Farrell A P
Zoology Department, 6270 University Boulevard, University of British Columbia, Vancouver, BC, V6T 1Z4, Canada.
J Exp Biol. 2007 May;210(Pt 10):1715-25. doi: 10.1242/jeb.02781.
The sensing and processing of hypoxic signals, the responses to these signals and the modulation of these responses by other physical and physiological factors are an immense topic filled with numerous novel and exciting discoveries. Nestled among these discoveries, and in contrast to mammals, is the unusual cardiac response of many fish to environmental hypoxia - a reflex slowing of heart rate. The afferent and efferent arms of this reflex have been characterised, but the benefits of the hypoxic bradycardia remain enigmatic since equivocal results have emerged from experiments examining the benefit to oxygen transfer across the gills. The main thesis developed here is that hypoxic bradycardia could afford a number of direct benefits to the fish heart, largely because the oxygen supply to the spongy myocardium is precarious (i.e. it is determined primarily by the partial pressure of oxygen in venous blood, Pv(O(2))) and, secondarily, because the fish heart has an unusual ability to produce large increases in cardiac stroke volume (V(SH)) that allow cardiac output to be maintained during hypoxic bradycardia. Among the putative benefits of hypoxic bradycardia is an increase in the diastolic residence time of blood in the lumen of the heart, which offers an advantage of increased time for diffusion, and improved cardiac contractility through the negative force-frequency effect. The increase in V(SH) will stretch the cardiac chambers, potentially reducing the diffusion distance for oxygen. Hypoxic bradycardia could also reduce cardiac oxygen demand by reducing cardiac dP/dt and cardiac power output, something that could be masked at cold temperature because of a reduced myocardial work load. While the presence of a coronary circulation in certain fishes decreases the reliance of the heart on Pv(O(2)), hypoxic bradycardia could still benefit oxygen delivery via an extended diastolic period during which peak coronary blood flow occurs. The notable absence of hypoxic bradycardia among fishes that breathe air during aquatic hypoxia and thereby raise their Pv(O(2)), opens the possibility that that the evolutionary loss of hypoxic bradycardia may have coincided with some forms of air breathing in fishes. Experiments are needed to test some of these possibilities. Ultimately, any potential benefit of hypoxic bradycardia must be placed in the proper context of myocardial oxygen supply and demand, and must consider the ability of the fish heart to support its routine cardiac power output through glycolysis.
缺氧信号的感知与处理、对这些信号的反应以及其他物理和生理因素对这些反应的调节，是一个充满众多新颖且令人兴奋的发现的庞大主题。在这些发现之中，与哺乳动物不同的是，许多鱼类对环境缺氧的异常心脏反应——心率反射性减慢。这种反射的传入和传出通路已得到表征，但缺氧性心动过缓的益处仍然不明，因为在研究其对鳃部氧气转运的益处的实验中出现了相互矛盾的结果。本文提出的主要论点是，缺氧性心动过缓可能为鱼类心脏带来一些直接益处，主要是因为海绵状心肌的氧气供应不稳定（即主要由静脉血中的氧分压Pv(O₂)决定），其次是因为鱼类心脏具有一种不寻常的能力，能够使心搏量（V(SH)）大幅增加，从而在缺氧性心动过缓期间维持心输出量。缺氧性心动过缓的假定益处包括增加心脏腔内血液的舒张停留时间，这为扩散提供了更长时间的优势，并通过负力 - 频率效应改善心脏收缩力。V(SH)的增加会拉伸心脏腔室，可能缩短氧气的扩散距离。缺氧性心动过缓还可以通过降低心脏dP/dt和心脏功率输出减少心脏的氧气需求，在低温下由于心肌工作负荷降低，这一点可能会被掩盖。虽然某些鱼类中存在冠状循环会降低心脏对Pv(O₂)的依赖，但缺氧性心动过缓仍可能通过延长舒张期（在此期间出现冠状血流峰值）来促进氧气输送。在水生缺氧期间呼吸空气从而提高其Pv(O₂)的鱼类中明显不存在缺氧性心动过缓，这表明缺氧性心动过缓的进化丧失可能与鱼类的某些形式的空气呼吸同时发生。需要进行实验来检验其中的一些可能性。最终，缺氧性心动过缓的任何潜在益处都必须置于心肌氧气供应和需求的适当背景下，并必须考虑鱼类心脏通过糖酵解支持其常规心脏功率输出的能力。
