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2. Hyperoxia blunts acute hypoxia- and PGF2α-induced pulmonary vasoconstriction in chronically hypoxic rats
- Creator:
- Žaloudíková, Marie, Martin Vízek, and Jan Herget
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, fyziologie, hypoxie, hyperoxie, human physiology, hypoxia, hyperoxia, isolated pulmonary arteries, hypoxic pulmonary vasoconstriction, 14, and 612
- Language:
- English
- Description:
- We investigated the influence of oxygenation of in vitro lung preparation on the pulmonary vascular reactivity. Small pulmonary vessels isolated from adult male Wistar rats exposed for 4 days to hypoxia (FiO2 = 0.1, group CH) were compared with those of normoxic controls (group N). The bath in the chamber of small vessel myograph was saturated with gas mixture containing either 21 % or 95 % of O2 with 5 % CO2 and we measured the reactions of vessels to acute hypoxic challenge with 0 % O2 or to PGF2α. We did not observe any difference of the contractile responses between both groups when the normoxic conditions were set in the bath. When the bath oxygenation was increased to 95 % O2, the contractions induced by hypoxic challenge and PGF2α decreased in chronically hypoxic rats and did not change in normoxic controls. We hypothesize that reduced reactivity of vessels from hypoxic rats in hyperoxia results from the effect of chronic hypoxia on Ca2+ signaling in the vascular smooth muscle, which is modulated by increased free radical production during the exposure to chronic hypoxia and further hyperoxia., M. Žaloudíková, M. Vízek, J. Herget., and Obsahuje seznam literatury
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public
3. The contractile response of isolated small pulmonary arteries induced by activated macrophages
- Creator:
- Žaloudíková, M., Jan Herget, and Martin Vízek
- Format:
- Type:
- article, články, model:article, and TEXT
- Subject:
- Fyziologie člověka a srovnávací fyziologie, tepny, kyslík, arteries, oxygen, isolated pulmonary arteries, reactive oxygen species, macrophage, 14, and 612
- Language:
- English
- Description:
- To test whether macrophages can play any role in hypoxic pulmonary vasoconstriction, we tested the in vitro response of rings from small pulmonary arteries to the activation of macrophages by FMLP, a substance stimulating predominantly membrane-bound NADPH oxidase. A small vessel myograph was used to measure the responses of rings from small pulmonary arteries (300-400 μ m) isolated from rat lungs. Rings from 5 rats were placed into both chambers of the myograph. The vessels were stabilized for 40 min and then normalized by automatic stretching to a wall tension equivalent to the intravascular pressure 30 mm Hg. At the start of each experiment, vessels were exposed to 80 mM K + to obtain maximal contractile response, which was used to normalize subsequent contractile responses. 2x10 6 viable macrophages, obtained by peritoneal lavage, were added into one chamber, then 5 μ M FMLP was administrated to both chambers and the tension measurement was started. The hydrogen peroxide concentration produced by stimulated macrophages was measured luminometrically. The concentrations of H 2 O 2 in specimens from chambers containing activated macrophages rose from 3.5±1.5 nM to 110±28 nM within 25 min of stimulation, while FMLP itself didn’t increase the H 2 O 2 concentration from the baseline value (4.5±3 nM) in samples from control chambers. After FMLP administration, the tension of the vessel rings in the presence of macrophages reached 0.23±0.07 of maximal contractile response, it did not change in controls. The additi on of ROS scavenger 4-hydroxy- TEMPO blocked the contractile response to the activation of macrophages. We conclude that the activation of macrophages stimulates the contraction of small pulmonary arteries and that this contraction is probably mediated by reactive oxygen species., M. Žaloudíková, J. Herget, M. Vízek., and Obsahuje bibliografii a bibliografické odkazy
- Rights:
- http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public