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. 1991 Oct;104(2):559–564. doi: 10.1111/j.1476-5381.1991.tb12468.x

Dissociation between the effects of zymosan on the systemic and pulmonary vessels of the rat.

J Damas 1, D Lagneaux 1
PMCID: PMC1908546  PMID: 1797319

Abstract

1. Zymosan, an activator of the alternative complement pathway, (2 to 16 mg kg-1) injected intravenously via the tail vein of anaesthetized rats, dose-dependently increased the vascular permeability of lung parenchyma, as measured by the accumulation of 125I-labelled albumin in lungs. 2. Pretreatment of the animals with cyclo-oxygenase inhibitors, indomethacin or ketoprofen (3 mg kg-1) or with the lipoxygenase and cyclo-oxygenase inhibitor, BW755C (40 mg kg-1) abolished the vascular permeability changes induced by zymosan (16 mg kg-1). Neither, the PAF antagonist, WEB 2086 (10 mg kg-1) nor the antagonist of mast cell amines, mepyramine and methysergide (3 mg kg-1) affected the plasma exudation in lungs. Zymosan did not induce any accumulation of labelled albumin in lungs of rats made leukopenic by rabbit anti-neutrophil serum. 3. Zymosan (16 mg kg-1) increased the haematocrit. This increase was not modified by indomethacin but reduced by WEB 2086. 3. Intravenous injection of zymosan (3 and 8 mg kg-1) in anaesthetized rats transiently increased right ventricular blood pressure and pulmonary arterial pressure, accelerated respiratory rate and decreased systemic blood pressure. 5. WEB 2086 largely reduced the systemic hypotension but did not affect the increase of pulmonary vascular resistance. Indomethacin inhibited the increase of blood pressure in the right ventricle and the modification of the respiratory rate. This drug did not inhibit but increased the systemic hypotension induced by zymosan. 6. Zymosan (16 mg kg-1) reduced serum complement haemolytic activity by 46%.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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