scholarly journals Effects of 1-S replaced and/or decarboxylated latamoxef on rabbit platelet aggregation in vitro.

1988 ◽  
Vol 46 (1) ◽  
pp. 71-77 ◽  
Author(s):  
Kiyohisa UCHIDA ◽  
Hisato KAKUSHI ◽  
Tsutomu SHIKE
Keyword(s):  
Platelet Aggregation ◽  
Rabbit Platelet

LY53857, a 5HT2 Receptor Antagonist, Delays Occlusion and Inhibits Platelet Aggregation in a Rabbit Model of Carotid Artery Occlusion

1991 ◽  
Vol 66 (03) ◽  
pp. 355-360 ◽  
Author(s):  
Harve C Wilson ◽  
William Coffman ◽  
Anne L Killam ◽  
Marlene L Cohen
Keyword(s):  
Electrical Stimulation ◽  
Platelet Aggregation ◽  
Carotid Artery ◽  
Receptor Antagonist ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Rabbit Platelet ◽  
Rabbit Platelets ◽  
5Ht2 Receptor

SummaryThe present study was designed to evaluate the effectiveness of the ergoline 5HT2 receptor antagonist, LY53857 in a rabbit model of vascular arterial occlusion. LY53857 (1 and 10 εM) inhibited serotonin amplified platelet aggregation responses to threshold concentrations of ADP in rabbit platelets in vitro. LY53857 (1 εM) not only inhibited the serotonin component of rabbit platelet aggregation, but also inhibited in vitro aggregation induced by ADP (48.7 ± 16.7% inhibition), collagen (76.1 ± 15.9% inhibition) and U46619 (65.2 ± 12.3% inhibition). The effectiveness of this ergoline 5HT2 receptor antagonist in blocking aggregation to ADP, collagen and U46619 may be related to its ability to inhibit a serotonin component of platelet aggregation since rabbit platelets possess high concentrations of serotonin that may be released during aggregation produced by other agents. Based on the effectiveness of LY53857 to inhibit rabbit platelet aggregation, we explored the ability of LY53857 to extend the time to carotid artery occlusion in rabbits following electrical stimulation of the artery. Reproducible carotid artery occlusion was induced in rabbits by moderate stenosis coupled to arterial cross clamping, followed by electrical stimulation. With this procedure, occlusion occurred at 47.0 ± 7 min (n = 30) after initiation of the electrical stimulation. Animals pretreated with LY53857 (50 to 500 εg/kg i.v.) showed a delay in the time to carotid artery occlusion (at 100 εg/kg i.v. occlusion time extended to 164 ± 16 min). Furthermore, ex vivo platelet aggregation from animals treated with LY53857 (300 εg/kg i.v.) resulted in 40.5% inhibition of platelet aggregation in response to the combination of ADP (1 εM) and serotonin (1 εM). These studies document the ability to obtain reproducible arterial occlusion in the rabbit and showed that intravenously administered LY53857 prolonged the time to carotid artery occlusion. Prolongation of carotid artery occlusion time was accompanied by inhibition of serotonin-amplified ADP-induced aggregation in rabbit platelets, an effect observed both in vitro and ex vivo. Thus, the rabbit is a useful model for studying the effectiveness of 5HT2 receptor antagonists in prolonging vascular occlusion induced by insult of the carotid artery.

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.

Enhanced Inhibition of in-Vitro Platelet Aggregation by a Targeted Antibody Conjugate Containing an Anti-Rabbit Platelet Glycoprotein Iib/Iiia Antibody

1994 ◽  
Vol 86 (s30) ◽  
pp. 18P-18P
Author(s):  
R S More ◽  
M A Azrin ◽  
M J Underwood ◽  
S Pringle ◽  
M D Ezekowitz ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Glycoprotein ◽  
Rabbit Platelet ◽  
Antibody Conjugate

Effects of Ethanol on Pathways of Platelet Aggregation In Vitro

1988 ◽  
Vol 59 (03) ◽  
pp. 383-387 ◽  
Author(s):  
Margaret L Rand ◽  
Marian A Packham ◽  
Raelene L Kinlough-Rathbone ◽  
J Fraser Mustard
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Secondary Phase ◽  
Primary Phase ◽  
Rabbit Platelet ◽  
Membrane Phospholipids ◽  
Rabbit Platelets ◽  
Induced Aggregation

