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Timothy W Evans - One of the best experts on this subject based on the ideXlab platform.
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Bleomycin induced lung injury in rats selectively abolishes hypoxic pulmonary vasoconstriction evidence against a role for platelet activating factor
Clinical Science, 1992Co-Authors: D G Mccormack, D E Crawley, Peter J. Barnes, Timothy W EvansAbstract:: 1. The role of platelet-activating factor in the attenuated hypoxic pulmonary vasoconstriction associated with lung injury was evaluated using specific platelet-activating factor antagonists and an isolated perfused lung preparation. 2. Intratracheal Bleomycin was administered to rats to produce acute lung injury. Animals received intratracheal saline (control), intratracheal Bleomycin or the platelet-activating factor antagonists BN 52021, WEB 2170 or WEB 2086 before and after Bleomycin treatment. Forty-eight hours after intratracheal administration of Bleomycin or saline the animals were killed. 3. The increases in pulmonary artery pressure during two periods of hypoxic ventilation and in response to 0.2 microgram of angiotensin II were measured. Acetylcholine-induced vasodilatation after pre-constriction with prostaglandin F2 alpha was also measured. To quantify lung injury, the wet/dry ratio of lung weight was determined. 4. Bleomycin treatment attenuated the first and second hypoxic pressor responses by 93% and 77%, respectively, but not the pressor response to angiotensin II nor the vasodilator response to acetylcholine. BN 52021 plus Bleomycin augmented the first hypoxic pressor response compared with Bleomycin treatment alone, but the structurally unrelated platelet-activating factor antagonists WEB 2170 and WEB 2086 had no significant effect on the Bleomycin-induced attenuation of hypoxic pulmonary vasoconstriction. None of the platelet-activating factor antagonists blocked the increase in the wet/dry lung weight ratio induced by Bleomycin. 5. Bleomycin-induced lung injury selectively attenuates hypoxic pulmonary vasoconstriction, an effect that does not appear to be mediated by platelet-activating factor. The mechanism remains to be elucidated, but may involve destruction of the hypoxic 'sensor' within the respiratory tract.
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Bleomycin induced lung injury in rats selectively abolishes hypoxic pulmonary vasoconstriction evidence against a role for platelet activating factor
Clinical Science, 1992Co-Authors: D G Mccormack, D E Crawley, Peter J. Barnes, Timothy W EvansAbstract:: 1. The role of platelet-activating factor in the attenuated hypoxic pulmonary vasoconstriction associated with lung injury was evaluated using specific platelet-activating factor antagonists and an isolated perfused lung preparation. 2. Intratracheal Bleomycin was administered to rats to produce acute lung injury. Animals received intratracheal saline (control), intratracheal Bleomycin or the platelet-activating factor antagonists BN 52021, WEB 2170 or WEB 2086 before and after Bleomycin treatment. Forty-eight hours after intratracheal administration of Bleomycin or saline the animals were killed. 3. The increases in pulmonary artery pressure during two periods of hypoxic ventilation and in response to 0.2 microgram of angiotensin II were measured. Acetylcholine-induced vasodilatation after pre-constriction with prostaglandin F2 alpha was also measured. To quantify lung injury, the wet/dry ratio of lung weight was determined. 4. Bleomycin treatment attenuated the first and second hypoxic pressor responses by 93% and 77%, respectively, but not the pressor response to angiotensin II nor the vasodilator response to acetylcholine. BN 52021 plus Bleomycin augmented the first hypoxic pressor response compared with Bleomycin treatment alone, but the structurally unrelated platelet-activating factor antagonists WEB 2170 and WEB 2086 had no significant effect on the Bleomycin-induced attenuation of hypoxic pulmonary vasoconstriction. None of the platelet-activating factor antagonists blocked the increase in the wet/dry lung weight ratio induced by Bleomycin. 5. Bleomycin-induced lung injury selectively attenuates hypoxic pulmonary vasoconstriction, an effect that does not appear to be mediated by platelet-activating factor. The mechanism remains to be elucidated, but may involve destruction of the hypoxic 'sensor' within the respiratory tract.
