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Biomedical subjects

F J Kuczler

Publications and source records attributed to F J Kuczler.

3 recordsLinked to original sources

Isoniazid overdose: recognition and management.

Since isoniazid is increasingly being used to control the spread of tuberculosis, physicians must be aware of its potentially fatal effects. The ingestion of toxic amounts of isoniazid causes recurrent seizures, profound metabolic acidosis, coma and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5 g of isoniazid. Doses larger than 30 mg per kg often produce seizures. When ingested in amounts of 80 to 150 mg per kg or more, isoniazid can be rapidly fatal. The first signs and symptoms of isoniazid toxicity usually appear 30 minutes to two hours after ingestion and include nausea, vomiting, slurred speech, dizziness, tachycardia and urinary retention, followed by stupor, coma and recurrent grand mal seizures. The seizures produced by isoniazid toxicity are often refractory to anticonvulsant therapy. Given in gram-per-gram amounts of the isoniazid ingested, pyridoxine (vitamin B6) usually eliminates seizure activity and helps to correct the patient's metabolic acidosis. Isoniazid toxicity should be suspected in any patient who presents with refractory seizures and metabolic acidosis.

Adolescent↗

Choline influx across the brush border of guinea pig jejunum.

Choline uptake across the mucosal border of guinea pig jejunum was measured to determine the characteristics of this step in intestinal absorption. Unidirectional influx of [14C]choline appears to proceed primarily by a saturable, carrier-mediated process at low mucosal choline concentrations; at high concentrations (greater than 4 mM) the influx rate is approximately linearly related to the mucosal choline concentration, suggesting that absorption by passive diffusion predominates. Influx was only minimally reduced by elimination of Na+ from the mucosal test solution or by reduction of the intracellular Na+ concentration. Preincubation of tissue samples with metabolic inhibitors or with ouabain did not markedly reduce influx. These results are consistent with a model of choline transport across the brush border membrane by a carrier-mediated mechanism which is similar to that involved in fructose absorption but different from the Na+-dependent mechanism which participates in active transport of sugars and amino acids. At low lumenal choline concentrations, influx into colonic mucosa is slower than in jejunum and appears to be attributed solely to simple diffusion.

Animals↗