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Biomedical subjects

J Lefort

Publications and source records attributed to J Lefort.

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

Enhancement by prostacyclin of the contractility of the guinea-pig airways smooth muscle.

Aerosolized prostacyclin (PGI2) potentiated the increase in pulmonary resistance to inflation induced by serotonin, prostaglandin F2 alpha (PGF2 alpha), acetylcholine and histamine in the guinea-pig. This was not due to a reflex, nor to further production of PG cyclooxygenase derivatives. PGI2 and PGF2 alpha induced contraction of the parenchyma lung strip of the guinea-pig, which could be inhibited by polyphloretin phosphate and by PGE1. Since PGF2 alpha failed to potentiate the bronchial responses to acetylcholine, histamine or serotonin, under conditions where PGI2 was effective, the in vitro similarities between the two PGs cannot explain the in vivo results. The ability of PGI2 to potentiate bronchial responses was not shared by the other PGs. Since the latter are either bronchoconstrictor agents by themselves (PGF2 alpha and PGD2), or bronchodilators (PGE1, PGE2), our hypothesis is that PGI2 potentiates the responses of the bronchi to various agonists by a mechanism similar to that which accounts for the potentiation of acute inflammation and pain by PGE1 and PGE2, the latter being ineffective in enhancing the bronchial responses because of the associated bronchodilator activity.

Animals↗
PubMed1981

Leukotrienes C and D induce aspirin-sensitive bronchoconstriction in the guinea-pig.

Branchoconstriction in the guinea-pig due to leukotrienes C4 and D4 in vivo and in vitro was suppressed by aspirin. Since contracting effects of putative mediators of bronchial asthma should be refractory to inhibition of cyclooxygenase, our results indicate that release of leukotrienes in the guinea-pig does not alone account for anaphylactic bronchoconstriction.

Airway Resistance↗
PubMed1981

[Interest of the sphincteromyectomy in the treatment of idiopathic constipation and short-segment Hirschsprung's disease (author's transl)].

During last 10 years, 33 children presenting with a severe constipation (19 of them with subobstruction episodes) have been treated with sphincteromyectomy at ages varying from 3 m. to 13 y. The aetiologic study of the constipation includes a barium enema, a manometric study (for the cases treated since 1975) and a histologic study of the muscular strip obtained during the sphincteromyectomy. The barium enema does not show any specific pattern of Hirschsprung's disease, on the other hand, the manometric study brings more constant arguments to distinguish the idiopathic constipation from the short-segment Hirschsprung's disease. The sphincteromyectomy is done by anal approach (28 times) or by posterior approach (6 times). One patient has had 2 sphincteromyectomies. 14 patients had a Hirschsprung's disease and we find among them 9 very good or good results. 5 failures needed a rectal resection by the Swenson's technique. 19 children had an idiopathic constipation. 2 have not been reviewed. Among the 17 others, we find 11 very good results. No postoperative complications have been observed particularly not any incontinence.

Adolescent↗
PubMed1980

Activation of guinea-pig platelets induced by convulxin, a substance extracted from the venom of Crotalus durissus cascavella.

Convulxin (Cx), a component of the venom of the snake Crotalus durissus cascavella, induced the concentration-dependent aggregation of guinea-pig platelets when used at and above 50 +/- 5 ng/ml, accompanied by the release of ATP and by the formation of thromboxanes (Tx). Platelet activation by Cx was not due to potential contaminants found in the crude snake venom, such as phospholipase A2 and clotting enzymes. Aspirin (50-100 microM) failed to interfere with the platelet effects of Cx, demonstrating independence from cyclo-oxygenase. In contrast, indomethacin (50 microM) displayed a distinct inhibitory activity on the effects of Cx, as compared to aspirin, and thus exerts cyclo-oxygenase-independent effects on platelet activation. The ADP scavenger creatine phosphate/creatine phosphokinase (CP/CPK) inhibited aggregation by Cx used at concentrations below 6-8 times the threshold, but failed to interfere with higher amounts. Platelet aggregation by Cx was inhibited and reversed once established by EDTA (5mM) and by prostacyclin (0.1-1 microM). Cx-induced activation of platelets is thus Ca2+-dependent and liable to control by the adenylate cyclase-cyclic AMP system. Convulxin induced hypotension, bronchoconstriction and thrombocytopenia when injected i.v. to the anesthetised guinea pig at 0.3-3 microgram/kg. Aspirin and indomethacin (20 and 5 mg/kg respectively) mepyramine and methysergide (02. mg/kg) failed to interfere with these effects, but the combination of either aspirin or indomethacin with methysergide and mepyramine, suppressed the bronchial effects of Cx, leaving the hypotensive and thrombopenic effects unchanged. This synergism remains unexplained. Bronchoconstriction was platelet-dependent, being suppressed by platelet depletion with antiplatelet serum or by i.v. prostacyclin (1-10 microgram/kg).

Adenosine Diphosphate↗
PubMed1980

Platelet-tissue interaction: role of platelet-activating factor (PAF-acether).

The platelet-activating factor, or PAF-acether, is a phospholipid derivative that is a potent aggregating agent. It is formed by platelets themselves and also by basophils, neutrophils, monocytes and macrophages including alveolar macrophages. A role for PAF-acether during inflammation is envisaged since its intravenous administration induces hypotension, thrombocytopenia and bronchoconstriction in anaesthetized guinea-pigs. It is hypothesized that platelets, which contain and synthetize many pro-inflammatory substances, play a primary role in some pathological states.

Anaphylaxis↗
PubMed1979

Mechanisms of bronchoconstriction and of thrombocytopenia induced by collagen in the guinea pig.

Collagen injected to guinea pigs i.v. increased the pulmonary resistance to inflation (bronchoconstriction) and induced thrombocytopenia. Immune platelet depletion protected against the effects of collagen, and has been shown not to prevent bronchoconstriction induced by the prostaglandin/thromboxane A2 precursor arachidonic acid. Use of inhibitors demonstrated that histamine, serotonin, acetylcholine and bradykinin were not involved with the effects of collagen in the guinea pig. Aspirin and indomethacin inhibited collagen-induced bronchoconstriction completely and thrombocytopenia partly, supporting the hypothesis that the former is prostaglandin cyclo-oxygenase dependent, whereas the latter has a thromboxane A2-independent mechanism as well. Carrageenan, heparin and reserpine inhibited the in vivo effects of collagen to various extents, but their precise mechanism of action could not be discovered. Collagen-induced bronchoconstriction is strictly platelet and thromboxane A2-dependent.

Airway Resistance↗