الفهرس 
introductionOnly 14 pages are availabe for public view
 |  | from | 88 |  |  |
| | | from | 88 | | |
Abstract
Platelets play an essential role in precipitating myocardial ischaemia, as platelet aggregation have frequently been found in coronary arteries after sudden death (Ekelandand Oro 1979 and Ikeda et al., 1981). They may also aggravate ischaemia by releasing a vasoconstrictor agent, thromboxane A2. (Lewy et 81.1 l98).
On the other hand, some studies postulate that, since platelet aggregation are Ca+4 dependant, therefore Ca antagonists can prevent thrombus formation (Kiyonoto et a!., 1983; and Mehta, 1985). They added that verapamil hydrochloride or any other Ca— channel blocking agent have inhibitory effect on all platelet functions mediated by calcium ions.
In contrary to that, Margolis et a!. (1980) reported an insignificant effects of verapamil hydrechloride on the platelet functions studied in their experiments.
Dale et a!. (1983) claimed that verapamil hydrochloride can affect some platelet functions and leave the others, as it can reduce aggregation and prolong bleeding time, cannot affect platelet adhesiveness.
Therefore, this work was planned to clarify these cortradictory reports and to demonstrate the exact effect of verapamil
hydrochloride as a Ca’- channel blocking agent, on platelet
functions as aggregation, adhesiveness, clot retraction and bleeding time, and to demonstrate its effect on other heamostatic parameter\?s Including clotting time and prothrornbin time.