Biphasic elimination pattern

Toxicokinetics of PCBs in rodents were altered when administered in mixtures (de Jongh et al. 1992). PCBs 153, 156, and 169 produced biphasic elimination patterns in mice when administered in combinations, but single-phase elimination when administered alone. Elimination of all PCBs was more rapid after coadministration. Mixtures of PCBs 153 and 156 raised EROD activity and lengthened retention of each congener in liver however, a mixture of PCB 153 and 169 lowered EROD activity (de Jongh et al. 1992). Selected PCBs of low acute toxicity may increase the toxicity of compounds such as 2,3,7,8-TCDD (Bimbaum et al. 1985). Thus, PCB 153 or 157 at sublethal dosages (20 to 80 mg/kg BW) did not produce cleft palate deformities in mouse embryos. But a mixture of PCB 157 and 2,3,7,8-TCDD produced a tenfold increase in the incidence of palate deformities that were expected of 2,3,7,8-TCDD alone palate deformities did not increase with a mixture of PCB 153 and 2,3,7,8-TCDD. The widespread environmental occurrence of PCB-PCDD and PCB-PCDF combinations suggests a need for further evaluation of the mechanism of this interaction (Bimbaum et al. 1985). 

A plasma calibration curve for ll-nor-A9-THC-9-carboxylic acid, 5a, is shown in Figure 9. There was reasonable linearity from 1.0-50 ng/ml plasma with detection limits of 0.5 ng or less per ml. Figure 10 presents similar data for a urine calibration curve. The method showed reasonable linearity between 2.0-100 ng/ ml urine. Figure 11 presents pharmacokinetic data. for plasma levels of a human volunteer, BS, over a 0.5 hour to 48 hour period comparing A9-THC and 11-nor acid levels after a dose of 5.0 mg of A9-THC by the intravenous route. Both parent compound and acid metabolite exhibited a biphasic elimination pattern although the levels of the acid did not fall as rapidly as parent compound. Elimination of the acid metabolite 5a in urine is shown in Figure 12. It is evident that urinary elimination proceeded rapidly as 80% of the total 11-nor-acid excreted was eliminated in the urine during... 

Disposition of paditaxel from plasma follows a biphasic elimination pattern. Approximately 97.5% of it is bound to plasma proteins. Clearance is triphasic and results mainly from hepatic extraction and biliary excretion. Eleven metabolites have been delected in plasma, but not identified. " ... 

I. Pharmacology. Pentobarbital is a short-acting barbiturate with anticonvulsant as well as sedative-hypnotic properties. It is used as a third-line drug in the treatment of status epilepticus. It may also reduce intracranial pressure in patients with cerebral edema by inducing vasoconstriction. After intravenous administration of a single dose, the onset of effect occurs within about 1 minute and lasts about 15 minutes. Pentobarbital demonstrates a biphasic elimination pattern the half-life of the initial phase is 4 hours, and the terminal phase half-life is 35-50 hours. Effects are prolonged after termination of a continuous infusion. 

Pharmacokinetis were evaluated in 15 pts. Mean plasma concentrations oftotal-DXR, free-DXR, encapsulated-DXR at level 4 was shown in Fig 2. Table 4 shows the mean pharmacokinetic parameters of total-DXR, free-DXR-and metabolites in plasma at level 1 to level 4. The plasma concentration of total-DXR at each level reached Cmax at the end of infusion. The plasma concentration profiles of total-DXR at level 1 to 3 showed biphasic elimination pattern but showed monophasic elimination pattern at level 4, because one subject at level 4 showed monophasic elimination pattern with a long half-life. CL, Vdss, and MRT of total-DXR were almost the same among dose levels. T1/2A.Z of total-DXR was prolonged by dose escalation, because the concentration of terminal phase was detected as dose increased (Table 4). Most oftotal-DXR could exist in circulating blood as an encapsulated form, because plasma concentration of... 

Transfer of the aquatic animals, after absorption of the cyclodiene, to insecticide-free water showed variations in elimination pattern related with the chemical as well as its concentration in the body. It follows a somewhat biphasic response, there is initial rapid elimination of high concentration followed by a slow elimination at lower body concentrations (Fig. 3)(21,22, 23). Xenopus, even at low body levels of cis-chlordane, eliminate it at slightly faster rate than fish. Photo-cis-chlordane seems to be eliminated at a faster rate than cis-chlordane by both goldfish and bluegill (Table 2). The elimination of photo-cis-chlordane by goldfish and bluegill and of photodieldrin by blue-gill shows a biphasic response (Fig. 3). 

Photoisomers seem to be more toxic than the parent form. For example, c -photochlordane was about twice as lethal to bluegiUs and goldfish as c -chlordane (Sudershan and Khan 1980). Bluegills exposed to 5 pg/L of radiolabeled CM-photochlordane or di -chlordane for 48 h accumulated c -chlordane from the medium by a factor of 78, and di -photochlordane by a factor of 140 (Sudershan and Khan 1980). During the next 6 weeks, 20% of the di -chlordane was eliminated in a linear pattern, and about 50% was eliminated in 46 days. Elimination of cw-photochlordane followed a biphasic pattern and was most rapid during the first 3 weeks 40% was eliminated in... 

Lynn et al. (1982) detected three major C-containing compounds in plasma and the pattern was dominated by bis(2,3-dibromopropyl) phosphate as early as 5 min after intravenous dosing. 2,3-Dibromopropanol was also detected up to 8 h after dosing. The elimination of bis(2,3-dibromopropyl) phosphate was biphasic, with half-lives of 6 and 36 h and it was detected up to five days after dosing. 

The phenothiazines have a long duration of effect compared with many of the other sedative-tranquillizers used in horses. The onset of effect is relatively slow after i.v. administration and the maximum clinical effect occurs 20-30 min after i.v. administration. Peak plasma drug levels occur 30 min after the i.m. injection of acepromazine (Chou et al 1998). Acepromazine has a biphasic concentration decay pattern after i.v. administration (Marroum et al 1994). The distribution half-life is 3-5 min (Ballard et al 1982, Marroum et al 1994) and the elimination half-life is 2-3 h. The terminal half-life of acepromazine after oral administration is approximately 6h. Acepromazine is highly protein bound in the plasma (>99%) with a large apparent volume of distribution (Vj, 6.61/kg) (Ballard et al 1982). 

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