Biomedical subjects

W M Kolling

Publications and source records attributed to W M Kolling.

5 recordsLinked to original sources

PubMed1998

Stability of undiluted and diluted adenosine at three temperatures in syringes and bags.

The stability of adenosine in various diluents in polypropylene syringes and polyvinyl chloride (PVC) bags at three temperatures was studied. Portions of pooled undiluted adenosine infusion (3 mg/ mL) were stored in 60-mL capped syringes, 20 for each storage condition. Adenosine infusions were prepared by mixing adenosine with 5% dextrose injection, 0.9% sodium chloride injection, lactated Ringer's injection, or 5% dextrose and lactated Ringer's injection to produce a concentration of 0.75 mg/mL. Samples of each infusion were stored in 60-mL capped syringes and 50-mL bags, 20 syringes and 20 bags for each storage condition. Syringes and bags were stored in the dark at 25, 5, and -15 degrees C. At various sampling times, three syringes and three bags of each infusion were removed for visual inspection, pH measurement, and high-performance liquid chromatographic analysis. At 10 and 16 days, fungal growth at 25 degrees C was suspected in the infusions prepared with 5% dextrose injection. For all other samples, there was no evidence of precipitation or change in pH. The concentration of adenosine remained constant in all samples at all storage conditions. Adenosine 3 mg/mL was stable in polypropylene syringes for 7 days at 25 degrees C, 14 days at 5 degrees C, and 28 days at -15 degrees C; adenosine 0.75 mg/ mL in 0.9% sodium chloride injection and in 5% dextrose injection was stable in polypropylene syringes and PVC bags for 16 days at 25, 5, and -15 degrees C; and adenosine 0.75 mg/mL in lactated Ringer's injection and in 5% dextrose and lactated Ringer's injection was stable in syringes and bags for 14 days at 25, 5, and -15 degrees C.

Adenosine↗

PubMed1994

Computer modeling of adsorption on an activated charcoal surface.

The molecular modeling program SYBYL was used to simulate the adsorption of various barbiturates by an activated charcoal surface. The compounds barbituric acid (BA), barbital (B), phenobarbital (PB), mephobarbital (M), and primidone (Pr) were modeled, and their structures were energetically minimized. These structures agreed with literature reports for the conformations of these molecules in dimethyl sulfoxide-d6, methanol-d4, and chloroform-d. The activated charcoal surface was modeled using graphitic crystallites which had either no oxygen-containing functional group, a C-OH functional group, or a C = O functional group. The presence of the C-O (presumably C-OH) and C = O functional states on activated charcoal surfaces had been previously determined by X-ray photoelectron spectroscopy. It was assumed that the crystallite was locally flat. Upon docking, conformational changes were observed for barbital, phenobarbital, mephobarbital, and primidone. Estimates for the heat of adsorption ranged from -62.3 kJ/mol for barbituric acid to -91.1 kJ/mol for mephobarbital on the hydroxylated surface. Allowance for the heat of desorption of the required number of water molecules from the surface, also determined by SYBYL, gave heat of displacement values of -19.4 kJ/mol for barbituric acid and -32.6 kJ/mol for mephobarbital. These values compared well to the heat of displacement values obtained by isoperibol calorimetry, which were -20.3 kJ/mol for barbituric acid and -31.6 kJ/mol for mephobarbital. Previous laboratory studies had demonstrated the greater importance of the C-O functional state for barbiturate adsorption compared to the C = O functional state. The computer-modeled system predicted the same result.

Adsorption↗

PubMed1981

Intraventricular levels of amikacin after intravenous administration.

Serum and ventricular fluid pharmacokinetic data for amikacin were evaluated prospectively in 10 hydrocephalic children with suspected ventriculitis. After the fourth or fifth intravenous 7.5-mg/kg dose of amikacin given every 8 h, mean peak serum levels were 24.3 +/- 3.2 microgram/ml (achieved at 0.5 h) with a calculated half-life of 2.2 +/- 1.1 h. Mean peak ventricular fluid levels in five patients with bacterial infection were 6.1 +/- 2.0 microgram/ml (achieved at 3 h). In the remaining five patients without bacterial ventriculitis, very low levels (less than or equal to 0.7 microgram/ml) of amikacin were detected. Ventricular fluid pleocytosis was directly correlated and glucose levels were inversely correlated with penetration of amikacin. Systemic therapy with amikacin may be the treatment of choice for children with ventriculitis meningitis caused by bacteria which are highly susceptible to this drug, thereby permitting the avoidance of the potentially hazardous intraventricular route of administration.

Amikacin↗

PubMed1981

Pharmacokinetic comparison of intravenous and oral chloramphenicol in patients with Haemophilus influenzae meningitis.

The pharmacokinetics of chloramphenicol following intravenous and oral administration were studied in 14 infants with Haemophilus influenzae meningitis. Following five days of treatment with intravenous chloramphenicol (100 mg/kg/day every six hours), oral chloramphenicol was substituted at the same dose. Multiple serum levels of chloramphenicol were determined after an intravenous dose on day 4 and after an oral dose on day 10. CSF levels were measured six hours after intravenous or oral chloramphenicol dose on those days (CSF trough). Following intravenous administration, the mean peak serum level of 15.0 micrograms/ml was reached at 45 minutes. In comparison, after oral chloramphenicol in the same dosage, the mean peak serum level of 18.5 micrograms/ml was achieved at two to three hours. The mean serum half-life of the drug (6.5 hours) was significantly longer after oral administration than after intravenous chloramphenicol (4.0 hours) (P less than .001). The increased serum half-life following orally administered chloramphenicol was occasionally associated with drug accumulation. In addition, mean trough CSF levels were somewhat higher when the patient received oral medication (6.6 micrograms/ml) compared to intravenous administration (4.2 micrograms/ml) (P less than .001). For any treatment regimen for H influenzae meningitis that includes a period of oral chloramphenicol therapy the patient should be hospitalized to ensure compliance. Because of the wide range of individual variation in serum half-life that may result in accumulation, periodic monitoring of serum chloramphenicol levels is also recommended.

Administration, Oral↗

PubMed1978

Aspirin hepatotoxicity.

A case of aspirin hepatotoxicity in a 46-year-old male with rheumatoid arthritis is discussed, and this adverse reaction is reviewed. The patient was started on 900 mg aspirin four times daily; five days later the dose was increased to 1200 mg four times daily. After six days' therapy of 4.8 g aspirin daily, the serum salicylate level rose to 25 mg/100 ml and liver enzymes became elevated. Aspirin was discontinued and ibuprofen, 600 mg four times daily, begun. Eight days after cessation of aspirin therapy, the patient's liver enzyme values returned to normal. Previous case reports and studies of aspirin-induced hepatotoxicity are reviewed. It is concluded that aspirin-induced hepatotoxicity occurs much more frequently in patients with rheumatoid arthritis and other connective tissue disorders than previously recognized.

Adolescent↗