Hypersensitivity of Platelets to Arachidonate /AA/ in Acute Myocardial infarction /MI/

1979 ◽  
Author(s):  
A. Szczeklik ◽  
W. Łukasiewicz ◽  
M. Serwonska ◽  
J. Musiaŀ
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Initial Velocity ◽  
Acute Mi ◽  
Circulating Platelet Aggregates ◽  
Irreversible Aggregation ◽  
Platelet Aggregates

We studied for 17 consecutive days platelet aggregation induced by AA and compared it with that induced by ADP in 20 patients with acute MI. Within 3-7 days following MI platelets required less AA to aggregate irreversibly in vitro. They also aggregated to greater extent 3 min after addition of 2 μM ADP, although the initial velocity /Vmax/ following ADP was not increased. Threshold AA concentrations causing irreversible aggregation correlated with the extent of aggregation induced by ADP, but not with ADP-Vmax. No uniform pattern of behaviour of circulating platelet aggregates was noted. These results suggest that platelet hypersensitivity in MI might be due to the activation of AA mechanisms. Use of anti-platelet drugs in MI might prevent these changes in platelet function limiting in this way the extension of MI.

Platelet Function in Childhood Migraine

Cephalalgia ◽  
1985 ◽  
Vol 5 (2_suppl) ◽  
pp. 99-101 ◽  
Author(s):  
Pietro Carrieri ◽  
Fulvio Sorge ◽  
Giuseppe Orefice ◽  
Salvatore De Feo
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Plasma Levels ◽  
Childhood Migraine ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates

Platelet function in vitro and in vivo (ADP-induced platelet aggregation, circulating platelet aggregates, β-thromboglobulin plasma levels) has been studied in children with common migraine, in headache-free intervals. Migraine patients demonstrated increased circulating platelet aggregates when compared with controls. Moreover, two of ten patients had pathological β-thromboglobulin levels. These data indicate that in some children with migraine there is an abnormality of platelet function during headache-free periods.

Abstract 697: Mobilization of Oct-4 + Bone Marrow-Derived Very Small Embryonic-Like Stem Cells in Patients with Acute Myocardial Infarction

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Wojciech Wojakowski ◽  
Magda Kucia ◽  
Boguslaw Machalinski ◽  
Edyta Paczkowska ◽  
Joanna Ciosek ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stem Cells ◽  
Bone Marrow ◽  
Pluripotent Stem Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Small Cells ◽  
Acute Mi

Bone marrow-derived CD34 + CXCR4 + progenitor cells are mobilized into peripheral blood early in acute myocardial infarction (MI). Adult murine bone marrow contains population of small CD34 + lin − CD45 − CXCR4 + cells expressing markers of pluripotent stem cells (PSC) SSEA, Oct-4 and Nanog. This population of very small embryonic-like cells (VSEL) has unique morphology (small size 2– 4 μm, large nucleus, euchromatin) and capability to form embrioid bodies (EB). Murine EB-derived cells can in vitro differentiate into cells from all three germ layers including cardiomyocytes. We hypothesized that in patients with acute MI small cells expressing the VSEL immunophenotype and PSC markers are present in bone marrow and mobilized into peripheral blood. Blood samples (20 mL) from 18 patients with acute MI were obtained after 12 hours, 2 and 5 days after symptoms onset. Bone marrow samples (20 mL) were obtained from 2 patients with acute MI and 3 healthy volunteers. Mononuclear cells were isolated using hypotonic lysis and samples were analyzed by FACS. Mobilization of following cell populations was confirmed: hematopoietic lin − CD45 + CXCR4 + , lin − CD45 + CD133 + , lin − CD45 + CD34 + and non-hematopoietic (VSEL) lin − CD45 − CXCR4 + , lin − CD45 − CD133 + , lin − CD45 − CD34 + . Analysis of the cell number using lymphocyte gate showed more significant increase of CD45 + (hematopoietic) populations of lin − CD34 + , lin − CD133 + and lin − CXCR4 + cells. After gating for small events (VSEL size range) we found more significant mobilization of small, non-hematopoietic populations of lin − CD34 + , lin − CD133 + and lin − CXCR4 + cells (Table ). The expression of PSC markers (Oct-4, Nanog, SSEA-1) in VSEL was confirmed using real-time RT-PCR. Conclusion: We report for the first time that acute MI is associated with mobilization of non-hematopoietic VSELs expressing pluripotent stem cells markers.

Platelet Function Parameters In Diabetic Patients

1981 ◽  
Author(s):  
A I Woods ◽  
S S Meschengieser ◽  
N M Sutton ◽  
M A Lazzari
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Diabetic Patients ◽  
Circulating Platelet Aggregates ◽  
Diabetic Population ◽  
Platelet Aggregates ◽  
Spontaneous Platelet Aggregation ◽  
Age Range ◽  
Induced Aggregation ◽  
Ristocetin Cofactor

Abnormalities in platelet function tests have already been described in diabetic patients reflecting platelet hyperreactivity. An attempt to determine which of the tests seemed to be more affected in the diabetic population was done in a group of 34 diabetic patients (20 men and 14 women, age range 15-76). The tests performed included assay of Ristocetin Cofactor (McFarlane et al.) circulating platelet aggregates (CPA) (Wu-Hoak) and platelet aggregation induced by ADP in low concentration (0.6 x 10-6M) and Bovine Factor VIII (0.001 U/ml). In matched controls only 3.5% had a positive aggregation induced by Bovine F VIII and with ADP (0.6 x 10-6M% ) the extent of maximum aggregation was 30%.In 15 of the 34 patients (44%) aggregation induced by ADP in high dilution was greater than 50% and this was the test more frequently affected. The level of Ristocetin Cofactor was increased (>160%) in 12 of 34 patients (35%) and aggregation induced by BF VIII was positive also in 12 patients (35%). The detection of CPA was positive in 9 patients (26%). Two patients had spontaneous platelet aggregation and in them all the other tests performed were also positive. Three patients had 3 of the tests altered, and 11 patients only had 2 affected tests.The assay more affected was the ADP induced aggregation followed by the Ristocetin Cofactor levels and BF VIII induced aggregation. The test less affected was the CPA. A correlation with clinical data will be mentioned.

