Biomedical subjects

J Jentzen

Publications and source records attributed to J Jentzen.

3 recordsLinked to original sources

PubMed1987

Myocardial necrosis due to intraperitoneal administration of phenylpropanolamine in rats.

Overdose with the sympathomimetic agent phenylpropanolamine (PPA) may cause arrhythmias and myocardial injury in humans. To study the mechanism of these toxic effects, unanesthetized rats (6 animals per group) were given single intraperitoneal doses of 1, 2, 4, 8, 16, or 32 mg/kg PPA. Increases in blood pressure, measured by tail cuff, were dose related and comparable to increases reported in patients with PPA toxicity. Animals were killed at 24 hr and light microscopic examination showed diffuse, dose-related myocardial necrosis. Histology scores (a measure of severity of necrosis) in groups receiving 8, 16, and 32 mg/kg PPA were 1.4 +/- 0.5, 1.8 +/- 1.0, and 2.3 +/- 0.4, respectively, and were all significantly greater than the histology score of control animals (0.2 +/- 0.3, p less than 0.01). The observed lesion was similar in appearance to the myocardial necrosis produced by large doses of catecholamines or sympathomimetic agents in rats. In summary, single doses of PPA caused myocardial necrosis in rats at doses comparable to those causing toxicity in humans. Myocardial necrosis may contribute to the cardiac toxicity of PPA overdose.

Animals↗

PubMed1985

Fatal acute selenium toxicity.

Selenium is used widely in industry and as a dietary supplement. Reports of acute selenium toxicity are infrequent, however, and the relationship of toxicity to selenium concentrations in blood and tissues has not been established. We describe a patient who died eight days after ingesting selenious acid in the form of gun blueing. The patient's clinical course demonstrated many of the features of inorganic selenium toxicity described in animals; hypotension as a result of both vasodilation and decreased cardiac output, adult respiratory distress syndrome, severe myopathy which contributed to respiratory failure, and a garlicky odor to the breath. Four days after ingestion the serum selenium concentration was twenty times normal and urinary excretion seventy times normal. Postmortem tissue selenium concentrations were up to 40 times normal.

Female↗

PubMed1984

Pulmonary oxygen toxic effect. Occurrence in a newborn infant despite low PaO2 due to an intracranial arteriovenous malformation.

A newborn infant with a massive left to right shunt secondary to a cerebral arteriovenous malformation required continuous oxygen therapy in high concentrations. Despite high PO2, the infant maintained low to normal PaO2 concentrations. Light and ultrastructural studies of the lungs demonstrated typical changes of acute pulmonary oxygen toxicity, including degeneration of capillary endothelium and type I pneumonocytes, interstitial edema, and alveolar exudation. These observations confirm earlier experimental animal studies that demonstrated that the alveolar Po2 concentration and not the Pao2 is the major factor contributing to pulmonary oxygen toxic effect.

Humans↗