scholarly journals Prostaglandin I2 Metabolite

2020 ◽  
Author(s):  
Keyword(s):  
Prostaglandin I2

scholarly journals Significance of thromboxane A2 and prostaglandin I2 in acute necrotizing pancreatitis in rats

1990 ◽  
Vol 35 (9) ◽  
pp. 1078-1084 ◽  
Author(s):  
Bart Van Ooijen ◽  
Wil J. Kort ◽  
Cor J. Tinga ◽  
J. H. Paul Wilson
Keyword(s):  
Necrotizing Pancreatitis ◽  
Thromboxane A2 ◽  
Acute Necrotizing Pancreatitis ◽  
Prostaglandin I2 ◽  
Acute Necrotizing

Heparin enhances thrombin-stimulated prostaglandin I2 production by cultured endothelial cells

1990 ◽  
Vol 57 (4) ◽  
pp. 481-488 ◽  
Author(s):  
Fumiaki Itoh ◽  
Toshiyuki Kaji ◽  
Yumiko Hayakawa ◽  
Yutaka Oguma ◽  
Nobuo Sakuragawa
Keyword(s):  
Endothelial Cells ◽  
Prostaglandin I2 ◽  
Cultured Endothelial Cells

Successful Treatment of Intermittent Claudication Due to Spinal Canal Stenosis Using Beraprost Sodium, a Stable Prostaglandin I2 Analogue

Angiology ◽  
1997 ◽  
Vol 48 (5) ◽  
pp. 457-461 ◽  
Author(s):  
Hiroyuki Kato ◽  
Sei Emura ◽  
Kiyoko Ngashima ◽  
Hayato Kishikawa ◽  
Toshinobu Takashima ◽  
...  
Keyword(s):  
Intermittent Claudication ◽  
Successful Treatment ◽  
Spinal Canal ◽  
Spinal Canal Stenosis ◽  
Prostaglandin I2 ◽  
Canal Stenosis ◽  
Beraprost Sodium

scholarly journals Evidence that Ca2+-activated K+ channels play a major role in mediating vasorelaxation of guinea-pig aorta in response to prostaglandin I2

2000 ◽  
Vol 82 ◽  
pp. 209
Author(s):  
Fumiko Yamaki ◽  
Yoshio Tanaka ◽  
Kazuhide Nishimaru ◽  
Hikaru Tanaka ◽  
Koki Shigenobu
Keyword(s):  
Guinea Pig ◽  
Prostaglandin I2 ◽  
K Channels

Antithrombogenic Poly(vinyl chloride) with Heparin- and/or Prostaglandin I2-Immobilized in Hydrogels

1989 ◽  
Vol 4 (1) ◽  
pp. 4-16 ◽  
Author(s):  
Mitsuru Akashi ◽  
Shinji Takeda ◽  
Tsuyoshi Miyazaki ◽  
Eiji Yashima ◽  
Noriyuki Miyauchi ◽  
...  
Keyword(s):  
Vinyl Chloride ◽  
Prostaglandin I2 ◽  
Poly Vinyl Chloride

scholarly journals Synergistic inhibition of platelet activation by plasmin and prostaglandin I2

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1504-1507
Author(s):  
AI Schafer ◽  
GB Zavoico ◽  
J Loscalzo ◽  
AK Maas
Keyword(s):  
Cyclic Amp ◽  
Platelet Activation ◽  
Platelet Rich Plasma ◽  
Thromboxane A2 ◽  
Prostaglandin I2 ◽  
Synergistic Inhibition ◽  
Tissue Plasminogen ◽  
A Site ◽  
Induced Aggregation ◽  
Inhibition Of Thrombin

Endothelial cell prostacyclin (PGI2) inhibits platelet activation by raising platelet cyclic AMP. Previously, platelet activation was also shown to be blocked by plasmin formed by endothelium-derived tissue plasminogen activator (TPA). We have now studied interactions between PGI2 and plasmin in the control of platelet function. PGI2 and plasmin cause synergistic inhibition of thrombin- and ADP-induced aggregation of washed platelets. Inhibition by PGI2 is similarly potentiated by TPA added to platelet-rich plasma to generate plasmin. Thrombin-stimulated rise in platelet cytosolic Ca2+, measured by fura2 fluorescence, and thromboxane A2 formation, measured by radioimmunoassay (RIA), are likewise synergistically inhibited by PGI2 and plasmin. Plasmin neither increases nor potentiates PGI2-stimulated increases in platelet cyclic AMP. Thus, PGI2 and plasmin cause synergistic inhibition of platelet activation by both cyclic AMP-dependent and independent mechanisms. This interaction between two different endothelium-derived products may play an important role in localizing the hemostatic plug to a site of vascular injury by preventing further thrombin-mediated accrual of platelets.

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