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Biomedical subjects

J Lefort

Publications and source records attributed to J Lefort.

At least 127 records · Page 7Linked to original sources
PubMed1979

Differential effects of prostacyclin and prostaglandin E1 on bronchoconstriction and thrombocytopenia during collagen and arachidonate infusions and anaphylactic shock in the guinea-pig.

The antagonism by prostacyclin (PG12) and prostaglandin E1 (PGE1) of bronchoconstriction induced by serotonin (5HT), collagen, arachidonic acid (AA) and anaphylaxis, as well as of thrombocytopenia was studied in the guinea-pig. Under conditions where PGE1 prevented bronchoconstriction by 5HT, by collagen or by AA better than the accompanying thrombocytopenia, PG12 was a selective antagonist of bronchoconstriction due to collagen, but failed to interfere with that due to 5HT or to AA. Collagen-induced bronchoconstriction in the guinea-pig is platelet-dependent. PG12 blocks bronchoconstriction by collagen, because it prevents the platelet activation, and fails to interfere with bronchoconstriction by AA, even though it reduces the accompanying thrombocytopenia, because the role of platelets is negligible. PGE1 and PG12 failed to interfere with thrombocytopenia or with bronchoconstriction of anaphylactic shock, and were inactive even when the acute bronchial effect was suppressed by anti-histamine treatment. Anaphylactic thrombocytopenia is beyond the control of agents which stimulate the cyclic AMP system, and involves specific mechanism which are not stimulated in platelet-rich plasma.

Anaphylaxis↗
PubMed1979

Platelet-lung in vivo interactions: an artifact of a multi-purpose model?

The simultaneous evaluation of platelet behaviour in vivo and of the accompanying bronchoconstriction in the guinea pig is described. Arachidonic acid induces bronchoconstriction, accompanied by, but independent from, thrombocytopenia, whereas collagen induces bronchoconstriction also accompanied by, but dependent from, thrombocytopenia. In both cases bronchoconstriction is due to cyclo-oxygenase metabolites of arachidonic acid. Use of potential inhibitors of thromboxane synthetase failed to reveal which of prostaglandin endoperoxides or thromboxane A2 is responsible for aspirin-inhibitive bronchoconstriction and thrombocytopenia. In contrast to PGE1 prostacyclin failed to interfere with bronchoconstriction by serotonin or by arachidonic acid, even though thrombocytopenia by the latter was suppressed. Bronchoconstriction by collagen, in contrast, was inhibited by nanogram doses of prostacyclin, confirming platelet-dependency. The combined bronchoconstriction/thrombocytopenia test in guinea pigs can discriminate sites of action of anti-inflammatory drugs, of agents which block specific platelet and/or bronchial receptors, which stimulate the cyclic AMP system, or generically which interfere with the mechanisms of bronchoconstriction and of thrombocytopenia.

Adenosine Diphosphate↗
PubMed1979

[Idiopathic megaoesophagus in the child. A series of 17 cases treated surgically (author's transl)].

The authors undertook a retrospective study of a series of 17 cases of idiopathic megaoesophagus seen over a period of 25 years in two paediatric surgery departments. Age distribution was regularly between 20 months and 15 years. No neonatal nor familial forms were seen. Symptoms were dominated by regurgitation and dysphagia. Weight loss was an almost constant feature. Heller's operation, via an abdominal approach with retro-oesophageal valve of the tuberosity fixed to both edges of the myotomy, was the operation proposed. In one case of recurrent megaoesophagus operated upon elsewhere a Thal operation gave a good result with a follow up of 8 years. Immediate clinical and radiological results were favourable in the great majority of cases : 16 cases out of 17. Long term results (follow up of more than 5 years in 8 patients) were also favourable. However one patient was sometimes troubled by regurgitations due to persistent achalasia and a grave failure occured in a patient who five years after a Heller operation developed a peptic stenosis of the lower oesophagus. No recurrence of megaoesophagus was seen. The authors emphasise the importance of the prevention of gastro-oesophageal reflux and the value of oesophagoscopy and of manometry in cases where the result of a Heller's operation is imperfect.

Adolescent↗
PubMed1978

Role of platelets in aspirin-sensitive bronchoconstriction in the guinea-pig; interactions with salicylic acid.

