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PubMed1991

Hypercholesterolaemia, atherosclerosis and release of endothelium-derived relaxing factor by aggregating platelets.

In pig coronary arteries atherosclerosis developed progressively after an experimental mechanical injury to the endothelium, despite its regeneration. The atherosclerotic process can be considerably accelerated by a high cholesterol diet. In arteries with regenerated endothelium, there is a reduction of endothelium-dependent relaxations mediated by (a) pertussis toxin-sensitive G protein(s). As this includes the response to platelet-derived serotonin, the ability of the regenerated endothelium to prevent abnormal vasoconstrictions (and presumably to feedback on platelet aggregation) in response to aggregating platelets is seriously curtailed. These changes are exacerbated in atherosclerotic arteries. Bioassay studies demonstrate that reduced endothelium-dependent relaxations are due mainly to a reduced release of endothelium-derived relaxing factor. Thus, endothelial dysfunction, in particular the reduced ability to release endothelium-derived relaxing factor, is a key factor in determining the abnormal responsiveness of the atherosclerotic blood vessel wall.

Animals↗
PubMed1995

Balloon dilatation of porcine pulmonary arteries decreases endothelium-dependent relaxations and increases vasoconstriction to aggregating platelets.

BACKGROUND: Balloon dilatation of muscular coronary arteries disrupts endothelium and smooth muscle and allows platelet aggregation and adherence and cell proliferation, which can lead to restenosis. Balloon dilatation of the more distensible pulmonary artery is commonly performed, but the extent of damage to endothelium and its effect on the release of endothelium-derived nitric oxide (EDNO) and prostacyclin has not been studied. METHODS AND RESULTS: We dilated distal pulmonary arteries of intact ex vivo porcine lungs (n = 20; balloon-dilated [BD] group) using similar-sized adjacent vessels as controls with (E+group) and without (E- group) endothelium. Isolated rings were studied in vitro. Aggregating platelets caused constrictions of quiescent rings from the BD (27.4 +/- 8% of constriction to 80 mmol/L KCl) and E- groups (24 +/- 5%), which were inhibited by pyrilamine, a histamine blocker (11 +/- 4%; P < .05), and an intact endothelium (8 +/- 5%; P < .05). Constrictions to histamine and KCl were similar in the BD and E- groups. In rings with increased tone, platelets caused endothelium-dependent relaxations in the E+ group (70 +/- 6% relaxation), which were significantly (P < .05) inhibited in the BD group (20 +/- 7%), by L-nitro-arginine (EDNO blocker, 17 +/- 7%) and in the E- group (21 +/- 9%). Balloon dilatation markedly reduced endothelium-dependent relaxations to 5-hydroxytryptamine, thrombin, acetylcholine, and the calcium ionophore A23187, but relaxations to sodium nitroprusside were unaffected. CONCLUSIONS: Despite the distensibility of the pulmonary artery, balloon dilatation significantly damages the pulmonary endothelium, decreases EDNO production, impairs vasodilation, and favors platelet-induced vasoconstriction.

Animals↗
PubMed1984

Aggregating platelets contract isolated canine pulmonary arteries by releasing 5-hydroxytryptamine.

To examine the effect of platelets and 5-hydroxytryptamine on pulmonary arterial smooth muscle, rings of canine pulmonary arteries, with and without endothelium, were studied under isometric conditions in physiological salt solution. 5-Hydroxytryptamine, but not the thromboxane-like endoperoxide analogue U-46619, produced concentration-dependent contractions of the rings with a maximum averaging 93% of that obtained with KC1. Autologous platelets in concentrations comparable to that in plasma caused contractions averaging 70% of the maximal responses to KC1. Solution withdrawn from baths containing platelet-contracted rings, but not the supernatant from nonaggregated platelets, also caused contraction. The serotonergic antagonists cyproheptadine, ketanserin, and methysergide caused concentration-dependent inhibition and eventually abolition of contractions evoked by platelets and 5-hydroxytryptamine. Phentolamine and prazosin produced significantly less inhibition of the contractile response to platelets. Pretreatment of the platelets with indomethacin or meclofenamate reduced thromboxane release but had no effect on platelet-induced contractions. Removal of the endothelium did not affect contractile responses to platelets or 5-hydroxy-tryptamine. These experiments demonstrate that in the canine pulmonary artery: (a) 5-hydroxytryptamine is the predominant mediator of the contractile response triggered by platelet aggregation; and (b) unlike in other blood vessels, the endothelium cannot curtail the contractile response to aggregating platelets.

