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Biomedical subjects

D Lundberg

Publications and source records attributed to D Lundberg.

88 records · Page 5Linked to original sources
PubMed1978

Haemodynamic effects of different corticosteroids in controlled haemorrhagic shock in the dog.

The haemodynamic effects of massive doses of hydrocortisone (80-320 mg.kg-1), methylprednisolone (4-32 mg.kg-1), betamethasone (1.6-12.8 mg.kg-1) and aldosterone (0.1-0.8 mg.kg-1) and the interaction with phenoxybenzamine and propranolol have been studied during controlled haemorrhagic shock in the anaesthetized dog. Hydrocortisone was the only steroid which showed any significant vasodilating ability when given alone. The alpha-receptor blocking agent phenoxybenzamine distinctly decreased the total peripheral resistance. The effect of the phenoxybenzamine was increased in combination with hydrocortisone or methylprednisolone, especially if the steroid was given as the first drug. The vasodilation found was efficiently abolished by the beta-receptor blocking agent propranolol. The ability of hydrocortisone or methylprednisolone to potentiate phenoxybenzamine was not shared by betamethasone or aldosterone. Thus, the haemodynamic effect of the steroid does not seem to be correlated to either a glucocorticoid nor a mineralocorticoid effect. It is suggested that the steroid effect studied is related to the ability of hydrocortisone or methylprednisolone to block the extra neuronal amine uptake which decreases the rate of elimination of the sympathetic transmitter from the vicinity of the adrenergic receptor of the vascular smooth muscle.

Adrenal Cortex Hormones↗
PubMed1976

Haemodynamic effects of massive doses of hydrocortisone and the interaction with phenoxybenzamine in controlled haemorrhagic shock in the dog.

Haemorrhagic shock was produced in anaesthetized dogs by bleeding into a blood reservoir system. The blood level of the reservoir was adjusted at a level above the heart, corresponding to a mean arterial blood pressure of 6.7 kPa (50 mm Hg). The dogs were treated with hydrocortisone and the adrenergic alpha-receptor blocking agent phenoxybenzamine during the hypotension period. Hydrocortisone (80-160 mg kg-1) was found to induce vasodilation, which, however, was of a very small magnitude and was of short duration. Phenoxybenzamine given after hydrocortisone caused very pronounced vasodilation. Hydrocortisone (80 mg kg-1) given after phenoxybenzamine also showed a vasodilator activity, which seemed to be greater than that of the same dose of hydrocortisone given alone. Thus, the vasodilator action of hydrocortisone does not seem to be due to an alpha-receptor blockade of the drug. The vasodilator action of phenoxybenzamine given after hydrocortisone was greater than that of even higher doses of the drug given alone. From the present findings and the fact that corticosteroids are known to potentiate the sympathomimetic action of catecholamines, it is suggested that the hydrocortisone-induced potentiation of the vasodilation action of phenoxybenzamine found is related to an increased vascular adrenergic beta-receptor tone.

Animals↗
PubMedDate not supplied

Changes in cerebrospinal fluid homovanillic acid in children with Ondine's curse.

The cerebrospinal fluid (CSF) concentrations of three acid monoamine metabolites, two purines, and a group of amino acids were determined in two children with chronic central alveolar hypoventilation (Ondine's curse). The levels of all assayed neuroactive substances, metabolites, and amino acids, with one exception, were normal compared to an age-matched group of neurologically healthy children. The levels of the dopamine metabolite homovanillic acid in the children with Ondine's curse were approximately 2.4 times higher than expected for age range. The present findings may indicate a link between central nervous system dopamine activity and chronic central alveolar hypoventilation. Among other possible explanations, the changes seen might represent a primary alteration in dopamine activity or may reflect a change in dopamine turnover resulting from the chronic hypoventilation.

Adenosine↗
PubMedDate not supplied

Treatment of coccidioidomycosis with ketoconazole: clinical and laboratory studies of 18 patients.

Ketoconazole was given to 18 patients with coccidioidomycosis. Fourteen had received prior antifungal chemotherapy with amphotericin B, miconazole, or both. Ten patients had pulmonary disease, two had meningitis, and six had extrameningeal disseminated disease. The initial dose of ketoconazole was 200 mg per day; it was later increased to 400 mg per day for some patients. All strains of Coccididioides immitis tested were sensitive to ketoconazole. Approximately 2-4 hr after an oral dose of 200 mg of ketoconazole, levels of the drug in blood peaked at approximately 2 micrograms/ml. Higher concentrations in blood were achieved with a 400-mg dose. Improvement was measured by physical examination, conversion of cultures previously positive for C. immitis to negative, decrease in erythrocyte sedimentation rate by 50%, and decrease in titer of complement fixation antibody by two or more dilutions. One patient died after one week of treatment with ketoconazole and could not be evaluated; two other patients with coccidioidal meningitis could not be evaluated. Six of nine patients with pulmonary disease showed radiographic improvement, and their sputum cultures, which had been positive, became negative. Four of the six patients with disseminated disease improved. There were few adverse reactions to ketoconazole, which can be safely administered for prolonged periods to patients with coccidioidomycosis. These findings suggest that ketoconazole may be effective for treatment of this disease and indicate that trials comparing the efficacy of ketoconazole with that of amphotericin B are warranted.

Adult↗
PubMedDate not supplied

Effect of lumbar sympathetic blockade and chlorpromazine-induced adrenergic alpha-receptor blockade on skin temperature in peripheral arterial diseases.

The post-cooling toe temperature changes after lumbar sympathetic blockade and after intramuscular administration of an adrenergic alpha-receptor blocking substance (chlorpromazine) were studied in 14 patients with impending gangrene because of peripheral arterial insufficiency. The post-cooling temperature rise was similar after sympathetic blockage and chlorpromazine administration and significantly different from the basal toe temperature changes after cooling. It is concluded that administration of an adrenergic alpha-receptor blocking substance is as good as the lumbar sympathetic blockage for evaluation of a remaining sympathetic vasomotor tone in arterial disease patients.

Adrenergic alpha-Antagonists↗