Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation system and platelets play an important role in the stage of lodgement of tumor cells. We examined abilities of human and hamster pancreatic cancer cell lines to aggregate platelets in vitro, and investigated the effect of prostaglandin E1, I2, on artificial liver metastases of pancreatic cancer in Syrian golden hamster. Platelet aggregating activities were found in five out of six human pancreatic cancer cell line and thromboplastin likes activity in five cell lines. Diisopropanolnitrosamine induced hamster pancreatic cancer cells (HPK-1) were able to aggregate platelets both in vitro and in vivo and these activities were inhibited by prostaglandin I2. Hamster was inoculated intraportally with 1 X 10(6) HPK-1 cells. After two weeks autopsy of these hamsters revealed multiple metastatic nodules on liver surface. In this model we administered prostaglandin E1, I2 into the portal vein five minutes before cell inoculation. Number of liver surface nodules were significantly decreased to 33.1 + 7.0, 11.0 + 9.6 in hamster given 100g PGE1 PGI2 before cell inoculation, compared with control group of hamsters (62.0 + 6.6 PH9.3, 66.1 + 13.9 PH7.4). But administration of prostaglandin after cell injection was not effective. In all cases none of extrahepatic metastases were noted. Inhibitory action of PGE1 PGI2 on liver metastasis is suspected to be related to inhibition of platelet aggregation.
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PMID:[Inhibitory effect of anti-platelet prostaglandin on liver metastasis of hamster pancreatic cancer]. 250 99

Discontinuous plasma exchange with prostaglandin I2 (5 ng/kg/min) and low dosage heparin (5-6 IU/kg/min) (treatment I), and ACD solution alone (treatment II) was studied. During both treatments the activated partial thromboplastin time remained within the normal range. After treatment I platelet count was not decreased but in vitro platelet aggregation was reduced (p less than 0.001). After treatment II platelet count was reduced and in vitro platelet aggregation unchanged. Prostaglandin I2 at this dosage caused no cardiovascular complications. The physiopathological implications of these differences are discussed.
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PMID:Plasma exchange with prostaglandin I2 and ACD solution: comparative effects. 354 62

Platelet sensitivity to adenosine di-phosphate (ADP), thrombin, collagen, arachidonic acid and prostaglandin I2 (PGI2) and the activity of the coagulation system as measured by the activated partial thromboplastin time, prothrombin time, Russell's viper venom time and plasma fibrinogen have been examined in male and female rats, female rats during the oestrous cycle and female rats treated with oestrogen and a progestogen. Male rat platelets were less sensitive to thrombin and more sensitive to inhibition by PGI2 than those from females and fibrinogen levels in male rat plasma were approximately twice those seen in females. During the oestrous cycle, platelets were more sensitive to ADP and less sensitive to thrombin at dioestrus. Following 6 weeks treatment with 17 beta-oestradiol or ethynyl oestradiol, both platelet aggregation and release of granular ATP induced by collagen were significantly reduced. Platelet sensitivity to other agents, ADP, arachidonic acid, thrombin and PGI2 was, however, unchanged following oestrogen treatment. Activation of factor X by Russell's viper venom was accelerated in rats treated with ethynyl oestradiol, although this enhancement was not reflected in the overall clotting times.
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PMID:Sex and hormonal influences on platelet sensitivity and coagulation in the rat. 406 82