Human platelet rich plasma and human serum protects from inactivation the antiaggregatory capacity of prostacyclin-like material (PGI2) produced by the rat stomach fundus.
Prostacyclin (PGI2) synthetizing capacity of rat stomach fundus in Krebs-Ringer-Bicarbonate (KRB); human platelet rich plasma (PRP) or human serum (HS), was explored. The basal production of PGI2-like material was similar in the three media, suggesting the absence of any special substance in plasma or serum able to modify prostacyclin synthesis from tissue substrate. On the other hand it was also documented that in PRP and in HS the antiaggregatory activity of the PGI2-like material declined in its capacity less than 50% following 60 minutes of incubation at 37 degrees C, whereas it almost disappeared when incubated in KRB. Possible explanations underlying such finding are discussed.
D000818:Animals; D000925:Anticoagulants / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism*; D001798:Blood Proteins / Q000378:metabolism; D011464:Epoprostenol / Q000494:pharmacology*; D004903:Erythrocyte Aggregation / Q000187:drug effects*; D005753:Gastric Mucosa / Q000378:metabolism*; D006801:Humans; D008297:Male; D011453:Prostaglandins / Q000494:pharmacology*; D051381:Rats
D000925:Anticoagulants; D001798:Blood Proteins; D011453:Prostaglandins; D011464:Epoprostenol