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R Foltz

Publications and source records attributed to R Foltz.

8 recordsLinked to original sources
PubMed1995

Quantitative determination of codeine and its major metabolites in human hair by gas chromatography-positive ion chemical ionization mass spectrometry: a clinical application.

A highly sensitive method was developed for the quantitative analysis of codeine and morphine in human hair. After addition of deuterated internal standards, hair samples were digested overnight in 1N NaOH at 37 degrees C. Hydrolysis was performed on certain digests by addition of 1 mL 6N HCl. Digest solutions were extracted using a solid-phase procedure with Bond Elut Certify extraction columns. Derivatized extracts were analyzed on a Finnigan ion trap mass spectrometer (Magnum) in the positive ion chemical ionization mode using acetone as the reagent gas, helium as the carrier gas, and a DB-5 MS (30 m x 0.25-mm i.d.) capillary column. The assay was linear to 75 ng/mg (r = 0.99) and was capable of detecting 10 pg of codeine and morphine on-column. Intra-assay precision ranged from 8 to 20%. The method was used to quantitate codeine in human hair obtained from two male volunteers with dark brown to black hair after a single oral dose of 120 mg codeine phosphate liquid. Hair samples were plucked from the scalp for 28 days and then cut at the scalp. Codeine was detectable in 1-cm long hair (containing the bulb) at 12 h following the dose and remained detectable in the hair shaft for at least 8 weeks. Codeine metabolites were not detected in the hair of these two subjects. The method is currently being used in dose-response disposition studies to quantitate codeine and its major metabolites in human subjects.

Administration, Oral↗
PubMed1995

Quantitative analysis of THC, 11-OH-THC, and THCCOOH in human hair by negative ion chemical ionization mass spectrometry.

A sensitive and specific method was developed for the quantitative analysis of delta9-tetrahydrocannabinol (THC), 11 -hydroxy-THC (11-OH-THC), and 11-nor-9-carboxy-THC (THCCOOH) in human hair. Deuterated internal standards were added to hair samples, and samples were digested overnight in 1 N NaOH at 37 degrees C. Digest solutions were extracted with a liquid-liquid extraction procedure, which was previously developed in our laboratory for the analysis of plasma and whole blood. Derivatized extracts were analyzed on a Finnigan 4500" mass spectrometer in negative ion chemical ionization mode using methane as the reagent gas, hydrogen as the carrier gas, and a Restek Rtx 200-15M-0.25-microm capillary column. The assay was linear up to 50 ng/mg hair (r, 0.99) for all three compounds and was capable of detecting 10 pg THC and THCCOOH and 100 pg 11-OH-THC on column. The intra-assay precision ranged from 2.1 to 11.2% for the three analytes; the interassay precision ranged from 4.4 to 13.0%. The method was used to detect and quantitate the presence of THC, 11-OH-THC, and THCCOOH in human hair obtained from eight regular users of cannabis. THC, but not 11-OH-THC or THCCOOH, was detectable in the hair shaft above the assay limit of quantitation. Four laboratory wash procedures were also evaluated for their effect on the measured concentration of THC in hair. in seven of eight subjects, a methylene chloride wash procedure substantially reduced the measured THC concentration by up to 50%. The gas chromatographic-mass spectrometric assay is currently being used to support pharmacokinetic studies of drug disposition into the hair of humans and animals.

Boranes↗
PubMed1986

Protection against experimental ischemic spinal cord injury.

The authors have studied the protection against ischemic damage to rabbit spinal cord by pretreatment with agents that block neuronal activity and directly or indirectly reduce tissue metabolism. Hypothermia, thiopental, magnesium, lidocaine, and naloxone were used to pretreat the spinal cord prior to ischemia. Hypothermia and thiopental provided comparable protection: they each increased the duration of ischemia required to produce neurological deficits in 50% of the animals from 26 to 41 minutes. They also increased from 10 to 30 minutes the time that the postsynaptic waves of the spinal somatosensory evoked potential (SSEP) could be absent and the animal still have neurological recovery. Hypothermia and thiopental, when used together, increased the duration of ischemia required to produce neurological deficits to 57 minutes in 50% of the animals. Naloxone increased the duration of ischemia required to produce neurological deficits to 36 minutes in 50% of the animals, and increased to 20 minutes the time that the postsynaptic waves of the SSEP could be absent and the animal still have neurological recovery. Magnesium pretreatment improved neurological outcome, possibly by improving collateral circulation as the SSEP did not fail completely during aortic occlusion in all animals. Lidocaine was not beneficial, perhaps because of the prolonged hypotension that resulted.

Animals↗
PubMed1984

The metabolic response to severe head injury.

Caloric expenditure and nitrogen balance were measured in 14 steroid-treated comatose head-injured patients acutely and up to 28 days after injury. During this period patients were fed with a continuous enteral infusion of a formula containing 2 Kcal/cc and 10 gm nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated nonparalyzed patients was 138% +/- 37% of that expected for an uninjured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 135 patient-days. The mean excretion was 20.2 +/- 6.4 gm/day. The mean protein caloric contribution was 23.9% +/- 6.7% and was greater than 25% for six patients, compared to normal values of 10% to 15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with enterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20% to 40% of the body surface.

Adolescent↗
PubMed1984

Neurological outcome correlated with spinal evoked potentials in a spinal cord ischemia model.

Occlusion of the abdominal aorta of the rabbit by inflating the balloon of a Swan-Ganz catheter positioned in the aorta is a simple and reliable method of producing spinal cord ischemia. The electrophysiological, neurological, and neuropathological correlates of ischemia with progressively longer durations and of ischemia after drug interventions were studied with the goal of developing an easily monitored, reproducible model for central nervous system ischemia. The percentage of animals developing paraplegia after varying periods of ischemia was zero after 15 minutes, 30% after 17 minutes, 33% after 20 minutes, 38% after 25 minutes, and 100% after 60 minutes of ischemia. After 25 minutes of ischemia the percentage of animals developing paraplegia was 87% when they were awake and not ventilated during ischemia and reperfusion, but dropped to 38% in animals that were paralyzed, sedated with ketamine, and ventilated, and when the metabolic acidosis that follows aortic occlusion was corrected during reperfusion. Pretreatment with thiopental, hypothermia, naloxone, methylprednisolone, and verapamil changed the percentage of animals developing paraplegia after 25 minutes of ischemia to 0%, 0%, 25%, 40%, and 100%, respectively. The component waves of the spinal somatosensory evoked potential (SSEP) disappeared sequentially during ischemia in the following order: P2, N4, N3, N2, and N1. After reperfusion, the SSEP components returned in reverse order of their disappearance. In the untreated animals, absence of the N3 wave for more than 10 minutes during ischemia was always followed by a neurological deficit. Pretreatment with thiopental or hypothermia permitted longer periods of electrophysiological silence without permanent neurological deficit. The ratio of the amplitude of N3 to N1 (N3/N1) was at least 70% of the control level, and N4 and P2 amplitudes were at least 30% of the control level at 120 minutes after reperfusion in all animals that had a normal outcome. Return of the N3/N1 amplitude to at least 90% of the control level or return of N3/N1 to 70% to 89% of control and P2 to at least 60% of control at 120 minutes after reperfusion reliably correlated with a normal 48-hour motor examination in animals with and without drug interventions.

Animals↗