The effect of acute alcohol intoxication on psychometric testing and 5-HT-induced platelet aggregation in normal subjects: Modulatory role of evening primrose oil

1990 ◽  
Vol 5 (3) ◽  
pp. 245-248
Author(s):  
R. Corbett ◽  
J. B. A. Meagher ◽  
B. E. Leonard
1995 ◽  
Vol 19 (3) ◽  
pp. 759-762 ◽  
Author(s):  
Hanna Taivainen ◽  
Kalevi Laitinen ◽  
Riitta Tahtela ◽  
Kalervo Kiianmaa ◽  
Matti J. Valimaki

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Andrew L Frelinger ◽  
Youfu Li ◽  
Matthew D Linden ◽  
Inge Tarnow ◽  
Marc R Barnard ◽  
...  

Background: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a platelet function test) has been widely reported, but the underlying mechanism is unclear. We examined the role of pre-existent platelet hyperreactivity in aspirin “resistance”. We also determined the correlation between aspirin resistance defined by serum thromboxane (TX) B 2 (the most specific test of aspirin’s effect) and other assays of platelet function. Methods: Platelet function measured before and after aspirin 81 mg daily for 7 days was analyzed by Spearman’s rank correlation. Normal subjects (n=165) were studied because virtually all clinically relevant patients are already taking aspirin. An additional advantage of the use of normal subjects is that the platelet response to stimuli is not influenced (with resultant increased scatter of the data) by an underlying disease, e.g. coronary artery disease, which causes platelet hyperreactivity. Results: The proportion of the post-aspirin platelet function predicted by the pre-aspirin platelet function was 28.3 ± 7.5% (mean ± asymptotic standard error) for serum TXB 2 , 39.3 ± 6.8% for urinary 11-dehydro TXB 2 , 4.4 ± 7.7% for arachidonic acid-induced platelet aggregation, 40.4 ± 7.1% for ADP-induced platelet aggregation, 26.3 ± 9.2% for the VerifyNow Aspirin Assay®, and 45.0 ± 10.9% for the TEG® PlateletMapping ™ System with arachidonic acid. Spearman rank order correlations were highly significant for comparisons between assays when both pre-aspirin and post-aspirin results were included in the analysis. However, residual serum TXB 2 levels post-aspirin treatment were not significantly associated with post-treatment results of any of the other assays. Platelet count correlated with pre-aspirin serum TXB 2 and VerifyNow Aspirin Assay, but not with any post-aspirin platelet function test. Conclusions: Aspirin “resistance” (i.e. hyporesponsiveness to aspirin in a laboratory test) is in part unrelated to aspirin but is the result of underlying platelet hyperreactivity prior to the institution of aspirin therapy. Individuals identified as aspirin “resistant” defined by serum TXB 2 are not the same individuals identified by the other tests.


1954 ◽  
Vol 32 (4) ◽  
pp. 465-469 ◽  
Author(s):  
E. J. Masoro ◽  
Henry Abramovitch

The role of insulin in ethanol metabolism was investigated with the aid of C14-labeled ethanol. Surviving kidney and liver slices prepared from insulized rats oxidized ethanol to carbon dioxide at approximately the same rate as slices prepared from control rats. The data on the effect of insulin on the conversion of ethanol to lipids are equivocal since the P value is 0.036. There appears to be some increase in lipogenesis but not of an appreciable magnitude. The possibility that the beneficial effects noted in the treatment of acute alcohol intoxication with insulin may be the result of an increased synthetic metabolism is discussed.


Blood ◽  
1988 ◽  
Vol 72 (5) ◽  
pp. 1717-1725 ◽  
Author(s):  
HJ Weiss ◽  
B Lages

Abstract Aggregation responses and thromboxane (Tx) formation in ten patients with storage pool deficiency (SPD) specific to the dense granules (delta-SPD) were studied to assess further the role of dense granule adenosine diphosphate (ADP) in mediating platelet aggregation by epinephrine. The ability of epinephrine to elicit secondary aggregation (SA) responses was highly variable in delta-SPD when tested at 5 mumol/L epinephrine, but was consistently abnormal when tested over a range of concentrations. The occurrence of SA in both delta-SPD patients and normal subjects was correlated with the magnitude of the rate of primary aggregation (PA). This PA rate was normal, on average, for the entire patient group but was greater in patients with more consistent SA responses. The PA findings were related to the Kd value obtained in binding studies with 3H-yohimbine, but not with the number of alpha 2-receptor sites. Studies on Tx production (assessed by radioimmunoassay of TxB2) showed that the ability to synthesize Tx from arachidonate was not impaired in delta-SPD, and that there was an absolute positive correlation between epinephrine-induced SA and Tx production. Aggregation in delta-SPD platelets in response to the Tx receptor agonist U44069 was consistently decreased, but could be corrected by addition of ADP. The results of the study suggest that dense granule-derived ADP is not required for PA by epinephrine, but mediates SA as a synergistic agonist with TxA2. This role of ADP in SA may be elucidated more precisely by further studies on platelet activation processes in delta-SPD.


2016 ◽  
Vol 176 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Bettina Grüne ◽  
Daniela Piontek ◽  
Oliver Pogarell ◽  
Armin Grübl ◽  
Cornelius Groß ◽  
...  

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4105-4105
Author(s):  
Xiaoxu Lu ◽  
De Pei Wu ◽  
Yue Han ◽  
Lan Dai ◽  
Wenhong Sheng

Abstract Objective In order to compare the functions of ADP in platelet aggregation and platelet membrane surface glycoproteins expression after thrombin receptors activation, then to investigate the role of ADP in thrombin signal transmission. Methods Peptide SFLLRN (PAR1-AP, TRAP) and AYPGKF(PAR4-AP)were used for stimulating platelet at different time points (0~30minute) in 12 normal subjects, then the alterations of platelet aggregation and GPIbα, P-selectin were analyzed in the involvement of ADP inhibitor, ApyraseVII, which was observed by aggregometer and flowcytometry respectively. Results Either PAR1 or PAR4 peptide can lead to platelet activation, inducing absolute platelet aggregation, together with a persistent increase of P-selectin and reversible interlisation of GPIb. Platelet aggregation was partly inhibited by ApyraseVII and showed a reversible curve upon PAR1 activation, and no change upon PAR4 activation. In addition, ApyraseVII accelerated the return of GPIb to platelet surface in PAR1 pathway, produced weak effect on GPIbα internalisation, … ltogether with little effect on GPIb alteration in PAR4 pathway. Meanwhile, no change of P-selectin was obtained in the involvement of Apyrase for both peptides. Conclusion All the results confirm a critical role of ADP in thrombin signal transmission through the process of PAR1 pathway. ADP induces platelet aggregation and slows down the restoration of GPIb to platelet surface.


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