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Biomedical subjects

G E Isom

Publications and source records attributed to G E Isom.

At least 109 records · Page 6Linked to original sources
PubMed1981

Characterization of the respiratory activity of (D-Ala2)methionine-enkephalinamide.

The effects of central administration of (D-Ala2)methionine-enkephalinamide (EA) on respiration were studied in the unanesthetized rat. EA induced a dose-dependent depression of respiratory rate and tidal volume which was reversed by the subcutaneous administration of naloxone HCl (10 mg/kg). Increasing atmospheric CO2 concentration stimulated EA-induced respiratory depression and the peptide produced a parallel shift to the right of both the respiratory rate -- PaCO2 and tidal volume -- PaCO2 curves. Following chronic administration of EA tolerance to the respiratory depression was observed and chronic exposure to morphine produced partial tolerance to the respiratory depression induced by EA. It was concluded that EA desensitizes the central chemoreceptors to CO2 and the action of EA on respiration parallels that of morphine.

Animals↗
PubMed1979

Studies on the central pressor activity of dibutyryl cyclic AMP.

The effects of the central administration (i.c.v.) of dibutyryl cyclic AMP (DBcAMP) on arterial blood pressure and heart rate were studied in the rat. The cyclic nucleotide produced a dose-dependent rise in blood pressure and an accompanying tachycardia. Maximal pressor effect of a single dose of DBcAMP (350 micrograms) was observed 25 min post injection and the duration of the response was 60 min. Chemical degeneration of central catecholaminergic neurons with 6-hydroxydopamine treatment abolished the pressor response to DBcAMP. Partial chemical degeneration of central serotonin pathways with 5,6-dihydroxytryptamine did not significantly alter the effect. The pressor activity of the cyclic nucleotide was attenuated by central administration of phentolamine. Spinal cord section at the C6-C7 level or peripheral chemical degeneration of catecholaminergic neurons combined with bilateral adrenalectomy abolished the pressor response to DBcAMP. It was concluded that the pressor response to i.c.v. administration of DBcAMP is mediated by central catecholaminergic pathways and is the result of an increase in efferent sympathetic outflow and release of catecholamines from the adrenal medulla.

Animals↗
PubMed1978

Influence of immune stimulation and suppression on morphine physical dependence and tolerance.

The role of the immune system in the development of physical dependence and tolerance to morphine was studied in mice in which the immune response was either stimulated or suppressed. Immunization of mice against morphine increased the blood and brain levels of morphine as compared to controls. However, the development of physical dependence and tolerance was decreased. The chronic responses to morphine were also decreased by nonspecific immunosuppression (vincristine-cyclophosphamide treatment and gamma-irradiation exposure) and specific immunosuppression (antithymocyte and antilymphocyte sera treatment). Immunosuppressive treatments did not alter the rate of morphine absorption from the subcutaneous depot used to induce chronic exposure to the drug. However, the blood and brain levels of morphine were higher than control after 72 hours of morphine pellet implantation. It is apparent that manipulation of the immune system can alter the physical dependence and tolerance development to morphine.

Animals↗