Lograno M D, Mosconi C, Marangoni F, Medini L, Grassi G, Galli C
Pharmaco-Biological Department, University of Bari, Italy.
Eur J Pharmacol. 1991 Sep 24;202(3):311-6. doi: 10.1016/0014-2999(91)90272-r.
We studied the aggregation of collagen and ADP-stimulated platelet-rich plasma (PRP) and the formation of thromboxane B2 (TxB2) by collagen-stimulated PRP in spontaneously hypertensive rats (SHR) and in Wistar-Kyoto control rats (WKY). In addition, we evaluated the inhibition of the aggregation of PRP following homologous or heterologous perfusions through isolated aortas, the release of 6-keto-prostaglandin (PG)F1 alpha from these arteries perfused with PRP, and the sensitivity of PRP to the antiaggregatory activity of the stable PGI2 analogue, iloprost, in both SHR and WKY. The lower activities (aggregation induced by ADP and collagen, collagen-stimulated TxB2 production) of SHR platelets, were not accompanied by morphological differences from WKY platelets. These changes were associated with a greater release of arterial 6-keto-PGF1 alpha, with greater platelet antiaggregatory activity of the arterial wall and with higher sensitivity of platelets to iloprost. The lower reactivity of platelets to aggregating agents, and the greater sensitivity to prostacyclin, associated with a greater production of arterial prostacyclin were the major changes observed in SHR animals. These alterations in the SHR vs. normotensive WKY may lead to an enhanced risk of hemorrhage in the hypertensive state.
我们研究了自发性高血压大鼠（SHR）和Wistar-Kyoto对照大鼠（WKY）中胶原蛋白诱导的富含血小板血浆（PRP）聚集以及ADP刺激的PRP中血栓素B2（TxB2）的形成。此外，我们评估了通过离体主动脉进行同源或异源灌注后PRP聚集的抑制情况、用PRP灌注这些动脉后6-酮-前列腺素（PG）F1α的释放，以及SHR和WKY中PRP对稳定的前列环素类似物伊洛前列素抗聚集活性的敏感性。SHR血小板较低的活性（ADP和胶原蛋白诱导的聚集、胶原蛋白刺激的TxB2产生），并未伴随与WKY血小板在形态上的差异。这些变化与动脉6-酮-PGF1α的更大释放、动脉壁更高的血小板抗聚集活性以及血小板对伊洛前列素更高的敏感性相关。血小板对聚集剂的反应性较低，以及对前列环素的敏感性较高，同时伴随着动脉前列环素产生增加，是在SHR动物中观察到的主要变化。与血压正常的WKY相比，SHR的这些改变可能导致高血压状态下出血风险增加。
