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A Pilot Study of Piracetam in Cuprophan Hemodialysis
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Abstract: Twelve patients, 8 male and 4 female, aged from 26 to 70 years were studied. They were on hemodialysis (HD) 4 h three times weekly with cuprophan hollow fiber dialyzers (Gambro 120M) and dialysate containing 35 mEq/L of acetate. The study compares two random HD sessions on each patient. Sixty minutes prior to one random session a placebo was administered orally, and prior to another random session piracetam was given at a dose of 8 g. Heparin dosage was not reduced during HD using QB 200 ml, QD 500 ml, and no ultrafiltration. Blood samples for leukocyte and platelet counts, serum C3, arterial paO2 and paCO2, thromboxane‐B2 (TxB2), and β‐thromboglobulin (β‐TG) were taken from the arterial line before and at 15, 60, and 240 min during HD. Leu‐kopenia at 15 min of HD was found to be less severe (p < 0.01) in the piracetam study than in the placebo, whereas platelet count did not change. Serum C3 was slightly increased in both studies. Arterial oxygen was preserved close to the initial levels by piracetam (91.66 mm Hg versus 81.08, p < 0.01 at 60 min, and 93.08 versus 80.17 mm Hg, p < 0.01 at 240 min of HD sessions) but paCO2 did not change significantly. TxB2 increased less with piracetam in comparison to placebo (p < 0.01 or p < 0.001), but (J‐TG was reduced significantly by piracetam at any time during HD (p < 0.001). The above statistical analysis was done by paired t‐test. Using the ANOVA test, significance was found only in plasma TxB2 levels between the two groups (p < 0.001). It is suggested that piracetam is a potent inhibitor of some HD‐associated bioincompat‐ibility parameters.
Title: A Pilot Study of Piracetam in Cuprophan Hemodialysis
Description:
Abstract: Twelve patients, 8 male and 4 female, aged from 26 to 70 years were studied.
They were on hemodialysis (HD) 4 h three times weekly with cuprophan hollow fiber dialyzers (Gambro 120M) and dialysate containing 35 mEq/L of acetate.
The study compares two random HD sessions on each patient.
Sixty minutes prior to one random session a placebo was administered orally, and prior to another random session piracetam was given at a dose of 8 g.
Heparin dosage was not reduced during HD using QB 200 ml, QD 500 ml, and no ultrafiltration.
Blood samples for leukocyte and platelet counts, serum C3, arterial paO2 and paCO2, thromboxane‐B2 (TxB2), and β‐thromboglobulin (β‐TG) were taken from the arterial line before and at 15, 60, and 240 min during HD.
Leu‐kopenia at 15 min of HD was found to be less severe (p < 0.
01) in the piracetam study than in the placebo, whereas platelet count did not change.
Serum C3 was slightly increased in both studies.
Arterial oxygen was preserved close to the initial levels by piracetam (91.
66 mm Hg versus 81.
08, p < 0.
01 at 60 min, and 93.
08 versus 80.
17 mm Hg, p < 0.
01 at 240 min of HD sessions) but paCO2 did not change significantly.
TxB2 increased less with piracetam in comparison to placebo (p < 0.
01 or p < 0.
001), but (J‐TG was reduced significantly by piracetam at any time during HD (p < 0.
001).
The above statistical analysis was done by paired t‐test.
Using the ANOVA test, significance was found only in plasma TxB2 levels between the two groups (p < 0.
001).
It is suggested that piracetam is a potent inhibitor of some HD‐associated bioincompat‐ibility parameters.
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