Effects of Magnesium on Platelet Aggregation and Adhesion

1994 ◽  
Vol 72 (06) ◽  
pp. 912-918 ◽  
Author(s):  
M Gawaz ◽  
I Ott ◽  
A J Reininger ◽  
F-J Neumann
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Platelet Function ◽  
Platelet Adhesion ◽  
Bleeding Time ◽  
Magnesium Deficiency ◽  
Ex Vivo ◽  
Surface Expression ◽  
Activated Platelets

SummaryMagnesium deficiency and its association with platelet hyperreactivity has been well recognised in a variety of diseases including myocardial infarction, preeclampsia, and diabetes. In order to investigate potential effects of intravenous Mg2+ supplementation, platelet function was studied by measurements of in vitro bleeding time (BT) and of fibrinogen (Fg)-mediated aggregation of washed platelets. In addition, the effect of Mg2+ on platelet adhesion onto immobilised Fg, on Fg binding to activated platelets, and on surface expression of GMP-140 or GP53 was evaluated. Mg2+(4 mM) prolonged in vitro BT by 30% and inhibited Fg-mediated aggregation significantly, independent of the agonist used to initiate platelet aggregation (ADP, collagen, epinephrine, thrombin, phorbol ester). Adhesion of resting platelets to immobilised Fg was reduced by 50% in the presence of 2 mM Mg2+. Moreover, Mg2+ reduced Fg binding to ADP- or collagen-stimulated platelets as well as surface expression of GMP-140 with an IC50 of approximately 3 mM. Intravenous administration of Mg2+ to healthy volunteers inhibited both ADP-induced platelet aggregation (p <0.05) by 40% and binding of Fg or surface expression of GMP-140 by 30% (p <0.05). Thus, pharmacological concentrations of Mg2+ effectively inhibit platelet function in vitro and ex vivo.

INCREASED PLASMA CONCENTRATION OF CROSSLINKED FIBRIN POLYMERS IN ACUTE MYOCARDIAL INFARCTION

1987 ◽  
Author(s):  
C W Francis ◽  
D G Connadhan ◽  
W L Scott ◽  
V J Marder
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Plasma Concentration ◽  
Factor Xiiia ◽  
Soluble Polymers ◽  
Electrophoretic Technique ◽  
Direct Demonstration ◽  
Acute Mi ◽  
Subendocardial Mi

Thrombin cleaves fibrinopeptides from fibrinogen, converting it to fibrin monomer, and activates factor XIII which catalyzes the formation of intermolecular e-(y-glutamyl)-lysine bonds to stabilize the fibrin polymer. The formation of factor XIIIa-catalyzed fibrin polymers during clotting of plasma and purified fibrinogen in vitro was followed using an SDS agarose gel electrophoretic technique with radiolabeled antifibrinogen antibody overlay. Prior to clot formation an increase in both total amount and sizes of crosslinked fibrin polymers was demonstrated with at least 10 distinct polymeric forms identifiable by a time corresponding to .92 of the clotting time. Soluble polymers were shown to be crosslinked through y dimer formation by two dimensional electrophoresis with proportionately more dimer in each successively larger polymer. Plasma from patients initially presenting with acute myocardial infarction (MI) showed increases in the plasma concentration of fibrin polymer and in the proportion of total fibrinogen present as polymer, as determined by a quantitative adaptation of the electrophoretic technique. The plasma concentration of crosslinked fibrin dimer in patients with subendocardial or transmural MI showed significant (p <.005) increases to 4.0 ± 1.0% and 3.6 ± .8%, respectively, as compared to the concentration in normal plasma (.8 ± .1%). No difference in plasma concentration of fibrin polymer was found in samples from patients with transmural compared to subendocardial MI. This study provides the first direct demonstration and quantitation of factor XIIIa crosslinked fibrin polymers in thrombotic disease and the findings are indicative of increased activity of both thrombin and factor XIIIa in acute MI.

Platelet Function in Acute Myocardial Infarction Patients Compared with Controls

1980 ◽  
Vol 44 (02) ◽  
pp. 096-099 ◽  
Author(s):  
John R O'Brien ◽  
Michael D Etherington ◽  
Robert D Shuttleworth ◽  
William H Calwell
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Chest Pain ◽  
Acute Phase ◽  
Platelet Function ◽  
Acute Phase Proteins ◽  
Platelet Factor ◽  
Acid Glycoprotein ◽  
Platelet Poor Plasma ◽  
Acute Mi

SummaryA considerable number of tests were carried out comparing 33 patients with acute myocardial infarction (MI), 13 patients with chest pain (CP) and 47 controls. There was some evidence that the plasma platelet factor 4 (PF4) was different in the three groups. The heparin neutralizing activity (HNA) of platelet poor plasma was increased in the MI patients relative to the controls and the intra-platelet HNA was decreased. Malondialdehyde (MDA) formation by platelets maximally stimulated by thrombin was decreased in MI whilst the plasma 5-hydroxyindoles (5HIs) in MI was greatly increased. The acute phase proteins α1 acid glycoprotein and fibrinogen were significantly raised in MI. The results in the CP group were intermediate between the MI and the controls. These findings define more precisely the changes in acute MI and are relevant to the concept of exhausted platelets.

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