Animals↗
PubMed2002

Disaggregation of aggregated platelets by savignygrin, a alphaIIbeta3 antagonist from Ornithodoros savignyi.

Ticks control their host's hemostatic system by secretion of bioactive components during feeding that inhibit blood coagulation and platelet aggregation. Dissolution of platelets that have already aggregated can enhance control over the hemostatic system. It has been shown that disaggregation of aggregated platelets by the enzyme apyrase was accompanied by a shape change from the aggregated spherical form back to the discoid form associated with un-activated platelets. The present study concerns the disaggregation effect of the alpha IIb/beta3 antagonist, savignygrin. Aggregated platelets that were disaggregated by savignygrin and platelets pre-incubated with savignygrin before activation with ADP, retained a spherical form similar to platelets disaggregated by the fibrinogenolytic enzyme plasmin. The number of pseudopods were however, markedly reduced suggesting a disruption of the focal adhesion points that act as a localization point of alpha IIb/beta3. These results are concurrent with targeting of alpha IIb/beta3 and dissociation of fibrinogen from its receptor, once aggregation has taken place. This is the second mediator of platelet disaggregation found in soft ticks and suggests that disaggregation of aggregated platelets might play an important part in the anti-hemostatic strategy of ticks.

Animals↗
PubMed2000

P-Selectin expression, platelet aggregates, and platelet-derived microparticle formation are increased in peripheral arterial disease.

Platelet volume has been reported to be increased in vascular disease. Therefore, we studied the relationship of mean platelet volume and platelet count as well as flow cytometrically measured platelet size and platelet function in 50 patients with peripheral arterial disease and 50 healthy volunteers. Platelet activation was measured by P-selectin expression analysis on resting and on stimulated platelets, and the determination of platelet aggregates and platelet-derived microparticles using flow cytometry. P-Selectin expression on platelets was significantly elevated in patients suffering from peripheral arterial disease (all P<0.0001). Platelet aggregates (P<0.0001) and platelet-derived microparticles (P<0.0001) were significantly higher in the patient group compared with controls, whereas mean platelet volume and platelet count showed no significant differences. Platelet count was inversely related to mean platelet volume in patients and controls (r = -0.43, P<0.001). The present study supports the hypothesis of platelet hyperreactivity and circulating activated platelets in peripheral arterial disease. Mean platelet volume, and platelet count cannot be used as predictive markers for platelet activation in peripheral arterial disease patients.

Adult↗
PubMed2002

Platelet aggregating response to platelet activating factor participates in activation of the 12-lipoxygenase pathway in platelets from rabbits.

BACKGROUND: Many thrombotic angiopathies are known to originate from abnormalities in platelet-blood vessel interaction. The present study focuses on the platelet activating factor (PAF)-induced platelet aggregating mechanism and the arachidonate metabolic pathways activated by it in platelets from a male rabbit. METHODS: Blood vessel contractility was examined using perfused arterial segments dissected from rabbit ear central arteries. Autologous platelet rich plasma (PRP) was infused into the perfusion system. Vascular contractilities were examined during infusion of PRP with a platelet agonist such as collagen or PAF. Platelet aggregation was measured with a platelet aggregometer. RESULTS: Vasocontractile response to noradrenaline (NA) during infusion of PRP with PAF was initially augmented but gradually became attenuated, whereas repetitive vasocontractile responses to NA in the presence of PRP with collagen gradually increased. Platelet aggregation in response to PAF was moderately inhibited by both nordihydroguaiaretic acid (NDGA) and baicalein, 12-lipoxygenase (LOX) inhibitors, was unaffected by indomethacin (IM), a cyclo-oxygenase (COX) inhibitor, and was markedly diminished by EGTA, a calcium chelator. CONCLUSIONS: PAF-induced platelet aggregation may participate in the activation of the 12-LOX pathway rather than the COX pathway in platelets, and is remarkably sensitive to intracellular Ca2+ levels.

