The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform

Thomas J. Divers - One of the best experts on this subject based on the ideXlab platform.

  • The effects of pentoxifylline on equine Platelet Aggregation
    Journal of veterinary internal medicine, 2010
    Co-Authors: Bruce G. Kornreich, M Enyeart, Sophy A. Jesty, Daryl V. Nydam, Thomas J. Divers
    Abstract:

    Background: Pentoxifylline (PTX) possesses a number of vasomotor, immunomodulatory, and hemorheologic properties. Based upon the hypothesis that equine laminitis and navicular disease result from microthrombosis, the inhibitory effects of PTX on inflammatory cytokines, and its inhibitory effects on human Platelet Aggregation, PTX has been widely used to treat equine endotoxemia, navicular disease, and laminitis. Despite this, the effects of PTX on equine Platelet Aggregation have not been investigated previously. Hypothesis: PTX decreases Platelet Aggregation in equine whole blood at concentrations approximating those achieved in horses given clinically relevant doses of PTX. Animals: Seven healthy adult horses from a research herd. Methods: Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate Aggregation. Results: The onset time of collagen-induced equine Platelet Aggregation was significantly shortened by PTX. The maximum slope of resistance change (dR/dt) and total resistance change of collagen-induced Platelet Aggregation were unaffected by PTX. No effects of PTX on ADP-induced onset time of Aggregation, dR/dt, or total resistance change were observed. Conclusions and Clinical Importance: Our hypothesis is not supported by the results. PTX hastens the onset of collagen-induced Platelet Aggregation in equine whole blood, but has no effect on the rate of collagen-induced Aggregation. PTX does not affect ADP-dependent equine Platelet Aggregation. Given these findings, PTX may not be a reasonable therapeutic option to decrease Platelet Aggregation in horses.

Chanwit Roongsritong - One of the best experts on this subject based on the ideXlab platform.

  • Gender differences in Platelet Aggregation in healthy individuals
    Journal of Thrombosis and Thrombolysis, 2010
    Co-Authors: Mohammad Otahbachi, Jan Simoni, Grace Simoni, John F. Moeller, Cihan Cevik, Gary Meyerrose, Chanwit Roongsritong
    Abstract:

    This study evaluated gender variability in Platelet Aggregation in response to common agonists. Platelet Aggregation was measured in 36 healthy men and women free of any antiPlatelet medication, aged 22–36 years, of Caucasian (White not of Hispanic origin), Hispanic, and African-American not of Hispanic origin. In this ex-vivo study, we investigated Platelet Aggregation in response to adenosine-5′-diphosphate (ADP), epinephrine (EPI), arachidonic acid (AA) and collagen (COL), using a Platelet ionized calcium aggregometer (Chrono-Log Co.). Platelet Aggregation response to all tested agonists was higher in females than in males regardless of ethnicity. The most significant differences were observed with collagen ( P  

  • Gender differences in Platelet Aggregation in healthy individuals.
    Journal of thrombosis and thrombolysis, 2009
    Co-Authors: Mohammad Otahbachi, Jan Simoni, Grace Simoni, John F. Moeller, Cihan Cevik, Gary Meyerrose, Chanwit Roongsritong
    Abstract:

    This study evaluated gender variability in Platelet Aggregation in response to common agonists. Platelet Aggregation was measured in 36 healthy men and women free of any antiPlatelet medication, aged 22-36 years, of Caucasian (White not of Hispanic origin), Hispanic, and African-American not of Hispanic origin. In this ex-vivo study, we investigated Platelet Aggregation in response to adenosine-5'-diphosphate (ADP), epinephrine (EPI), arachidonic acid (AA) and collagen (COL), using a Platelet ionized calcium aggregometer (Chrono-Log Co.). Platelet Aggregation response to all tested agonists was higher in females than in males regardless of ethnicity. The most significant differences were observed with collagen (P < 0.01). Among the ethnic groups, Caucasian women were most prone to Platelet Aggregation. Gender is a determinant of agonist effects on Platelet aggregability in healthy subjects.

Michael Aviram - One of the best experts on this subject based on the ideXlab platform.

  • fosinopril reduces adp induced Platelet Aggregation in hypertensive patients
    Journal of Cardiovascular Pharmacology, 1996
    Co-Authors: Shlomo Keidar, J Oiknine, Adi Leiba, Chen Shapira, Marcel Leiba, Michael Aviram
    Abstract:

    : Platelets are intimately involved in atherosclerosis, and hypertension is a known risk factor for coronary artery disease. The angiotensin-converting enzyme (ACE) inhibitors were demonstrated to reduce hypertension and attenuate atherosclerosis. Because increased Platelet Aggregation was shown in hypertensive patients, the effect of a new ACE inhibitor, fosinopril, on Platelet Aggregation was studied. Fosinopril therapy (10 mg/day for 4 weeks) in 18 male hypertensive patients showed > or = 31% reduction in ADP-induced Platelet Aggregation. In vitro studies showed that fosinopril had similar inhibitory effect on ADP-induced Platelet Aggregation. No inhibitory effect could be detected with collagen as the aggregating agent. Finally, inhibition of Platelet Aggregation by fosinopril was less effective in Platelets derived from hypertensive patients as compared with Platelets derived from normal subjects. We conclude that fosinopril possesses a significant inhibitory activity on ADP-induced Platelet Aggregation both in vitro and in vivo.

