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Biomedical subjects

H R Keiser

Publications and source records attributed to H R Keiser.

At least 199 records · Page 11Linked to original sources

Effects of dietary sodium and of acute saline infusion on the interrelationship between dopamine excretion and adrenergic activity in man.

The effects of dietary sodium and of saline infusion on urinary dopamine and norepinephrine and on the relationship of these catecholamines to adrenergic activity were determined. In seven normal subjects on a 9-meq sodium intake, urinary dopamine and norepinephrine were 136+/-18 (SE) and 37.4+/-5.3 mug/day, respectively. When sodium intake was increased to 209 or 259 meq/day, urinary dopamine increased to 195+/-20 mug/day (P<0.01) whereas urinary norepinephrine decreased to 21.1+/-3.0 mug/day (P<0.01). Infusion of saline in seven subjects increased sodium excretion and urinary dopamine (from 2.18+/-0.22 to 2.79+/-0.19 mug/20 min, P<0.01), but decreased plasma dopamine-beta-hydroxylase by 33% and urinary norepinephrine insignificantly. The clearance of inulin and p-aminohippurate did not change significantly and filtration fraction was the same. The data indicate that an increase in dietary sodium or infusion of saline results in an apparent decrease in adrenergic activity and an increase in urinary dopamine. Dopamine excretion would thus appear to relate inversely to adrenergic activity and to parallel sodium excretion. These findings suggest a possible role for dopamine and norepinephrine in the regulation of renal sodium excretion.

Adult↗

Response of plasma histaminase activity to small doses of heparin in normal subjects and patients with hyperlipoproteinemia.

The release of histaminase activity in plasma after small intravenous of heparin was studied in 85 normal subjects and patients. In normal subjects, plasma histaminase activity (basal level, 1.7+/-0.1 U/ml, mean +/-SEM) increased 1.6+/-0.2 U/ml after 10 U of heparin/kg, 8.5+/-2.4 U/ml after 20 U/kg, and 33+/-4.9 U/ml after 75 U/kg. The extent of the increase varied widely among individuals but in a particular individual the response was constant and dose-dependent. Histaminase activity rose to peak levels within 7-15 min and then declined exponentially with a half-life of 40-120 min. This pattern of response was also observed in two patients with the histaminase-producing tumor, medullary carcinoma of the thyroid. A significantly reduced response was observed, however, in 14 patients with type I hyperlipoproteinemia, a disorder in which high plasma triglyceride levels are associated with low postheparin plasma lipolytic activity. After 10 U heparin/kg, plasma histamine activity increased 0.5+/-0.2 U/ml, and after 75 U heparin/kg, 10.9+/-5.6 U/ml. In contrast, in 27 patients with other types of hyperlipoproteinemia in whom postheparin lipolytic activity was normal, the increase (2.4+/-0.6 U/ml) in plasma histaminase activity after 10 U heparin/kg was not significantly different from that of normal subjects. The reduced response of the plasma histaminase activity to heparin in patients with type I hyperlipoproteinemia did not appear to be due to the presence of lipemia or to an inhibitor of the enzyme in plasma. These findings suggest that many patients with type I hyperlipoproteinemia may have deficient release of both lipolytic and histaminase activities into plasma after heparin administration.

Adolescent↗