21,364 research outputs found
VASOCONSTRICTION AND BRONCHOCONSTRICTION INDUCED BY 2,5-DI-(TERT-BUTYL)1,4-BENZOHYDROQUINONE, AN ENDOPLASMIC RETICULAR CA2+-ATPASE INHIBITOR, IN ISOLATED AND PERFUSED RAT LUNG
No full textThe microsomal Ca2+-ATPase inhibitor 2,5-di-(tert-butyl)-1,4-benzohydroquinone (tBuBHQ) induced bronchoconstriction and vasoconstriction in the isolated perfused and ventilated rat lung. Thes effects were accompanied by increased levels of thromboxane and prostacyclin in the effluent perfusate. The effect of tBuBHQ was inhibited by L-655,240, a thromboxane receptor antagonist, indicating thromboxane-A2-mediated bronchoconstriction and vasoconstriction. Accordingly, the cyclooxygenase inhibitor indomethacin largely blocked the effects of tBuBHQ. The involvement of a phospholipase in the generation of thromboxane A2 (TXA2) was supported by dibucaine protection on tBuBHQ effects. The results from this study indicate that tBuBHQ, probably by inhibiting the microsomal Ca2+-ATPase, can trigger the arachidonic acid cascade leading to the formation of TXA2, which in turn causes bronchoconstriction and vasoconstriction in rat lung
SULFUR DIOXIDE-INDUCED BRONCHOCONSTRICTION IN THE ISOLATED PERFUSED AND VENTILATED GUINEA-PIG LUNG
No full textSO2 exposure (50-500 ppm) of isolated, perfused and ventilated guinea pig lungs, via the air passages, caused a concentration-related reduction in dynamic compliance and conductance. No changes in pulmonary perfusion flow was noted at any SO2 concentration. Formed sulfite was detected in lung lavage fluid as well as in the perfusate. Pretreatment of the lungs with a low concentration of SO2 (10 ppm) for 30 min protected against bronchoconstriction by a high concentration of SO2 (250 ppm). A similar protective effect was noted by pretreatment with sodium sulfite (3 mM) in the lung perfusate
Thiol modifications in H2O2 and thromboxane induced vaso-and bronchocosntriction in rat perfused lung
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MECHANISMS OF PCBS MIXTURE TOXICITY ON ISOLATED RAT HEPATOCYTES
No full textExposure of isolated hepatocytes to a polychlorinated biphenyl mixture induced a rapid loss of cell viability. The effect was not dose-dependent. The biochemical effects in the cellular toxicity did not involve glutathione content, protein sulfhydryl groups and lipid peroxidation. A transient increase in cytosolic Ca2+ was observed after exposing the hepatocytes to the polychlorinated biphenyl mixture. Our findings indicate that polychlorinated biphenyls are able to kill hepatocytes and suggest that elevation of cytosolic Ca2+ concentration could be responsable of the toxicity
Sodium Metabisulfite and citric acid induce bronchoconstriction via a sulfite sensitive pathway in the isolate guinea pig lung
No full textSULFUR DIOXIDE-INDUCED BRONCHOCONSTRICTION VIA RUTHENIUM RED-SENSITIVE ACTIVATION OF SENSORY NERVES
No full textThe mechanism of sulfur dioxide-induced bronchoconstriction was studied using isolated perfused and ventilated guinea-pig lungs. They were exposed to sulfur dioxide after pretreatment with different compounds, either via the pulmonary artery or via the air passages. Neither the cyclooxygenase inhibitor indomethacin (30 muM) nor the H-1-receptor antagonist diphenhydramine (15 muM), given via the perfusate, attenuated the sulfur dioxide-induced bronchoconstriction. Furthermore, sulfur dioxide exposure did not cause a release of either thromboxane or histamine into the perfusate. In experiments with atropine equivocal results were obtained with regard to protection against sulfur dioxide-evoked bronchoconstriction. Intratracheal instillation of the local anesthetic agent lidocaine (1 mg/50 mul) markedly reduced the sulfur dioxide-induced bronchoconstriction. Also, ruthenium red (10 muM), an agent with calcium entry-blocking properties and an inhibitor of capsaicin-induced bronchoconstriction, was able to inhibit the effect of sulfur dioxide. The sulfur dioxide-induced bronchoconstriction was associated with release of calcitonine gene-related peptide, a sensory neuropeptide. The effect of sulfur dioxide was also inhibited by a Ca2+-free buffer plus EGTA. These results suggest that sulfur dioxide-induced bronchoconstriction in the guinea-pig lung is the result of a local effect on sensory nerves (C-fiber activation). The mechanism seems to be dependent on the Ca2+-dependent release of sensory neuropeptides and to be linked to opening of the cation channel, which is associated with the proposed capsaicin receptor on sensory nerves as revealed by the inhibitory effect of ruthenium red
Protecting Animals 36: Author Witi Ihimaera
No full textIn this very special episode of Knowing Animals I am joined by beloved New Zealand author Witi Ihimaera. Witi has written many books featuring nonhuman animals. He offers us a non-colonial lens through which to think about the human/nonhuman relationship
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