Bruce G. Kornreich - One of the best experts on this subject based on the ideXlab platform.

  • The effects of pentoxifylline on equine Platelet Aggregation
    Journal of veterinary internal medicine, 2010
    Co-Authors: Bruce G. Kornreich, M Enyeart, Sophy A. Jesty, Daryl V. Nydam, Thomas J. Divers
    Abstract:

    Background: Pentoxifylline (PTX) possesses a number of vasomotor, immunomodulatory, and hemorheologic properties. Based upon the hypothesis that equine laminitis and navicular disease result from microthrombosis, the inhibitory effects of PTX on inflammatory cytokines, and its inhibitory effects on human Platelet Aggregation, PTX has been widely used to treat equine endotoxemia, navicular disease, and laminitis. Despite this, the effects of PTX on equine Platelet Aggregation have not been investigated previously. Hypothesis: PTX decreases Platelet Aggregation in equine whole blood at concentrations approximating those achieved in horses given clinically relevant doses of PTX. Animals: Seven healthy adult horses from a research herd. Methods: Whole blood impedance aggregometry using whole equine blood incubated with varying concentrations of PTX. Adenosine diphosphate (ADP) and collagen were used to initiate Aggregation. Results: The onset time of collagen-induced equine Platelet Aggregation was significantly shortened by PTX. The maximum slope of resistance change (dR/dt) and total resistance change of collagen-induced Platelet Aggregation were unaffected by PTX. No effects of PTX on ADP-induced onset time of Aggregation, dR/dt, or total resistance change were observed. Conclusions and Clinical Importance: Our hypothesis is not supported by the results. PTX hastens the onset of collagen-induced Platelet Aggregation in equine whole blood, but has no effect on the rate of collagen-induced Aggregation. PTX does not affect ADP-dependent equine Platelet Aggregation. Given these findings, PTX may not be a reasonable therapeutic option to decrease Platelet Aggregation in horses.

Amelia Filippelli - One of the best experts on this subject based on the ideXlab platform.

  • Effects of nebivolol on human Platelet Aggregation.
    Journal of cardiovascular pharmacology, 2001
    Co-Authors: M. Falciani, F. Rossi, Barbara Rinaldi, Bruno D'agostino, Filomena Mazzeo, Settimio Rossi, Brúno Nobili, Amelia Filippelli
    Abstract:

    It has been documented that beta-adrenergic antagonists can influence Platelet Aggregation by a mechanism independent of their ability to antagonize beta-adrenoceptors. Nebivolol, a selective beta1-adrenergic receptor antagonist with additional hemodynamic effects, is able to vasodilate human forearm vasculature by acting on the L-arginine/nitric oxide pathway. Constitutive nitric oxide synthase is present also in human Platelets, resulting in the formation of nitric oxide, an endogenous inhibitor of Platelet Aggregation. The aim of this study was to investigate the effects of nebivolol on Platelet Aggregation and in particular to determine the involvement of the Platelet L-arginine/nitric oxide pathway. Propranolol, a nonselective beta-adrenergic antagonist, and carvedilol, a beta-blocker with vasodilating properties, were compared with nebivolol on Platelet activity. Plasma from healthy male subjects was used. Platelet Aggregation was achieved with adenosine diphosphate (ADP) (3 microM) and collagen (1 microg/ml), using the Born turbidimetric method to measure Platelet Aggregation. Our results showed that nebivolol, propranolol, and carvedilol all had an inhibitory effect on both ADP- and collagen-induced Platelet Aggregation. Nebivolol exhibited the greatest inhibition effect on Platelet Aggregation. The mechanism responsible for the inhibitory effect of nebivolol appeared to involve a nitric oxide-dependent pathway. Indeed, L-arginine augmented the inhibitory effects of nebivolol on Platelet Aggregation induced by collagen and ADP. Furthermore, the inhibitory effect of nebivolol on Platelet Aggregation was reduced in the presence of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA). In conclusion, we have demonstrated in this study that nebivolol's mechanism of Platelet Aggregation inhibition differs from that of other beta-adrenergic antagonists by being partially dependent on nitric oxide production.