Blood & Vessel
Online ISSN : 1884-2372
Print ISSN : 0386-9717
The role of platelets on the vascular injuries caused by arachidonic acid or ADP
Tsukasa FUJIMOTOHidenori SUZUKISetsuko ALIGAKenjiro TANOUEYoshiharu FUKUSHIMAHiroh YAMAZAKI
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1983 Volume 14 Issue 4 Pages 425-430

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Abstract
Experimental vascular iujuries induced by activation of platelets were observed under electron microscopy. Twenty eight rabbits were divided into two groups. In the first group, 0.7mg/kg of sodium arachidonate (AA) or 20-40mg/kg of ADP was injected into right carotid artery. AA was injected for 5 seconds and ADP was injected for one minute. In the second group, blood in the carotid arteries was washed out with saline throughout from 10 seconds before to one minute after the injection of AA or ADP. Immediately after, and 5 and 60 minutes after the injection, middle cerebral arteries in the subarachnoid space were isolated and observed under electron microscopy.
Immediately after the AA injection, deendothelialization, edematous changes in subendothelial layer and convolution of internal elastic lamina were seen in both groups. Adhesion of platelets on the deendothelialized inner surface was observed frequently. Sixty minutes after, abundant platelet thrombi with fibrin formation were seen. The results suggest the direct effect of AA, as a detergent agent, caused vascular injuries. Immediately after the ADP injection, small aggregates of platelets were seen in the vascular lumen in the first group, whlie the vascular wall showed completely normal finding in the second group. After 5 minutes, remarkable intracytoplasmic vesicular formation in endothelial cells was observed. Edematous changes in subendothelium and even in smooth muscle cells and sporadic deendothelialization were also seen. Adhesion of platelets on the deendothelialized site was seen. After 60 minutes, platelet thrombi with fibrin formation were observed. On the other hand, such injuries were not seen in any of the second group after the ADP injection. The results suggest that the presence of blood, especially aggregation of platelets, must be necessary to produce these vascular injuries.
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© The Japanese Society on Thrombosis and Hemostasis
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