SummaryEthanol, at physiologically tolerable concentrations, did not affect the primary phase of ADP-induced aggregation of human or rabbit platelets, which is not associated with the secretion of granule contents. Potentiation by epinephrine of the primary phase of ADP-induced aggregation of rabbit platelets was also not inhibited by ethanol. However, ethanol did inhibit the secondary phase of ADP-induced aggregation which occurs with human platelets in citrated platelet-rich plasma and is dependent on the formation of thromboxane A2. Inhibition by ethanol of thromboxane production by stimulated platelets is likely due to inhibition of the mobilization of arachidonic acid from membrane phospholipids, as ethanol had little or no effect on aggregation and secretion induced by arachidonic acid or the thromboxane mimetic U46619. Rabbit platelet aggregation and secretion in response to low concentrations of collagen, thrombin, or PAF were inhibited by ethanol. Inhibition of the effects of thrombin and PAF was also observed with aspirin-treated platelets. Thus, in addition to inhibiting the mobilization of arachidonate for thromboxane formation that occurs with most agonists, ethanol can also inhibit aggregation and secretion through other effects on platelet responses.

scholarly journals Inhibition of Endotoxic Lipopolysaccharide-mediated Platelet Aggregation by Cobra Venom Anticomplementary Factor

Blood ◽  
1974 ◽  
Vol 44 (3) ◽  
pp. 399-409 ◽  
Author(s):  
Jack S. C. Fong ◽  
James G. White ◽  
Robert A. Good
Keyword(s):  
Platelet Aggregation ◽  
Critical Time ◽  
Protein S ◽  
Cobra Venom ◽  
In Vivo Studies ◽  
Rabbit Platelet ◽  
Response Curves ◽  
Complement Components

Abstract Aggregometry studies on endotoxic lipopolysaccharide (LPS)-mediated rabbit platelet aggregation were performed. Different preparations of LPS showed characteristic aggregometry profiles, and LPS with potent anticomplementary activities generally had a more vigorous platelet aggregation function than did LPS preparations with lesser anticomplementary functions. Cobra venom anticomplementary factor (CVF) inhibited LPS-platelet interaction, and the inhibition was both time and dose dependent. Dose-response curves of CVF inhibition on LPS or zymosan-mediated platelet aggregation were essentially identical. In vitro and in vivo studies showed that CVF inhibition persisted even when hemolytic complement activities reached more than 70% of those originally present. At the critical time of days 5 or 6 following CVF administration, the lack of platelet responses towards LPS could be restored by addition of fresh plasma from normal or C6-deficient rabbits, but not with plasma that had been treated with antigen— antibody complexes, zymosan, or heating at 56° for 30 min. The experimental data indicate that serum protein(s) other than the terminal complement components are involved in LPS-platelet interaction. It seems most likely that the factor(s) perturbed reside in the mechanisms involved in activation of the alternate pathway. Furthermore, it appears quite possible that LPS-platelet interactions can be inhibited by manipulating the humoral factor(s) involved rather than by altering the platelets themselves.

The Effect of Phenylpropanoid Glycosides on Rabbit Platelet Aggregation In Vitro.

1993 ◽  
Vol 27 ◽  
pp. 113-114 ◽  
Author(s):  
A. Capasso ◽  
A. Di Giannuario ◽  
D. De Medici ◽  
S. Pieretti ◽  
M. Nicoletti
Keyword(s):  
Platelet Aggregation ◽  
Rabbit Platelet ◽  
Phenylpropanoid Glycosides

A Pharmacologic Approach To The Modification Of The Electrokinetic And Aggregability Characteristics Of Rabbit Platelets In Vitro

1981 ◽  
Author(s):  
Thomas R Lucas ◽  
D Firriolo ◽  
Philip N Sawyer
Keyword(s):  
Platelet Aggregation ◽  
Surface Charge ◽  
Platelet Function ◽  
Rabbit Platelet ◽  
Secondary Wave ◽  
Platelet Surface ◽  
Rabbit Platelets ◽  
Membrane Changes ◽  
Pharmacologic Agents

An attempt was made to correlate changes in the electrokinetic characteristics of rabbit platelets with alterations in platelet function. In an effort to modify the surface charge characteristics of the rabbit platelet, several pharmacologic agents were used, i.e., heparin, chlorpromazine, and neuraminidase. A Seaman microelectrophoresis apparatus and a chronolog platelet aggregometer were used to measure platelet membrane changes and aggregation. The control electrophoretic mobility (EM) was 0.875±0.005µ for 18 independent blood samples. Heparin increased the EM to 0.99±0.005 in 10 samples. Chlorpromazine decreased the EM to 0.860±0.005 and neuraminidase decreased the EM to 0.73±0.001. The results were significant when compared to baseline (p=0.005). Heparin inhibited thrombin induced platelet aggregation while neuraminidase enhanced primary aggregation and chlorpromazine blocked the secondary wave of platelet aggregation. The results indicate that increased surface negativity reduces platelet aggreg-ability, while a decrease in surface negativity results in altered platelet function affecting primary platelet interaction. The results suggest altered platelet surface charge characteristics as a possible mechanism for platelet aggregation and thrombosis. This study also suggests in part the role of heparin in reducing thrombosis formation by inhibiting platelet-platelet interaction via increased surface negativity.

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