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.

On the Measurement of Spontaneous Platelet Aggregation. The Platelet Aggregation Test III.

1976 ◽  
Vol 35 (03) ◽  
pp. 669-691 ◽  
Author(s):  
K Breddin ◽  
H Grun ◽  
H. J Krzywanek ◽  
W. P Schremmer
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Age Groups ◽  
Diabetic Patients ◽  
Measuring Device ◽  
Chart Recorder ◽  
Additional Equipment ◽  
Platelet Aggregates ◽  
Spontaneous Platelet Aggregation ◽  
Induced Aggregation

SummaryA new measuring device was developed for the study of “spontaneous” aggregating activity of thrombocytes. In the photometric platelet aggregation test (PAT III) 0.6 ml of platelet-rich plasma (PRP) are rotated in a disc-shaped cuvette at 20 rpm and 37° C. Changes in optical density of PRP which are induced by the formation of platelet aggregates are continuously registered using a chart recorder. PAT III was developed for the detection of enhanced platelet aggregation, indicating a risk of thrombosis and thromboembolic complications.In 146 healthy individuals a certain percentage showed slight primary aggregation (α1) which in some cases was followed by marked aggregation (α2) at a certain time (Tr) after the beginning of rotation. The percentage of individuals showing α2 increased with age. An increase of plasma pH in the rotating sample, which was caused by diffusion of CO2, was an important conditioning factor for aggregation. The test results depended on the platelet count in PRP. Aggregation curves were suppressed by admixture of erythrocytes and lipid turbidity. The tendency of platelets to aggregate increased within 60–90 min following blood sampling. During this period the interval to the onset of aggregation (Tr) became shorter and the maximum aggregation speed (α2) increased with time. PAT III yielded reproducible results when it was carried out more than 60 min after blood drawing.In a group of 327 diabetic patients “spontaneous” aggregation occurred more frequently in all age groups as compared with the controls.Additional equipment was available for the registration of ADP-, collagen-, or epine-phrine-induced aggregation similar to Born’s and O’Brien’s method. The device can easily be mounted on an Eppendorf photometer without further alterations.

Effect of Indobufen (K 3920) A New Antiplatelet Agent After Oral Administration in Patients with Vascular Diseases

1979 ◽  
Author(s):  
S. Coccheri ◽  
G.C. Fortunato
Keyword(s):  
Platelet Aggregation ◽  
Antiplatelet Agent ◽  
Vascular Diseases ◽  
Maximal Amplitude ◽  
Marked Inhibition ◽  
Lysis Time ◽  
Euglobulin Lysis Time ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Induced Aggregation

The antiaggregating effect of a new butyric acid derivative, indobufen (K 3920), was investigated in 30 patients with vascular diseases. A between-patient study was performed by administering 50 mg b.i.d. or 100 mg b.i.d. for 14 days to 2 groups of patients. A series of platelet function and clotting parameters were recorded at the end of the treatment period, both 2 and 24 h after the last administration.A marked inhibition of platelet aggregation was observed in both groups, as shown from the significant changes in maximal amplitude, reaction time and slope of ADP- and collagen-induced aggregation wave.Similar results were observed at the Breddin test in both groups of patients and at all experimental times.Platelet adhesiveness was also reduced and circulating platelet aggregates were normalized in all patients who had abnormal basal values.A shortening of euglobulin lysis time was observed 2 h but not 24 h after administration of both doses.Tolerability was excellent.Indobufen appears to be a promising drug for treatment of vascular diseases where platelet aggregation is involved.

Prevention of in vivo Platelet Aggregation by Indobufen in Angina Patients during Exercise

1981 ◽  
Vol 9 (2) ◽  
pp. 113-119 ◽  
Author(s):  
E M Pogliani ◽  
R Fantasia ◽  
C Perini ◽  
G Corvi
Keyword(s):  
Platelet Aggregation ◽  
Bicycle Ergometer ◽  
Crossover Design ◽  
Double Blind ◽  
Before And After ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions

Platelet aggregation induced by 3 concentrations of ADP and collagen was assessed in thirty patients with stable angina, before and after exercise with a bicycle ergometer. The patients received a single oral 200 mg dose of indobufen and placebo according to a crossover design in double-blind conditions. Platelet sensitivity to both aggregating agents increased when exercise was carried out after placebo, whereas indobufen markedly inhibited ADP- and collagen-induced aggregation. Circulating platelet aggregates increased in some patients during exercise after placebo but not after indobufen. These results suggest that effort may be an important factor in activation of platelet functions and that the use of drugs blocking the arachidonate pathway and the release reaction may be appropriate in patients with angina.

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.

Intravascular Thrombosis and Platelet function in Diabetic Neuropathy

1975 ◽  
Author(s):  
F. E. Preston ◽  
W. R. Timperley ◽  
B. C. O’Malley ◽  
J. D. Ward
Keyword(s):  
Platelet Aggregation ◽  
Diabetic Neuropathy ◽  
Platelet Function ◽  
Sural Nerve ◽  
Platelet Rich Plasma ◽  
Biopsy Material ◽  
Intravascular Thrombosis ◽  
Temperature Controlled ◽  
Spontaneous Platelet Aggregation ◽  
Induced Aggregation

Peripheral neuropathy is a serious complication of Diabetes Mellitus, The precise pathogenesis is unknown. Histological examination of biopsy material obtained from patients with diabetic neuropathy has revealed intravascular fibrin in vessels supplying the sural nerve in 10 out of 25 cases. This finding prompted us to study platelet function in this same group of patients.Blood samples were obtained from fifteen patients. After preparation of platelet-rich plasma, platelet aggregation was measured following the addition of various concentrations of ADP, collagen and adrenaline. The responses were assessed photoelectrically in a temperature-controlled, constantly stirred, non-glass system. In addition the samples were tested for spontaneous platelet aggregation.Spontaneous platelet aggregation was detected in one-third of samples studied, but in none of the controls. Enhanced ADP-induced aggregation was observed in 53% of samples and enhanced adrenaline-induced aggregation in 50%. Similar results were obtained with collagen.The data supports the view that enhanced platelet aggregation and intravascular thrombosis is of considerable importance in the pathogenesis of diabetic neuropathy.

