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Biomedical subjects

E H Herman

Publications and source records attributed to E H Herman.

90 records · Page 5Linked to original sources
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Characterization of the pulmonary lesions induced in rats by human recombinant interleukin-2.

Histologic, electron microscopic, and immunohistochemical studies were made to analyze the structural features and the cellular composition of the pulmonary lesions produced in rats by the administration of interleukin-2 (IL-2). This agent induced pulmonary edema; thickening of alveolar septa; damage to endothelial cells in capillaries and venules, marked interstitial infiltration by cytotoxic T lymphocytes, lymphokine-activated killer (LAK) cells, macrophages, and dendritic cells (as demonstrated by cell counting in preparations stained immunohistochemically with peroxidase- and fluorochrome-labeled antibodies); and injury to bronchiolar and alveolar epithelial cells. Granular and agranular lymphocytes often were closely apposed to endothelial cells in capillaries and venules. Contacts between lymphocytes and type II alveolar epithelial cells also were observed. Damaged type II alveolar epithelial cells showed nuclear and cytoplasmic features that are considered indicative of apoptosis (confirmed by nick end labeling). Phagocytosis of apoptotic bodies by macrophages was occasionally found. These results support the concept that IL-2 induces cytotoxic vascular and parenchymal cell damage that is mediated by LAK cells and cytotoxic T lymphocytes, which make contacts with endothelial cells and type II alveolar epithelial cells. This damage appears to be exacerbated by the secondary release of a variety of vasoactive agents and inflammatory mediators.

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Acute cardiovascular alterations induced by low doses of adriamycin, rubidazone, and daunorubicin in the anesthetized beagle dog.

Iv injections of Adriamycin (0.375-3.0 mg/kg), rubidazone (0.75-6.0 mg/kg), or daunorubicin (0.75-6.0 mg/kg) given within 1 minute produced immediate hypotension in anesthetized beagle dogs. The threshold hypotensive dose for Adriamycin (0.375 mg/kg, 7.5 mg/m2) was lower than that for either rubidazone (0.75 mg/kg) or daunorubicin (1.5 mg/kg). Recovery from hypotension was more rapid after administration of rubidazone or daunorubicin than after Adriamycin. Adriamycin (1.5-3.0 mg/kg) caused respiratory distress and depressed mean arterial pressure an average of 54%-82% for up to 30 minutes. The hypotension was almost eliminated when the Adriamycin (1.5 mg/kg) infusion period was extended to 15 minutes. Significant increases in plasma histamine concentrations, coinciding with the peak hypotensive response, were detected within 1 minute after infusion of either Adriamycin (1.5 mg/kg) or rubidazone (1.5 mg/kg). Similar effects were noted after 6.0 mg/kg of daunorubicin. It appears that the acute cardiovascular effects of the three anthracycline compounds are mediated through release of histamine.

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PubMedDate not supplied

Toxic cardiomyopathies.

Examples of toxic cardiomyopathies of various characteristics are presented. Daunomycin and doxorubicin, antineoplastic drugs, cause multifocal cardiomyopathies and intractable heart failure by cardiotoxic mechanisms; these effects are delayed and related to the cumulative dose. Cobalt caused diffuse vacuolar cardiomyopathy in chronic beer drinkers. The development of fulminant heart failure was the function of factors that increased the adsorption of cobalt or sensitized the myocardium to its cytotoxic effect. Beta-adrenergic receptor stimulant bronchodilators like isoproterenol or vasodilating antihypersensitive drugs like hydralazine are able to produce focal subendocardial necroses. This lesion is due to ischemia brought about by the acute exxagerated pharmacological effects of these compounds.

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