Enhanced 6-oxo-PGF1 alpha levels in plasma during hemodialysis.
The activation of platelets due to foreign surface interaction is a well known fact. Earlier, we found an increase of circulating platelet microaggregates (method of Wu and Hoak) during hemodialysis. Since this phenomenon might cause a PGI2-release by lung and/or vascular tissue, we studied the plasma 6-oxo-PGF 1 alpha-levels in 6 patients during hemodialysis. We found an initial increase of plasma 6-oxo-PGF 1 alpha. Coincidently, hypoxemia, fall in platelet and lekocyte count and a decrease in platelet count ratio were observed. An effect of heparin was excluded in a control group. The findings support the hypothesis that PGI2 acts as a defense mechanism against platelet deposition on vascular wall by a temporary increased synthesis which could be monitored by a temporarily enhanced plasma 6-oxo-PGF 1 alpha-level during the initial phase of hemodialysis.
D015121:6-Ketoprostaglandin F1 alpha; D000293:Adolescent; D000328:Adult; D002908:Chronic Disease; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood; D010974:Platelet Aggregation; D010976:Platelet Count; D011460:Prostaglandins F / Q000097:blood*; D006435:Renal Dialysis; D014511:Uremia / Q000628:therapy
D011460:Prostaglandins F; D015121:6-Ketoprostaglandin F1 alpha; D010100:Oxygen