platelet-vesseln wall interactions based on the perfusion of platelet rich plasma (PRP) through isolated segments obtained from the aorta of the same animal. The inhibition of aggregation of the perfused PRP, indicating prostacyclin (PGI2)-like material production by aortic wall, was quantified. The effect was not present when normal PRP was perfused through the vessels obtained from aspirin-treated animals. This experimental model was used in the study of platelet-vessel wall interaction in normal (N) and hypercholesterolemic (HC) rabbits (one month on a high cholesterol -2% W/W - diet).In the HC animals increased aggregating response coupled with reduced platelet sensitivity to the inhibitory effect of exogenous PGI2 was observed. When PRP of the two groups of animals was perfused through their own aortas, the inhibition of aggregation was significantly lower in HC samples, suggesting ever lower aortic production or lower sensitivity to the inhibitory effect of PGI2-like material in treated animals. In addition a lower inhibition of platelet aggregation occurred after perfusion of PRP from HC animals through aortas of N rabbits, indicating a decreased platelet sensitivity to the inhibitory effect of PGI2-like material released.It appears that in experimental HC rabbits, platelet aggregation and their sensitivity to the antiaggregatory effect of PGI2 are significantly affected. In our experimen tal conditions, production of PGI2-like material in the aorta is not reduced, but the overall outcome of plateletvessel wall interaction is a reduced inhibition of platelet aggregatory response.

ADPase Activity of Normal and Atherosclerotic Human Aorta intima

1977 ◽  
Vol 37 (03) ◽  
pp. 429-435 ◽  
Author(s):  
A. du P Heyns ◽  
C. J Badenhorst ◽  
F. P Retief
Keyword(s):  
Blood Platelets ◽  
Final Concentration ◽  
Human Aorta ◽  
Blood Vessel Wall ◽  
Anatomical Distribution ◽  
Intravascular Thrombosis ◽  
Tissue Extracts ◽  
Wall Interaction ◽  
Thoracic And Abdominal ◽  
Aortic Intima

SummaryADP plays a key role in platelet aggregation and the enzymatic removal of this nucleotide may be important in the pathogenesis of intravascular thrombosis and atherosclerosis. Aortic intima extracts have ADPase activity and is able to remove small quantities of ADP efficiently. ADPase activity was assayed by measuring the catabolism of 2 μM 14C-ADP (final concentration) by the tissue extracts. Extracts prepared from normal, moderately and severely atherosclerotic human aorta intimas showed a significant progressive decrease in ADPase activity with increasing atherosclerosis. ADPase activity of the arch, thoracic and abdominal regions of normal aortas did not vary significantly, and thus did not correlate with the anatomical distribution of atherosclerosis. Vascular ADPase activity seems relevant in thrombogenesis since it may be a link between blood platelets and blood vessel wall interaction.

Effects of Low-Dose EPA-E on Glycemic Control, Lipid Profile, Lipoprotein(a), Platelet Aggregation, Viscosity, and Platelet and Vessel Wall Interaction in NIDDM

Diabetes Care ◽  
1993 ◽  
Vol 16 (5) ◽  
pp. 683-688 ◽  
Author(s):  
H. T. Westerveld ◽  
J. C. de Graaf ◽  
H. H. Van Breugel ◽  
J. W. N. Akkerman ◽  
J. J. Sixma ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Glycemic Control ◽  
Lipid Profile ◽  
Vessel Wall ◽  
Low Dose ◽  
Lipoprotein A ◽  
Wall Interaction

The Action Mechanism of the Purified Platelet Aggregation Principle of Trimeresurus mucrosquamatus Venom

1979 ◽  
Vol 41 (03) ◽  
pp. 475-490 ◽  
Author(s):  
Chaoho Ouyang ◽  
Che-Ming Teng
Keyword(s):  
Platelet Aggregation ◽  
Adenine Nucleotides ◽  
Muscle Relaxants ◽  
Prostaglandin Synthesis ◽  
Action Mechanism ◽  
Crude Venom ◽  
Platelet Factor ◽  
Induce Platelet Aggregation ◽  
Minimal Concentration ◽  
Aggregation Principle

SummaryThe minimal concentration of the platelet aggregation principle (Platelet Aggregoserpen- tin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced platelet aggregation. PAS-induced platelet aggregation was independent on released ADP; it could occur in the ADP-removing systems, such as apyrase or a combination of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation could be inhibited by adenine nucleotides and adenosine.PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced platelet aggregation is due to prostaglandin synthesis. Recent literatures on the mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.

Thrombin Inhibition and Thrombin Generation by Cultured Aortic Endothelial and Smooth Muscle Cells from Minipig

1982 ◽  
Vol 48 (01) ◽  
pp. 101-103 ◽  
Author(s):  
B Kirchhof ◽  
J Grünwald
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vessel Wall ◽  
Thrombin Generation ◽  
Muscle Cells ◽  
Thrombin Inhibition ◽  
Generating Capacity ◽  
Wall Interaction ◽  
Cells Cultured

SummaryEndothelial and smooth muscle cells cultured from minipig aorta were examined for their inhibitory activity on thrombin and for their thrombin generating capacity.Endothelial cells showed both a thrombin inhibition and an activation of prothrombin in the presence of Ca++, which was enhanced in the presence of phospholipids. Smooth muscle cells showed an activation of prothrombin but at a lower rate. Both coagulation and amidolytic micro-assays were suitable for studying the thrombin-vessel wall interaction.

High-voltage electrophoresis of choline and its esters

1974 ◽  
Vol 89 (1) ◽  
pp. 96-98 ◽  
Author(s):  
Sheila E. Brooker ◽  
Keith J. Harkiss
Keyword(s):  
High Voltage ◽  
High Voltage Electrophoresis

scholarly journals Isolation, Characterization and Pathology of the Toxin From a Microcystis Aeruginosa (= Anacystis Cyanea) Bloom

1978 ◽  
Vol 31 (3) ◽  
pp. 209 ◽  
Author(s):  
TC Elleman ◽  
IR Falconer ◽  
ARB Jackson ◽  
MT Runnegar
Keyword(s):  
High Voltage ◽  
Algal Bloom ◽  
Lethal Dose ◽  
Acid Precipitation ◽  
Blue Green Alga ◽  
Laboratory Mice ◽  
Ammonium Sulphate Fractionation ◽  
Tyrosine D ◽  
Simple Amino Acid ◽  
High Voltage Electrophoresis

The nature of the toxicity of a bloom of blue-green alga, M. aeruginosa (= Anacystis cyanea), that occurred in a man-made lake was investigated. Crude algal bloom extracts were toxic to laboratory mice when injected intraperitoneaIIy. The lethal dose (LDlOO) of these extracts was 15-30 mg of lyophilized algal bloom per kilogram body weight. The toxin was purified by a procedure that included ammonium sulphate fractionation, solvent extraction, acid precipitation, Sephadex G25 and DEAE-Sephadex chromatography, and high-voltage electrophoresis at pH 6�5. The preparation gave a single spot on high-voltage electrophoresis at pH 9�0, had no free amino group, and was characterized by a simple amino acid composition of equimolar quantities of L-methionine, L-tyrosine, D-alanine, D-glutamic acid, erythro fi-methyl aspartic acid and methylamine.

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