PATHOGENETIC SIGNIFICANCE OF LYMPHOCYTE-TO-PLATELET ADHERENCE

SummaryWe have shown previously that washed human platelets resuspended in Tyrode solution containing albumin and apyrase maintain their disc shape and their ability to aggregate upon the addition of low concentrations of ADP, providing fibrinogen is added to the suspending medium. We have now examined their responses to other aggregating and release-inducing agents. Collagen, arachidonate, thrombin, immune serum globulin, the ionophore A 23, 187 and phytohaemagglutinin from Phaseolus vulgaris caused aggregation and release of granule contents. The response to adrenaline was variable. Serotonin caused the platelets to change shape but no aggregation or release occurred. Addition of a small amount of plasma was necessary for ristocetin-induced aggregation. Polylysine caused immediate platelet-to-platelet adherence with little or no release of granule contents. Responses to collagen or thrombin were greater in a modified medium containing magnesium but no calcium; in this medium, aggregation caused by ADP or polylysine was followed by the release of granule contents whereas these agents caused aggregation without release in a medium with both calcium and magnesium. When protein was omitted from the suspending medium, platelet aggregation in response to ADP was variable. In this medium, collagen and thrombin caused more extensive release than in the albumin-containing medium. Aggregation by polylysine was accompanied by release and extensive lysis in the protein-free medium. Thus, the composition of the final resuspending medium has a major effect on the responses of washed human platelets to aggregating agents.

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Interactions Between Blood Platelets and Vascular Endothelium in vitro Studies

10.1055/s-0039-1684685 ◽

1979 ◽

Author(s):

M.A. Gimbrone ◽

K.D. Curwen ◽

R. I. Handin

Keyword(s):

Platelet Aggregation ◽

Vascular Endothelium ◽

Potent Inhibitor ◽

Platelet Reactivity ◽

Blood Platelets ◽

Primary Cultures ◽

Adenosine Diphosphate ◽

Human Platelets ◽

Platelet Adherence

Endothelial cells (EC) can actively influence the hemostatic response at sites of vascular injury through multiple mechanisms. For example, EC can degrade adenosine diphosphate, release plasminogen activator, and synthesize prostacyclin (PGI2), a potent inhibitor of platelet aggregation. We have examined whether PGI2 also might account for the normal lack of platelet adherence to the uninjured EC surface. In a monolayer adherence assay, radiolabeled human platelets in citrated plasma showed minimal interaction with primary cultures of human EC (<1 platelet adhering per cell). Platelets from aspirin-treated and untreated donors behaved similarly. However, aspirin pretreatment of EC consistently resulted in ~2-fold increases in platelet adherence which could be completely abolished by exogenous PGI2 (0.5–1.0 μg/ml). SV40-transformed human EC (SVHEC), which are deficient in PGI2 production compared to primary EC, showed 10-30 times more platelet adherence. Exogenous PGI2 produced a dose - related (.001-1.0 μg/ml) decrease in platelet adherence to SVHEC but did not result in the basal levels observed with normal EC monolayers. These data suggest that : 1) In addition to its effects on platelet aggregation, PGI2 can influence platelet endothelial cell interactions; 2) The increased platelet reactivity of transformed EC is associated with, but not completely attributable, to decreased PGI2 production; and 3) Factors other than PGI2 may play a role in the thromboresistance of normal vascular endothelium.

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Effect of 13-hydroxyoctadeca-9,11-dienoic acid (13-hode) on thrombin induced platelet adherence to endothelial cells in vitro

Thrombosis Research ◽

10.1016/0049-3848(91)90151-l ◽

1991 ◽

Vol 62 (4) ◽

pp. 305-317 ◽

Cited By ~ 20

Author(s):

M.A. Tloti ◽

D.G. Moon ◽

L.K. Weston ◽

J.E. Kaplan

Keyword(s):

Endothelial Cells ◽

Dienoic Acid ◽

Platelet Adherence

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IMMUNE PARAMETERS AND LYMPHOCYTE-PLATELET ADHERENCE IN LARYNGEAL CARCINOMA

Medical Immunology (Russia) ◽

10.15789/1563-0625-2007-6-653-659 ◽

2014 ◽

Vol 9 (6) ◽

pp. 653

Author(s):

Yu. A. Vitkovsky ◽

L. V. Il’inykh ◽

B. I. Kuznik ◽

A. V. Solpov

Keyword(s):

Laryngeal Carcinoma ◽

Immune Parameters ◽

Platelet Adherence

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Scintigraphy of Platelet Adherence in Processed Dermal Sheep Collagen (PDSC) Grafts

Clinical Application of Radiolabelled Platelets ◽

10.1007/978-94-009-0581-8_20 ◽

1990 ◽

pp. 235-241

Author(s):

J. Bannenberg ◽

K. Breuker ◽

M. R. Hardeman ◽

J. Feijen ◽

P. J. Klopper

Keyword(s):

