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Biomedical subjects

L B Jaques

Publications and source records attributed to L B Jaques.

At least 55 records · Page 3Linked to original sources
PubMed1977

Heparin and sulfated mucopolysaccharides--a micro system for quantitative differentiation and determination.

Heparin (Hep), hyaluronic acid, chondroitins (sulfate) A, B, and C, and heparins (sulfate) A, B, C, and D were subjected to microelectrophoresis in barbital-agarose gel, fixed with cetylpyridinium chloride and stained with toluidine blue. The optical densities of the resulting bands were compared with optical densities obtained upon reaction with azure A in aqueous solution and with the carbazole reagent. A linear relation was obtained between optical density and concentration of purified sulfated mucopolysaccharide (SMP). Less than 1 microgram of Hep and 2 microgram of other SMPs are required for measurement by electrophoresis, while about 30 microgram of each is required with the carbazole reagent. The optical density of a mixture of SMPs was equal to the sum of the densities for the individual SMPs upon microelectrophoresis. It was demonstrated that the individual SMPs in mixtures were distinguishabed by reaction with specific enzymes and by changes in migration in agarose with barbital, phthalate, ethylenediamine, or propanediamine buffers, permitting ready demonstration and quantitation of various SMP species. Examples are shown of the application of the procedure to measure the total SMPs and individual SMPs in tissue extracts. The method is sensitive, reproducible, flexible, and measures quantities 1/30th of those measured colorimetrically, yet is relatively unaffected by protein, carbohydrate, or inorganic electrolytes.

Buffers↗
PubMed1976

Intrapulmonary heparin. A new procedure for anticoagulant therapy.

Heparin was administered by the intrapulmonary route to dogs, mice, and human volunteers. In all species, a single administration of a large quantity of heparin via the lung resulted in a prolonged state of moderate hypocoagulability (3 days in dogs, 14 days in man) due to the production of a sustained low concentration of heparin in plasma. The lengthening of clotting-time and duration of this response increased with dosage. Effective doses are above 8 mg (1300 units) per kg body-weight. Examination of the lungs, body-fluids, and tissues shows that the heparin is cleared rapidly from the lung and enters a body cellular compartment (probably the macrophages) from which it is slowly released to plasma. No evidence was found (symptomatic or on gross or histological postmortem examination) of haemorrhage or any heparin-related pathological change indicating either immediate or long-term toxic effects in the lung or other tissues. Suggestions are made for the clinical use of the unique features of anticoagulant treatment by intrapulmonary heparin.

Aerosols↗
PubMed1976

Blocking of olive oil induced plasma protein escape from the intestinal circulation by histamine antagonists and by a diamine oxidase releasing agent.

Earlier studies have shown that feeding of olive oil to rats substantially increased the plasma protein in the intestinal lymph. The possibility of histamine mediating this response was examined. The plasma protein escape from intestinal circulation after olive oil feeding was measured in rats in terms of the amount of Evans Blue labelled plasma protein found in the intestinal lymph. Animals treated with histamine antagonists (H1-receptor antagonist pyrilamine, 16-22 mg/kg i.p., plus H2-receptor antagonist Burimamide, 12-16 mg/kg i.p.) did not show an increase in the quantity of lymphatic plasma protein. Heparin pretreatment which releases the histaminolytic enzyme, diamine oxidase, into the interstitial space also prevented the increased accumulation of labelled plasma protein in the lymph after olive oil ingestion. Based on these observations, histamine appears to act on the intestinal microcirculation during olive oil absorption and allows larger quantities of plasma proteins to leave the intestinal circulation.

Amine Oxidase (Copper-Containing)↗
PubMed1976

Susceptibility to experimental atherosclerosis: relation to mast cells and heparin.

Fifteen chicken tissues were examined for mast cells. Numerous mast cells were found in peritoneum and spleen. The sulfated mucopolysaccharides extracted from these two tissues, corresponding in amount to that in mast cells, were found to be dermatan sulfate, chondroitin sulfate and heparitin sulfate but no evidence of heparin. We have shown a similar situation occurs in the rabbit which is also highly susceptible to the production of atherosclerosis by diet. These observations provide further evidence of a role for heparin and mast cells in limiting atherogenesis.

Animals↗
PubMed1976

Effects of acidity, cations and alcoholic fractionation on absorption of heparin from gastrointestinal tract.

Heparin was introduced into the stomach or duodenum of mice separately in doses of ca. 250 mg/kg. A slight anticoagulant effect in the systemic circulation was detected in whole blood clotting times and factor X inhibition. In contrast to most drugs, more heparin was absorbed from the stomach than from the intestine. Suppressing ionization of heparin by simultaneous administration of acid resulted in improved absorption of heparin from the small intestine. Heparin was separated with ethanol into five molecular weight fraction: I, 17 999; II, 13 i99; III, 10800, IV, 8 700; and V, 6 700. Each was introduced into the duodenum of mice with citric acid. The maximum hypocoagulability was produced with fraction IV. When administered in distilled water instead of in citric acid, this heparin fraction did not produce an anticoagulant effect. These studies demonstrated that improvement of heparin absorption from the gastrointestinal tract can be obtained by the combination of suppressing ionization and selecting molecular size.

Animals↗
PubMed1976

A new route of heparin administration--the lung.

Instillation of a single dose of heparin into the lungs of the dog resulted in a steady prolonged hypocoagulability as measured by the Lee and White clotting time, partial thromboplastin and activated partial thromboplastin times. 15 mg of heparin/kg increased clotting time three to five times control values. The anticoagulant effect occurred within one hour and lasted 48 h or more, in contrast to the short effect of intravenous heparin. For doses of 8, 10, 12, 15 and 20 mg/kg, there was a corresponding increase in the area under the response curve. The very prolonged moderate anticoagulant state with intrapulmonary heparin did not show the wide fluctuations in coagulation test values which occur with intravenous heparin.

Animals↗