Pinshern Chen - One of the best experts on this subject based on the ideXlab platform.
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folk medicine terminalia catappa and its major tannin component punicalagin are effective against Bleomycin induced genotoxicity in chinese hamster ovary cells
Cancer Letters, 2000Co-Authors: Pinshern Chen, Tsungyun Liu, Tachen LinAbstract:Terminalia catappa L. is a popular folk medicine for preventing hepatoma and treating hepatitis in Taiwan. In this paper, we examined the protective effects of T. catappa leaf water extract (TCE) and its major tannin component, punicalagin, on Bleomycin-induced genotoxicity in cultured Chinese hamster ovary cells. Pre-treatment with TCE or punicalagin prevented Bleomycin-induced hgprt gene mutations and DNA strand breaks. TCE and punicalagin suppressed the generation of Bleomycin-induced intracellular free radicals, identified as superoxides and hydrogen peroxides. The effectiveness of TCE and punicalagin against Bleomycin-induced genotoxicity could be, at least in part, due to their antioxidative potentials.
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folk medicine terminalia catappa and its major tannin component punicalagin are effective against Bleomycin induced genotoxicity in chinese hamster ovary cells
Cancer Letters, 2000Co-Authors: Pinshern Chen, Jihheng LiAbstract:Terminalia catappa L. is a popular folk medicine for preventing hepatoma and treating hepatitis in Taiwan. In this paper, we examined the protective effects of T. catappa leaf water extract (TCE) and its major tannin component, punicalagin, on Bleomycin-induced genotoxicity in cultured Chinese hamster ovary cells. Pre-treatment with TCE or punicalagin prevented Bleomycin-induced hgprt gene mutations and DNA strand breaks. TCE and punicalagin suppressed the generation of Bleomycin-induced intracellular free radicals, identified as superoxides and hydrogen peroxides. The effectiveness of TCE and punicalagin against Bleomycin-induced genotoxicity could be, at least in part, due to their antioxidative potentials.
Tachen Lin - One of the best experts on this subject based on the ideXlab platform.
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folk medicine terminalia catappa and its major tannin component punicalagin are effective against Bleomycin induced genotoxicity in chinese hamster ovary cells
Cancer Letters, 2000Co-Authors: Pinshern Chen, Tsungyun Liu, Tachen LinAbstract:Terminalia catappa L. is a popular folk medicine for preventing hepatoma and treating hepatitis in Taiwan. In this paper, we examined the protective effects of T. catappa leaf water extract (TCE) and its major tannin component, punicalagin, on Bleomycin-induced genotoxicity in cultured Chinese hamster ovary cells. Pre-treatment with TCE or punicalagin prevented Bleomycin-induced hgprt gene mutations and DNA strand breaks. TCE and punicalagin suppressed the generation of Bleomycin-induced intracellular free radicals, identified as superoxides and hydrogen peroxides. The effectiveness of TCE and punicalagin against Bleomycin-induced genotoxicity could be, at least in part, due to their antioxidative potentials.
Jihheng Li - One of the best experts on this subject based on the ideXlab platform.
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folk medicine terminalia catappa and its major tannin component punicalagin are effective against Bleomycin induced genotoxicity in chinese hamster ovary cells
Cancer Letters, 2000Co-Authors: Pinshern Chen, Jihheng LiAbstract:Terminalia catappa L. is a popular folk medicine for preventing hepatoma and treating hepatitis in Taiwan. In this paper, we examined the protective effects of T. catappa leaf water extract (TCE) and its major tannin component, punicalagin, on Bleomycin-induced genotoxicity in cultured Chinese hamster ovary cells. Pre-treatment with TCE or punicalagin prevented Bleomycin-induced hgprt gene mutations and DNA strand breaks. TCE and punicalagin suppressed the generation of Bleomycin-induced intracellular free radicals, identified as superoxides and hydrogen peroxides. The effectiveness of TCE and punicalagin against Bleomycin-induced genotoxicity could be, at least in part, due to their antioxidative potentials.
