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Biomedical subjects

T P Rohrig

Publications and source records attributed to T P Rohrig.

13 recordsLinked to original sources

Sudden death due to butane inhalation.

Sudden death due to the inhalation of halogenated hydrocarbons is a well-documented phenomenon in the scientific and medical literature. Recently, there has been sporadic information suggesting that nonhalogenated hydrocarbons may cause potentially fatal cardiac arrhythmias. This report documents five sudden deaths due to inhalation of nonhalogenated hydrocarbons: n-butane, isobutane and propane. The hydrocarbons were identified by headspace gas chromatography in blood, brain, and lung tissue. Case histories, toxicological findings and analytical procedures are discussed.

Administration, Inhalation↗

Gas flames, closed spaces, and hypoxia.

The investigation of the deaths of an elderly couple found in a small hotel room that was tightly sealed and heated by an open flame gas heater is presented. Autopsy and toxicologic studies did not reveal a definitive cause of death. Subsequent research and an experiment to duplicate the conditions support the contention that the cause of death was hypoxia due to oxygen depletion by the gas flame.

Aged↗

Postmortem distribution of mexiletine in a fatal overdose.

A case involving a fatal overdose of mexiletine is presented. Quantitation of the drug was accomplished by gas chromatography with a flame-ionization detector. The presence of mexiletine was confirmed by gas chromatography-mass spectrometry. Toxicological analysis revealed the following tissue distribution of mexiletine: heart blood, 44.8 micrograms/mL; femoral blood, 10.0 micrograms/mL; vitreous, 8.6 micrograms/mL; liver, 171.6 micrograms/g; brain, 84.0 micrograms/g; and gastric contents, 1464 mg.

Adult↗

Tissue distribution of ibuprofen in a fatal overdose.

A 26-year-old white man was found dead near his home. The decedent had had a history of ibuprofen overdose and had recently received a physician's order for 800 mg ibuprofen every 4 h for back pain. Postmortem examination was performed and was unrevealing except for heavy lungs (1,140 g combined weight) and a brownish-white granular residue in the stomach. Samples of heart blood, femoral blood, liver, brain, and gastric contents were submitted for toxicological analysis. Qualitative screening detected only the presence of ibuprofen. Quantitation of ibuprofen was performed using reverse-phase high-performance liquid chromatography (HPLC) with ultraviolet detection. The analytical column was an Econosphere C-8 column (150 mm, 4.6 mm I.D.) with 5 microns particle size preceded by a C-8 5 microns guard column. The mobile phase was 46% methanol and 54% 0.2 M acetate buffer at a flow rate of 2 ml/min. Fenoprofen was used as an internal standard at 200 mcg/ml. A linear response (r = 0.99) was achieved over a concentration range of 25-600 mcg/ml. Ibuprofen was identified and quantitated in the following tissues: heart blood (518.0 mcg/ml), femoral blood (348.3 mcg/ml), liver (942.1 mcg/g), brain (283.9 mcg/g), and gastric contents (131 mg total).

Adult↗

The in vitro metabolism of aflatoxin Q1 by mouse and rabbit liver preparations.

The investigation of the in vitro metabolism of aflatoxin Q1 by the post-mitochondrial fraction of mouse and rabbit liver is reported. Both animals metabolized this substance at a turnover similar to aflatoxin B1. There was a higher bound fraction and lower aqueous fraction from the metabolism of B1 than from aflatoxin Q1. The aqueous fraction of the metabolisms evidenced the beta-D-glucuronide of aflatoxin Q1. The rabbit metabolism of Q1 was characterized by high levels of chloroform soluble metabolites. In contrast, the mouse metabolism resulted in high glucuronide and bound Q1 metabolite levels.

Aflatoxins↗

In vitro metabolism of aflatoxin Q1 by rat liver post-mitochondrial homogenates.

An investigation of the in vitro biotransformation of aflatoxin Q1 by the post-mitochondrial fraction of rat liver is reported. These studies showed a 10 to 25 percent turnover of aflatoxin Q1, with the subsequent formation of five metabolites. A major metabolite was determined to be the beta-D-glucuronide of aflatoxin Q1.

Aflatoxins↗

Amoxapine overdose: report of two cases.

Two deaths are described involving amoxapine. Toxicological analysis in Case 1 revealed an amoxapine blood concentration of 5.7 micrograms/mL, and in Case 2, a concentration of 3.2 micrograms/mL. Qualitative analysis of other body fluids were performed.

Adult↗

Fatality resulting from metoprolol overdose.

A death due to an intentional overdose of metoprolol is described. The drug was quantified by gas chromatography, and identification was confirmed by gas chromatography/mass spectrometry. Metoprolol concentrations in blood, bile, urine, and vitreous humor were 19.8 mg/L, 83.1 mg/L, 1.6 mg/L, and 15.1 mg/L, respectively. A blood ethanol concentration of 0.25 g/100 mL was the only other significant toxicologic finding.

Gas Chromatography-Mass Spectrometry↗

Fluoxetine overdose: a case report.

A fatality due to the ingestion of fluoxetine and ethanol is reported. Quantitation of the drug and its active normetabolite was accomplished by gas chromatography with a flame ionization detector. Identification of the compounds was performed by gas chromatography/mass spectrometry. Tissue distribution of fluoxetine and norfluoxetine, as well as analytical details, is presented.

Adult↗

Tissue distribution of methylenedioxymethamphetamine.

Two cases of death involving methylenedioxymethamphetamine (MDMA) are reported; one case is a fatal acute overdose and the other is a drug-related death. The tissue distribution of MDMA is reported in both cases.

3,4-Methylenedioxyamphetamine↗

Tissue distribution of bupropion in a fatal overdose.

A fatality resulting from the ingestion of bupropion is reported. Quantitation of bupropion and its metabolites was accomplished by gas chromatography. The distribution of bupropion and its metabolites, along with analytical details, is presented.

Adult↗