Platelet Adherence

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Platelet adherence to cultured vascular cells: influence of prostacyclin (PGI2)

Blood ◽

10.1182/blood.v55.2.271.271 ◽

1980 ◽

Vol 55 (2) ◽

pp. 271-275 ◽

Cited By ~ 46

Author(s):

GL Fry ◽

RL Czervionke ◽

JC Hoak ◽

JB Smith ◽

DL Haycraft

Keyword(s):

Vascular Cells ◽

Platelet Adherence

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Reduced prostacyclin formation after reoxygenation of anoxic endothelium

AJP Cell Physiology ◽

10.1152/ajpcell.1990.259.5.c738 ◽

1990 ◽

Vol 259 (5) ◽

pp. C738-C745 ◽

Cited By ~ 28

Author(s):

S. L. Hempel ◽

D. L. Haycraft ◽

J. C. Hoak ◽

A. A. Spector

Keyword(s):

Arachidonic Acid ◽

Umbilical Vein ◽

Calcium Ionophore ◽

Calcium Ionophore A23187 ◽

High Rate ◽

Ionophore A23187 ◽

Arachidonic Acid Release ◽

Cyclooxygenase Activity ◽

Platelet Adherence ◽

Acid Release

Human umbilical vein endothelial cells subjected to 24 h of anoxia followed by reoxygenation released less prostacyclin (PGI2) in response to thrombin, calcium ionophore A23187, or arachidonic acid. This was associated with a substantial increase in stimulated platelet adherence. Increased lactate dehydrogenase and 51Cr release occurred after 1 h of reoxygenation, but the high rate of release did not persist during the subsequent 23 h of reoxygenation. The changes in platelet adherence and PGI2 release partially resolved over 24 h. PGI2 formation from prostaglandin H2 was not reduced, suggesting that cyclooxygenase activity, but not prostacyclin synthase, is affected by reoxygenation. A decrease in arachidonic acid release from cellular lipids also occurred. The reduction in cyclooxygenase activity, but not arachidonic acid release, was prevented by the presence of ibuprofen during reoxygenation. Addition of catalase or superoxide dismutase during reoxygenation increased PGI2 release but did not completely overcome the reduction relative to control cultures. These findings suggest that the increase in platelet adherence during reoxygenation may be mediated in part by a change in cyclooxygenase activity. This is only partly overcome by extracellular oxygen species scavengers but is prevented by the presence of a reversible cyclooxygenase inhibitor during reoxygenation.

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Effect Of Thrombin On Platelet Adherence To Cultured Vascular Cells: Modification By Dapa

10.1055/s-0038-1652167 ◽

1981 ◽

Author(s):

R L Czervionke ◽

J C Hoak ◽

D L Haycraft ◽

G L Fry

Keyword(s):

Endothelial Cells ◽

Platelet Activation ◽

Human Umbilical Cord ◽

Vascular Cells ◽

Aggregate Formation ◽

Platelet Adherence ◽

Vascular Origin ◽

Fast Acting ◽

Positive Controls

The role of thrombin in inducing adherence of platelets to cultured vascular cells is complex and may involve factors of both platelet and vascular origin. Dansylarginine N- (3-ethyl-l,5-pentanediyl)amide, DAPA, a fast-acting inhibitor of thrombin, was used in this study to evaluate platelet activation and endothelial PGI2 release induced by thrombin. Monolayers of endothelial cells and fibroblasts were cultured from human umbilical cord vessels. Empty culture dishes were used as a control. Some vascular cells were treated with aspirin (ASA) to inhibit PGI2 formation before they were incubated with 51Cr-platelets for platelet adherence studies. PGI2 was assayed by radioimmunoassay for 6-keto-PGF1α. In one study, endothelium was incubated with 0.3 U thrombin for 2 min. before 10 μM DAPA was added. Platelets were next mixed with this solution and adherence was determined. DAPA caused a decrease in thrombin-induced platelet adherence to normal endothelium from 8% to 2%. When ASA- treated endothelium was employed, DAPA decreased adherence from 59% to 2%. In another study, 51cr-platelets were first aggregated with 0.1 U thrombin, then 1.3 μM DAPA was added, and these aggregates were incubated with the monolayers. Similar experiments without DAPA served as positive controls. DAPA did not reverse the aggregate formation, but it did reduce platelet adherence to normal endothelium from 38% to 1%, and to ASA-treated endothelium from 68% to 11%. In contrast, DAPA had little effect with fibroblasts (81% to 71%), ASA-treated fibroblasts (82% to 67%), and the empty dish control (86% to 66%). These results suggest that thrombin-induced platelet adherence in this system involves more than just an effect upon platelets. In addition, they provide further evidence that the non-thrombogenic nature of endothelium persists despite the absence of PGI2.

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

10.1055/s-0039-1684486 ◽

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.

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