D G Mccormack - One of the best experts on this subject based on the ideXlab platform.
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Bleomycin induced lung injury in rats selectively abolishes hypoxic pulmonary vasoconstriction evidence against a role for platelet activating factor
Clinical Science, 1992Co-Authors: D G Mccormack, D E Crawley, Peter J. Barnes, Timothy W EvansAbstract:: 1. The role of platelet-activating factor in the attenuated hypoxic pulmonary vasoconstriction associated with lung injury was evaluated using specific platelet-activating factor antagonists and an isolated perfused lung preparation. 2. Intratracheal Bleomycin was administered to rats to produce acute lung injury. Animals received intratracheal saline (control), intratracheal Bleomycin or the platelet-activating factor antagonists BN 52021, WEB 2170 or WEB 2086 before and after Bleomycin treatment. Forty-eight hours after intratracheal administration of Bleomycin or saline the animals were killed. 3. The increases in pulmonary artery pressure during two periods of hypoxic ventilation and in response to 0.2 microgram of angiotensin II were measured. Acetylcholine-induced vasodilatation after pre-constriction with prostaglandin F2 alpha was also measured. To quantify lung injury, the wet/dry ratio of lung weight was determined. 4. Bleomycin treatment attenuated the first and second hypoxic pressor responses by 93% and 77%, respectively, but not the pressor response to angiotensin II nor the vasodilator response to acetylcholine. BN 52021 plus Bleomycin augmented the first hypoxic pressor response compared with Bleomycin treatment alone, but the structurally unrelated platelet-activating factor antagonists WEB 2170 and WEB 2086 had no significant effect on the Bleomycin-induced attenuation of hypoxic pulmonary vasoconstriction. None of the platelet-activating factor antagonists blocked the increase in the wet/dry lung weight ratio induced by Bleomycin. 5. Bleomycin-induced lung injury selectively attenuates hypoxic pulmonary vasoconstriction, an effect that does not appear to be mediated by platelet-activating factor. The mechanism remains to be elucidated, but may involve destruction of the hypoxic 'sensor' within the respiratory tract.
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Bleomycin induced lung injury in rats selectively abolishes hypoxic pulmonary vasoconstriction evidence against a role for platelet activating factor
Clinical Science, 1992Co-Authors: D G Mccormack, D E Crawley, Peter J. Barnes, Timothy W EvansAbstract:: 1. The role of platelet-activating factor in the attenuated hypoxic pulmonary vasoconstriction associated with lung injury was evaluated using specific platelet-activating factor antagonists and an isolated perfused lung preparation. 2. Intratracheal Bleomycin was administered to rats to produce acute lung injury. Animals received intratracheal saline (control), intratracheal Bleomycin or the platelet-activating factor antagonists BN 52021, WEB 2170 or WEB 2086 before and after Bleomycin treatment. Forty-eight hours after intratracheal administration of Bleomycin or saline the animals were killed. 3. The increases in pulmonary artery pressure during two periods of hypoxic ventilation and in response to 0.2 microgram of angiotensin II were measured. Acetylcholine-induced vasodilatation after pre-constriction with prostaglandin F2 alpha was also measured. To quantify lung injury, the wet/dry ratio of lung weight was determined. 4. Bleomycin treatment attenuated the first and second hypoxic pressor responses by 93% and 77%, respectively, but not the pressor response to angiotensin II nor the vasodilator response to acetylcholine. BN 52021 plus Bleomycin augmented the first hypoxic pressor response compared with Bleomycin treatment alone, but the structurally unrelated platelet-activating factor antagonists WEB 2170 and WEB 2086 had no significant effect on the Bleomycin-induced attenuation of hypoxic pulmonary vasoconstriction. None of the platelet-activating factor antagonists blocked the increase in the wet/dry lung weight ratio induced by Bleomycin. 5. Bleomycin-induced lung injury selectively attenuates hypoxic pulmonary vasoconstriction, an effect that does not appear to be mediated by platelet-activating factor. The mechanism remains to be elucidated, but may involve destruction of the hypoxic 'sensor' within the respiratory tract.