Roberts Jordan C, Syme Douglas A
Department of Biological Sciences, University of Calgary, 2500 University Dr. NW, Calgary, AB, T2N1N4, Canada.
Fish Physiol Biochem. 2018 Feb;44(1):49-62. doi: 10.1007/s10695-017-0412-x. Epub 2017 Aug 9.
Hypoxia results in elevated circulating epinephrine for many fish species, and this is likely important for maintaining cardiac function. The aims of this study were to assess how hypoxia impacts contractile responses of ventricular compact and spongy myocardium from rainbow trout (Oncorhynchus mykiss) and to assess how and if epinephrine may protect myocardial performance from a depressive effect of hypoxia. Work output and maximum contraction rate of isolated preparations of spongy and compact ventricular myocardium from rainbow trout were measured. Tissues were exposed to the blood PO that they experience in vivo during environmental normoxia and hypoxia and also to low (5 nM) and high (500 nM) levels of epinephrine in 100% air saturation (PO 20.2 kPa) and during hypoxia (PO 2 kPa, 10% air saturation). It was hypothesized that hypoxia would result in a decrease in work output and maximum contraction rate in both tissue types, but that epinephrine exposure would mitigate the effect. Hypoxia resulted in a decline in net work output of both tissue types, but a decline in maximum contraction rate of only compact myocardium. Epinephrine restored the maximum contraction rate of compact myocardium in hypoxia, appeared to slightly enhance work output of only compact myocardium in air saturation but surprisingly not during hypoxia, and restored net work of hypoxic spongy myocardium toward normoxic levels. These results indicate hypoxia has a similar depressive effect on both layers of ventricular myocardium, but that high epinephrine may be important for maintaining inotropy in spongy myocardium and chronotropy in compact myocardium during hypoxia.
对于许多鱼类来说，缺氧会导致循环肾上腺素水平升高，这可能对维持心脏功能很重要。本研究的目的是评估缺氧如何影响虹鳟（Oncorhynchus mykiss）心室致密心肌和海绵状心肌的收缩反应，并评估肾上腺素是否以及如何保护心肌性能免受缺氧的抑制作用。测量了虹鳟海绵状和致密心室心肌分离制剂的功输出和最大收缩率。组织暴露于它们在环境常氧和缺氧期间在体内所经历的血液氧分压，以及在100%空气饱和度（氧分压20.2 kPa）和缺氧期间（氧分压2 kPa，10%空气饱和度）低（5 nM）和高（500 nM）水平的肾上腺素中。据推测，缺氧会导致两种组织类型的功输出和最大收缩率下降，但肾上腺素暴露会减轻这种影响。缺氧导致两种组织类型的净功输出下降，但仅致密心肌的最大收缩率下降。肾上腺素恢复了缺氧时致密心肌的最大收缩率，在空气饱和状态下似乎仅略微增强了致密心肌的功输出，但令人惊讶的是在缺氧期间没有，并且将缺氧海绵状心肌的净功恢复到常氧水平。这些结果表明，缺氧对心室心肌的两层都有类似的抑制作用，但高浓度肾上腺素可能对在缺氧期间维持海绵状心肌的变力性和致密心肌的变时性很重要。
