The Ionoregulatory Responses to Hypoxia in the Freshwater Rainbow Trout Oncorhynchus mykiss
The Ionoregulatory Responses to Hypoxia in the Freshwater Rainbow Trout Oncorhynchus mykiss
复制标题
淡水虹鳟 Oncorhynchus mykiss 对缺氧的离子调节反应
DOI：
--
复制
发表时间：
2010
影响因子：
1.6
通讯作者：
C. Wood
中科院分区：
文献类型：
--
作者：
F. Iftikar;V. Matey;C. Wood
We utilized the rainbow trout, a hypoxia‐intolerant freshwater teleost, to examine ionoregulatory changes at the gills during hypoxia. Progressive mild hypoxia led first to a significant elevation (by 21%) in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} (measured with 22Na), but at 4‐h hypoxia when Po2 reached ∼110 mmHg, there was a 79% depression in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} . Influx remained depressed during the first hour of normoxic recovery but was restored back to control rates thereafter; there were no significant changes in
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$$J^{\mathrm{Na}\,}_{\mathrm{efflux}\,}$$
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$$J^{\mathrm{Na}\,}_{\mathrm{net}\,}$$
\end{document} . A more prolonged (8 h) and severe hypoxic (∼80 mmHg) exposure induced a triphasic response whereby
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} was significantly elevated during the first hour, as during mild hypoxia, but returned to control rates during the subsequent 3 h. Thereafter, rates started to gradually increase and remained significantly elevated by about 38% through to 8 h of hypoxia. A similar triphasic trend was observed with
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$$J^{\mathrm{Na}\,}_{\mathrm{efflux}\,}$$
\end{document} but with larger changes than in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} , such that negative Na+ balance occurred during the hypoxic exposure. Net K+ loss rates to the water approximately doubled. There were no significant alterations in ammonia excretion rates in either of the hypoxia regimes. Branchial Na+/K+‐ATPase activity did not change during 4 h at Po2 ∼ 80 mmHg or return to normoxia; H+‐ATPase activity also did not change during hypoxia but was significantly depressed by ∼75% after 6 h of normoxic recovery. Scanning electron microscopy revealed that within 1 h of exposure to Po2 ∼ 80 mmHg, exposed mitochondria‐rich cell (MRC) numbers increased by 30%, while individual MRC exposed surface area and total MRC surface area both increased by three‐ to fourfold. MRC numbers had decreased below control levels by 4 h of hypoxia, but surface exposure remained elevated by approximately twofold, a response that persisted through 6 h of normoxic recovery. Environmental hypoxia induces complex changes in gill ionoregulatory function in this hypoxia‐intolerant species that are very different from those recently reported in the hypoxia‐tolerant Amazonian oscar.
We utilized the rainbow trout, a hypoxia‐intolerant freshwater teleost, to examine ionoregulatory changes at the gills during hypoxia. Progressive mild hypoxia led first to a significant elevation (by 21%) in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} (measured with 22Na), but at 4‐h hypoxia when Po2 reached ∼110 mmHg, there was a 79% depression in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} . Influx remained depressed during the first hour of normoxic recovery but was restored back to control rates thereafter; there were no significant changes in
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$$J^{\mathrm{Na}\,}_{\mathrm{efflux}\,}$$
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$$J^{\mathrm{Na}\,}_{\mathrm{net}\,}$$
\end{document} . A more prolonged (8 h) and severe hypoxic (∼80 mmHg) exposure induced a triphasic response whereby
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} was significantly elevated during the first hour, as during mild hypoxia, but returned to control rates during the subsequent 3 h. Thereafter, rates started to gradually increase and remained significantly elevated by about 38% through to 8 h of hypoxia. A similar triphasic trend was observed with
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$$J^{\mathrm{Na}\,}_{\mathrm{efflux}\,}$$
\end{document} but with larger changes than in
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$$J^{\mathrm{Na}\,}_{\mathrm{influx}\,}$$
\end{document} , such that negative Na+ balance occurred during the hypoxic exposure. Net K+ loss rates to the water approximately doubled. There were no significant alterations in ammonia excretion rates in either of the hypoxia regimes. Branchial Na+/K+‐ATPase activity did not change during 4 h at Po2 ∼ 80 mmHg or return to normoxia; H+‐ATPase activity also did not change during hypoxia but was significantly depressed by ∼75% after 6 h of normoxic recovery. Scanning electron microscopy revealed that within 1 h of exposure to Po2 ∼ 80 mmHg, exposed mitochondria‐rich cell (MRC) numbers increased by 30%, while individual MRC exposed surface area and total MRC surface area both increased by three‐ to fourfold. MRC numbers had decreased below control levels by 4 h of hypoxia, but surface exposure remained elevated by approximately twofold, a response that persisted through 6 h of normoxic recovery. Environmental hypoxia induces complex changes in gill ionoregulatory function in this hypoxia‐intolerant species that are very different from those recently reported in the hypoxia‐tolerant Amazonian oscar.