TY - JOUR
T1 - Platelet-vessel wall interactions
T2 - Effects of platelets and plasma on the antiaggregatory activity and 6 keto-PGF1α production in isolated perfused aortas
AU - Galli, C.
AU - Petroni, A.
AU - Socini, A.
AU - Agradi, E.
AU - Colombo, C.
AU - Folco, G. C.
AU - Tremoli, E.
PY - 1981
Y1 - 1981
N2 - An experimental model for the study of platelet-vessel wall interactions has been developed, based on perfusion of rat platelet-rich plasma (PRP) through isolated rat aortas. In the perfused PRP, platelet aggregation was inhibited and levels of 6 Keto PGF1α and cAMP were elevated over the values found in non perfused PRP. When PPP or buffer were perfused through the isolated artery, elevations of 6 Keto PGF1α levels in the perfusate were smaller (in perfused PPP) or of shorter duration (in both perfused PPP and buffer). The presence of platelets in the perfusion fluids thus enhanced the formation of Prostacyclin by the arterial wall. Levels of 6 Keto PGF1α in PRP obtained from aspirin-treated animals and in PRP from normal animals, both perfused through normal aortas, were the same, and also levels of the above metabolite in normal PRP perfused through aortas of aspirin-treated animals did not differ from those found in non perfused PRP. It is concluded, from these data, that PRP does not stimulate PGI2 formation in perfused aortas by providing cyclic endoperoxides. The experimental model developed allows the study of interactions between normal platelets and aortas from experimentally treated animals or viceversa.
AB - An experimental model for the study of platelet-vessel wall interactions has been developed, based on perfusion of rat platelet-rich plasma (PRP) through isolated rat aortas. In the perfused PRP, platelet aggregation was inhibited and levels of 6 Keto PGF1α and cAMP were elevated over the values found in non perfused PRP. When PPP or buffer were perfused through the isolated artery, elevations of 6 Keto PGF1α levels in the perfusate were smaller (in perfused PPP) or of shorter duration (in both perfused PPP and buffer). The presence of platelets in the perfusion fluids thus enhanced the formation of Prostacyclin by the arterial wall. Levels of 6 Keto PGF1α in PRP obtained from aspirin-treated animals and in PRP from normal animals, both perfused through normal aortas, were the same, and also levels of the above metabolite in normal PRP perfused through aortas of aspirin-treated animals did not differ from those found in non perfused PRP. It is concluded, from these data, that PRP does not stimulate PGI2 formation in perfused aortas by providing cyclic endoperoxides. The experimental model developed allows the study of interactions between normal platelets and aortas from experimentally treated animals or viceversa.
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U2 - 10.1016/0090-6980(81)90209-4
DO - 10.1016/0090-6980(81)90209-4
M3 - Article
C2 - 6276925
AN - SCOPUS:0019793096
VL - 22
SP - 703
EP - 713
JO - Prostaglandins and Other Lipid Mediators
JF - Prostaglandins and Other Lipid Mediators
SN - 1098-8823
IS - 5
ER -