Search PubMed⌕ Search

Biomedical subjects

Huzoor-Akbar

Publications and source records attributed to Huzoor-Akbar.

27 records · Page 2Linked to original sources
PubMed1982

Potentiating effects of clofibrate on prostaglandin-dependent and -independent pathways of human platelet activation: evidence for involvement of cyclic AMP.

Although clofibrate has been shown to inhibit platelet aggregation that is caused by thrombin, ADP and epinephrine, by blocking the release of arachidonic acid from platelet phospholipids [8], here we have demonstrated that clofibrate enhanced platelet aggregation by arachidonic acid and PLC and reversed the effects of PGE1 on platelet cAMP concentration and on PLC-induced secretion of [14C]-5HT in similar, concentration-dependent manners. Taken together, these findings strongly suggest that the proaggregatory effect of clofibrate is mediated by a lowering of cAMP in platelets.

Arachidonic Acid↗
PubMed1977

The effect of halofenate--free acid on aggregation--the release reaction, coagulant activity, and lipid metabolism of human platelets.

Halofenate--free acid (HFA), the major metabolite of the hypolipidemic drug, halofenate, inhibited platelet aggregation induced by collagen and sodium arachidonate and blocked the second phase of aggregation caused by ADP, thrombin and epinephrine in human platelet-rich plasma. The aggregation of washed platelets by thrombin and collagen was also blocked. HFA also inhibited the release by thrombin and collagen of 5-hydroxytryptamine from dense granules of platelets and the release by thrombin of beta-glucuronidase from platelet alpha-granules. These inhibitory effects were concentration and time-dependent. HFA decreased platelet factor 3 activity by 31% and also inhibited the incorporation of 14C-acetate and U-14C-glucose into platelet lipids by 89% and 56% respectively. Thrombin-induced lipid peroxidation and prostaglandin formation was investigated by measuring the by-product malonyldialdehyde, and this was found to be inhibited by HFA. It is suggested that the effect of HFA on aggregation is attributable to inhibition of the release reaction which may in turn be a consequence of the effects of the drug on platelet lipid synthesis.

Aspirin↗
PubMed1977

Platelet activation in haemostasis: role of thrombin and other clotting factors in platelet-collagen interaction.

The mechanism of activation of platelets by collagen was examined. Hirudin interfered with the initial collagen-platelet interaction and both hirudin and heparin inhibited collagen-induced release of platelet granular contents. Hirudin completely inhibited the release of both [3H]5HT and beta-glucuronidase whereas heparin completely inhibited release of beta-glucuronidase but only partly inhibited release of [3H] 5HT. beta-Glucuronidase and maximal [3H] 5HT were only released when plasma was present. The results are compatible with an essential intermediary role for thrombin in collagen activation of platelets. Evidence was also obtained that von Willebrand factor may participate in this reaction.

Blood Coagulation Factors↗
PubMed1976

Evidence that colagen releases human platelet constituents by two different mechanisms.

Collagen is believed to be involved in the initial events in haemostasis and has been shown by others to cause platelet aggregation and release, and also to initiate the intrinsic pathway of coagulation. The present experiments provide evidence whihc suggests how these many effects of collagen may be involved in haemostasis. It is shown here that collagen releases platelet constituents by two different pathways. Collagen causes platelets washed free of loosely adsorbed coagulation factors to release constituents. This activity, is therefore, independent of the intrinsic pathway of coagulation, and is not inhibited by heparin or hirudin. Collagen also releases platelet constituents by an alternative pathway which is inhibited by heparin and hirudin and is independent of factor XII, but is dependent on factor XI, subsequent factors in the intrinsic pathway of coagulation and calcium. These results suggest that collagen-induced release of platelet constituents is in part due to a direct effect on the platelet, and , in part, to an indirect effect involving coagulation factors and mediated by thrombin. The present results suggest that irreversible aggregation by collagen is also mediated by thrombin. The possible significance of this dual action of collagen in the haemostatic process is shown in Fig 7.

Blood Platelets↗