Animals↗
PubMed1997

Glutathione S-transferase-rhodostomin fusion protein inhibits platelet aggregation and induces platelet shape change.

Rhodostomin (RHO) from Agkistrodon rhodostoma venom, consisting of 68 amino acids with an arginine-glycine-aspartic acid (RGD) sequence and 12 cysteine residues, is a potent inhibitor of platelet aggregation. We previously demonstrated that cell culture plates coated with the bacterially produced fusion protein of glutathione S-transferase-RHO [GST-RHO(RGD)] can facilitate human hepatoma cell attachment via intergrin interaction within 15 min. In this study, we further characterized the effect of RHO fusion protein on platelet cells by creating two other related fusion proteins, GST-RHO(RGE) and GST-(PS)RHO. The former was a single amino acid-substituted mutant, in which the aspartic acid residue of RGD was replaced by glutamic acid, and the latter was an insertion mutant, in which a pentapeptide of protein kinase A phosphorylation site was inserted between GST and RHO. These two mutant proteins together with a wild-type of GST-RHO(RGD) and native form of RHO were used to study effects on the inhibition of ADP-induced platelet aggregation. Results indicated that GST-RHO(RGD) inhibited platelet aggregation as potently as the native RHO, while the two other mutants were inactive. Furthermore, when unactivated platelet cells attached on the GST-RHO(RGD)-coated plate, they became a flattened pancake shape. From the results of facilitation of cell attachment on fusion protein-coated plates, we concluded that: (1) the GST-RHO(RGD) fusion protein is equally functional in inhibition of platelet aggregation and facilitation of cell attachment, which is through the interaction of RGD and integrins on the cell membrane; (2) the GST-RHO(RGE) mutant protein is unable to bind with integrins and results in loss of function; (3) the insertion mutant of GST-(PS)RHO may disrupt a proper conformation of RHO and also results in loss of function; (4) the bacterially produced fusion protein GST-RHO(RGD) can be properly used as an antithrombotic agent and an extracellular matrix.

Animals↗
PubMed1986

Morphological changes of platelets during the process of platelet aggregation in gray platelet syndrome.

Morphological changes of platelets during the process of platelet aggregation in gray platelet syndrome were observed by means of light microscopy, and scanning and transmission electronmicroscopy. Light microscopic examinations showed normal platelets and slightly enlarged, gray colored ones due to a deficiency in alpha-granules by May-Giemsa stain. At the time of maximum aggregation, normal platelets aggregated completely to form a mass by addition of ADP. On the other hand, patient's platelets only aggregated loosely and each platelet could be recognized separately, resembling primary aggregation of normal platelets. When collagen was added, almost no aggregation was noted in the patient's platelets. Scanning electronmicroscopic examinations revealed the same results as seen by light microscopy. Centralization of platelet organelles and almost complete aggregation and degranulation of platelets were noted immediately after 30 sec and 3-4 min after addition of ADP and collagen on the transmission electronmicrographs in normal platelets, whereas most patient's platelets remained to be unchanged. From these results, we concluded that these morphological changes were consistent with the changes of "release abnormalities" as shown in the functional examinations. Although some relationships between alpha-granule deficiency and functional abnormalities are considered, there is no definitive opinion.

Adenosine Diphosphate↗
PubMed1983

Study of platelet aggregation induced by platelet activating factor (PAF) after administration of ticlopidine or aspirin.

Platelet aggregation induced by platelet activating factor (PAF) was studied in 95 subjects: 39 controls, 23 patients receiving aspirin and 33 receiving ticlopidine. Potentiation of aggregation by concentrations of adrenaline unable to induce aggregation when used alone was also assessed. The 33 patients treated with ticlopidine showed a highly significant fall of platelet aggregation (p less than 0.001) at the three concentrations of PAF used. The 23 subjects receiving aspirin showed a diminution of platelet aggregation induced by PAF due to inhibition of ADP release. In these last two groups, adrenaline often potentiated platelet aggregation. However, this phenomenon was absent in subjects having taken aspirin in the hours before blood was drawn. This study demonstrates ticlopidine's inhibitory action on PAF-induced aggregation and confirms ticlopidine's role in reducing platelet aggregation by ADP, which has previously been demonstrated.

Adult↗