Nebulisers for lung aerosol therapy.
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Biomedical subjects
Publications and source records attributed to R Lewis.
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A hyperemic stress test was used to determine vasculogenic impotence in 100 men (50 potent, 50 impotent). Normal potent males had a resting penile:brachial index ratio of 0.75 and uniformly demonstrated a hyperemic response to the cuff occlusion stress test with a mean of 20 per cent increase in penile pressure. Penile blood pressure did not increase in impotent men, and often it decreased in response to the stress test.
Rat mast cells, stimulated for histamine release by compound 48/80 or lysosomal cationic protein, take up 45Ca2+ from he extracellular fluid. This uptake is inhibited by diisopropyl fluorophosphate, phenylmethylsulfonyl fluoride, and the inhibitors of energy metabolism. It was seen previously, when the release process is divided into two stages by activating the cells at 0 degrees C, the uptake of 45Ca2+ occurs during the release stage of the reaction. In the present studies, it was found that when cells activated at low temperatures were allowed to stand at 10 degrees C in the presence of 45Ca2+, the uptake of radioactive calcium increased in the first 15 min and then decreased to the levels of unstimulated cells. On the other hand, the release of histamine from the activated cells upon warming to 37 degrees C progressively decreased with an increase in time at 10 degrees C. These results suggest that during the decay of the active state the levels of intracellular exchangeable calcium pool are increased. For 45Ca2+ to be pumped out after the decay, there has to be net gain in intracellular calcium concentration during the first 15 min at 10 degrees C. The increase in membrane permeability to calcium appears to be due to the activation of a transient event.
The effects of changes in the extracellular concentration of calcium on activation of rat mast cells by compound 48/80 were studied. The intracellular exchangeable Ca2+ pools at various concentrations of extracellular Ca2+ were determined by equilibration of the cells with 45Ca2+. The cells stimulated by compound 48/80 in the presence of 2.5 microM and 1.6 mM extracellular Ca2+ released comparable amounts of histamine. However, the intracellular Ca2+ pool was doubled in 2.5 microM Ca2+ and was increased sixfold in 1.6 mM Ca2+. In 14.4 mM extracellular Ca2+, there was neither release of histamine nor uptake of Ca2+ which suggested an impairment in activation. The kinetics of Ca2+ influx in the presence of 2.5 microM Ca2+ did not reveal intracellular mobilization of calcium. The cells activated in 1.6 mM Ca2+ at 0 degrees C when allowed to stand in 14.4 mM extracellular Ca2+ released decreased amounts of histamine upon warming to 37 degrees C. The inhibition of the release progressively increased with time of standing at 0 degrees C. The decrease in histamine release was not seen with the cells standing in 1.6 mM Ca2+ at 0 degrees C. The effect of 14.4 mM Ca2+ added prior to tha challenge with compound 48/80 did not depend on the time of incubation. The data presented in this paper suggest that the high concentration of Ca2+ inhibits the histamine release from mast cells by interfering with membrane-associated phenomena.
The effect of equal (1.1 +/- 0.1 g/kg body wt) amounts of glucose administered orally, or by peripheral intravenous or intraportal infusion on hepatic glucose uptake and fractional hepatic extraction of insulin and glucagon was studied in conscious dogs with chronically implanted Doppler flow probes on the portal vein and hepatic artery and catheters in the portal vein, hepatic vein, carotid artery, and superior mesenteric vein. Portal vein and hepatic vein plasma flow increased only after oral glucose administration. Arterial plasma glucose increased equally to 150-160 mg/100 ml after all three routes of glucose administration. Portal vein glucose was similar after oral (195 +/- 15 mg/100 ml) and intraportal glucose infusion (215 +/- 11 mg/100 ml) and significantly higher than after peripheral intravenous glucose. Hepatic glucose uptake after oral (68 +/- 4%) and intraportal glucose administration (65 +/- 7%) significantly exceeded that after peripheral intravenous glucose infusion (23 +/- 5%). The amount of insulin above basal presented to the liver during the 180 min after oral glucose was 7.6 +/- 1.3 U, 4.3 +/- 0.6 U after intraportal glucose, and 4.1 +/- 0.6 U after peripheral intravenous glucose. Hepatic extraction of insulin increased significantly after oral glucose (42 +/- 3 to 61 +/- 4%), but was unchanged after intraportal and peripheral intravenous glucose administration. When the portal vein glucose levels achieved during peripheral intravenous glucose infusion for 90 min were maintained by a subsequent 90-min intraportal glucose infusion, hepatic glucose uptake was significantly greater during the intraportal glucose infusion. Glucagon secretion was suppressed equally after oral glucose, intraportal glucose, and peripheral intravenous glucose administration; fractional hepatic extraction of that hormone, which was significantly less than that of insulin, was unchanged. These results indicate that hepatic glucose uptake is significantly greater after oral and intraportal glucose administration than after peripheral intravenous glucose infusion. This difference is not simply related to the amount of glucose or insulin presented to the liver and the increased hepatic glucose uptake did not depend solely upon the augmented fractional hepatic extraction of insulin. Hepatic extraction of insulin and hepatic glucose uptake appear to be regulated independently.
The molecular weights of the soluble proteins from cranial and caudal prostate and seminal vesicle tissues of several species of nonhuman primates were separated by electrophoresis. The tissues of animals belonging to the genus Macaca were found to be similar and are compared to those of other species. The molecular weights of these proteins are discussed with regard to known concentrations of prostate and seminal vesicle proteins.
We investigated whether dialyzate obtained from patients undergoing CAPD had any harmful effects on the function of their own lymphocytes and granulocytes and on those of normal controls. When tested in dialyzate obtained after a 4 hr intraperitoneal residence, lymphocyte viability and transformation responses to phytohemagglutinin and protein A were similar for patients and controls. Neutrophil function assessed by the nitroblue tetrazolium test (NBT) was not altered. Our results suggest that dialyzate, after a 4 hr intraperitoneal stay, does not impair lymphocyte and granulocyte function.
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