1 The bronchoconstriction caused in the guinea-pig by arachidonic acid (AA), bradykinin, adenosine diphosphate (ADP) and adenosine triphosphate (ATP) was correlated with effects on platelets. ATP and ADP produced a brief thrombocytopenia and AA a more prolonged one. Bradykinin had no effect on platelets.2 Aspirin inhibited bronchoconstriction and thrombocytopenia produced by AA and part of the bronchoconstriction produced by ATP, but had no effect against ADP. Thrombocytopenia produced by ADP and ATP was not affected by aspirin or indomethacin.3 Platelet depletion by antiserum prevented bronchoconstriction in response to ADP and to ATP, but not in response to bradykinin or to AA, showing that platelets are not involved in aspirin-sensitive bronchoconstriction. Infusions of ADP reduced bronchoconstriction and thrombocytopenia in response to ADP itself and to ATP, but not to AA. Bronchoconstriction by ADP or ATP involves an action on platelets. Only that due to ATP is partially dependent on the activity of prostaglandin synthetase.4 ATP induced aggregation in vitro in guinea-pig platelet-rich plasma (PRP). Rabbit PRP responded only when ATP was first incubated with guinea-pig plasma. The aggregating compound formed was probably ADP, since it was destroyed by apyrase. Its formation was not inhibited by aspirin or indomethacin, indicating that aspirin inhibits ATP-induced bronchoconstriction by a different mechanism.5 The aggregating effect of ATP on guinea-pig platelets was inhibited by concentrations of apyrase that block ADP-induced aggregation, and potentiated by lower concentrations of apyrase.6 Adenosine 5'-tetraphosphate did not aggregate platelets in vivo or in vitro. In vitro aggregation occurred when apyrase was added, suggesting transformation into ADP. Adenosine 5'-tetraphosphate and apyrase inhibited aggregation due to ADP, but failed to affect that due to AA. This suggests that aggregation involving products of prostaglandin synthesis does not require ADP.7 Salicylic acid did not interfere with bronchoconstriction or aggregation due to AA, but prevented inhibition by aspirin when the weight ratio, salicylic acid:aspirin was 4:1. Salicyclic acid may be useful in studies of potential inhibitors of thromboxane A2 synthesis and of thromboxane A2-dependent processes in vivo and in vitro.

Adenosine Diphosphate↗
PubMed1978

[Gastroschisis. Analysis of 19 cases (author's transl)].

Since 10 years, 19 cases of gastroschisis have been observed in the surgical paediatric unit of Rouen. 12 children are alive and 7 died. It is possible to classify the lesions of the alimentary tract in four groups of increasing gravity. For the first two groups, survival is probable when the treatment is correct. The third group, including bowel resections and risk of short bowel is more difficult to treat. The last group, with necrosis of the main part of the bowel is uncurable. Surgical treatment of choice is immediate closure with small enlargement of the initial parietat defect. It was possible without complication in 8 cases (9 trials). Delayed closure is now employed when immediate closure is impossible. Post-operative treatment is marked by risks of infectious problems and chronic subocclusion. In this last occurence, reintervention must not be too much delayed. Parenteral feeding, with occasionnal continuous enteral feeding must be sufficient.

Birth Weight↗
PubMed1976

Haemorrhagic and inflammatory properties of collagenase from C. histolyticum.

Collagenase from Clostridium histolyticum induced haemorrhages when applied to the surface of dog lung; it exerted a similar effect on mouse lung when injected intrathoracically. Injected into rat paws, bacterial collagenase induced haemorrhage and oedema. Effects of collagenase were prevented by several procedures that inhibit collagenolytic activity (heating at various temperatures and incubation with metal-complexing agents such as EDTA, penicillamine and dithiothreitol). Protein protease inhibitors, dexamethasone and standard acidic anti-inflammatory drugs had only a slight or no effect on collagenase-induced haemorrhages; dexamethasone and acidic anti-inflammatory drugs blocked collagenase-induced oedema. Inhibition of endogenous kinin-releasing mechanisms by administration of hexadimethrine, a recognized inhibitor of the activation of clotting Factor XII, and depletion of kininogen by administration of carrageenin blocked collagenase-induced oedema. Collagenase did not increase permeability of rat skin vessels, nor did it release potential inflammatory mediators, such as bradykinin or prostaglandins, from plasma or platelets. Bacterial collagenase-induced haemorrhage presumably resulted from enzymatic destruction of membranous structures; at least a portion of the inflammatory response may be due to activation of a kinin-like system.

Animals↗
PubMed1976

[Fibula aplasia and associated malformations. 62 cases].

The authors have studied 62 cases of aplasia of hypoplasia of the fibula. They note that developmental abnormalities affect the whole of the lower limb. They describe the evolution of the bony deformities and of anomalies of the soft tissues. They conclude that discrepancy in limb length is the major factor in the prognosis and that it increases uniformally. Surgery is indicated even when a definitive prosthesis is planned. The possibility of leg lengthening must be approached with caution.

Adolescent↗