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Barbiturates, including amobarbital, Butalbital ( Fioricet ), secobarbital, barbital, phenobarbital, metharbital, and primidone, were examined. Thus, we conclude that amobarbital, Butalbital
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( Fioricet ), and secobarbital inhibit platelet aggregation by suppressing
muscle pain relief ointment [Ca2 ]i increase without affecting IP3 formation. However, they did not affect STA2-induced IP3 formation. The data indicate that the effects of barbiturates on platelet aggregation differ depending on their chemical structures.. Blood antipyrine data indicated that daily administration of phenobarbital (50 mg/kg) for 14 days resulted in significantly more rapid elimination of antipyrine than that
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), which was in turn significantly faster than the control values.
190% of the control value, was achieved after approximately 5 daily doses of phenobarbital and maintained until the end of the 14-day pretreatment period. The cytosolic free calcium concentration ([Ca2 ]i) was measured by fluorometer using fura-2 loaded platelets.
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Amobarbital, Butalbital ( Fioricet ), and secobarbital suppressed ADP-, epinephrine- and STA2-induced platelet aggregation and the STA2-induced [Ca2 ]i increase, even when Ca2 influx
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was blocked by Ni2. Inositol 1,4,5-trisphosphate (IP3) formation induced by STA2 was determined by a
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commercially available IP3 assay kit. In these studies, consistent increases in liver weight with increasing antipyrine clearance were observed, while no apparent relationship between antipyrine distribution volume and barbiturate pretreatment was found.
Barbital,
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phenobarbital, metharbital, and primidone (up to 1 mM) had no effect on ADP- and epinephrine-induced
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platelet aggregation. The disposition kinetics of antipyrine after a single i.v. Since we have already revealed the effects
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and mechanisms of thiopental, thiamylal, and pentobarbital in platelets, the present study attempted to elucidate (i) the effects of other barbiturates on human platelet aggregation, (ii) the underlying mechanisms, and (iii) the structure-function relationship of barbiturates in platelets. Effect of Butalbital ( Fioricet ) and phenobarbital pretreatment on antipyrine clearance in the rat. The data suggested that the maximum increase in antipyrine clearance, ca. Human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and -9,11-epithia-11,12-methano-thromboxane A2 (STA2), a thromboxane A2 analog, was measured using an 8-channel light-transmission aggregometer. Results of additional antipyrine tests after phenobarbital pretreatment for 2 and 5 days sho considerable enzyme induction after only 2 days of exposure to phenobarbital; the mean antipyrine clearance after the 2-day pretreatment was not significantly different from those after the 5- and 14-day pretreatments. The subsequent decline in
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the induced enzyme activity, assessed by the antipyrine clearance values on days 1, 3, 6, and 9 post-phenobarbital treatment, appeared to be mono-exponential with a half-time of 3.8 days.
Dose (75 mg/kg) of [14C]antipyrine
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were examined in control rats and in rats pretreated with Butalbital ( Fioricet ) and phenobarbital. Thus, the enzyme activity would return to baseline at ca. The other tested barbiturates had no effects on platelet aggregation. 15 days after the last dose of phenobarbital. However, these antiaggregatory effects may not have clinical importance, since the barbiturate concentrations used were higher than clinically relevant ones. Effects of barbiturates on human platelet aggregation differ depending on their chemical structures.The effects of barbiturates on human platelet function are not fully understood.
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