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.

Effect of Indobufen on Platelet Functions in Angina Patitents at Rest and During Exercise

1979 ◽  
Author(s):  
E. Pogliani ◽  
R. Fantasia ◽  
E. Polli
Keyword(s):  
Platelet Aggregation ◽  
Stable Angina ◽  
Serotonin Release ◽  
Double Blind ◽  
Before And After ◽  
Circulating Platelet Aggregates ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions ◽  
Stimulation Of

Platelet aggregation induced by 3 concentrations of ADP and collagen was assessed in 30 patients with stable angina before and after exercise with bicyle ergometer. The patients received a single Oral 200 mg dose of indobufen and placebo according to a cross-over design in double-blind conditions. An increase in platelet sensitivity to both aggregating agents occurred when exercise was carried out after placebo, whereas indobufen markedly inhibited ADP- and collagen-induced aggregation. Circulating platelet aggregates increased in some patients during exercise after placebo but not after indobufen. In 20 patients 14C-serotonin release induced by collagen in PRP was investigated. The release was increased when placebo was administered before exercise but it was inhibited when indobufen was given before exercise. In the same patients MDA levels after thrombin-induced stimulation of platelets in PRP increased during exercise after placebo but decreased during exercise after indobufen. These results suggest that effort may be an important factor in activation of platelet functions and that the use of drugs blocking the arachidonate pathway and the release reaction may be appropriate in patients with angina.

Ticlopidine Facilitates the Deaggregation of Human Platelets Aggregated by Thrombin

1994 ◽  
Vol 71 (01) ◽  
pp. 091-094 ◽  
Author(s):  
M Cattaneo ◽  
B Akkawat ◽  
R L Kinlough-Rathbone ◽  
M A Packham ◽  
C Cimminiello ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Platelet Aggregation ◽  
Prostaglandin E1 ◽  
Human Platelet ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Before And After ◽  
Normal Human ◽  
Platelet Aggregates ◽  
Induced Aggregation

SummaryNormal human platelets aggregated by thrombin undergo the release reaction and are not readily deaggregated by the combination of inhibitors hirudin, prostaglandin E1 (PGE1) and chymotrypsin. Released adenosine diphosphate (ADP) plays an important role in the stabilization of thrombin-induced human platelet aggregates. Since ticlopidine inhibits the platelet responses to ADP, we studied thrombin-induced aggregation and deaggregation of 14C-serotonin-labeled platelets from 12 patients with cardiovascular disease before and 7 days after the oral administration of ticlopidine, 250 mg b.i.d. Before and after ticlopidine, platelets stimulated with 1 U/ml thrombin aggregated, released about 80–90% 14C-serotinin and did not deaggregate spontaneously within 5 min from stimulation. Before ticlopidine, hirudin (5× the activity of thrombin) and PGE1 (10 μmol/1) plus chymotrypsin (10 U/ml) or plasmin (0.06 U/ml), added at the peak of platelet aggregation, caused slight or no platelet deaggregation. After ticlopidine, the extent of platelet deaggregation caused by the same inhibitors was significantly greater than before ticlopidine. The addition of ADP (10 μmol/1) to platelet suspensions 5 s after thrombin did not prevent the deaggregation of ticlopidine-treated platelets. Thus, ticlopidine facilitates the deaggregation of thrombin-induced human platelet aggregates, most probably because it inhibits the effects of ADP on platelets.

Effects of Bupranolol, a New β-Blocker, on Platelet Functions of Rabbit and Human in Vitro

1976 ◽  
Vol 36 (02) ◽  
pp. 376-387 ◽  
Author(s):  
Teruhiko Umetsu ◽  
Kazuko Sanai ◽  
Tadakatsu Kato
Keyword(s):  
Platelet Aggregation ◽  
Platelet Adhesion ◽  
Human Platelets ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
Β Blocker ◽  
Platelet Aggregates ◽  
Induced Aggregation ◽  
Platelet Functions

SummaryThe effects of bupranolol, a new β-blocker, on platelet functions were investigated in vitro in rabbits and humans as compared with propranolol, a well-known β-blocker. At first, the effect of adrenaline on ADP-induced rabbit platelet aggregation was studied because adrenaline alone induces little or no aggregation of rabbit platelets. Enhancement of ADP-induced rabbit platelet aggregation by adrenaline was confirmed, as previously reported by Sinakos and Caen (1967). In addition the degree of the enhancement was proved to be markedly affected by the concentration of ADP and to increase with decreasing concentration of ADP, although the maximum aggregation (percent) was decreased.Bupranolol and propranolol inhibited the (adrenaline-ADP-)induced aggregation of rabbit platelets, bupranolol being approximately 2.4–3.2 times as effective as propranolol. Bupranolol stimulated the disaggregation of platelet aggregates induced by a combination of adrenaline and ADP, but propranolol did not. Platelet adhesion in rabbit was also inhibited by the β-blockers and bupranolol was more active than propranolol. With human platelets, aggregation induced by adrenaline was inhibited by bupranolol about 2.8–3.3 times as effectively as propranolol.From these findings. We would suggest that bupranolol might be useful for prevention or treatment of thrombosis.

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