Axelsson M, Davison W, Forster M E, Farrell A P
Department of Zoology, University of Canterbury, Christchurch, New Zealand.
J Exp Biol. 1992 Jun;167:179-201. doi: 10.1242/jeb.167.1.179.
The aim of this study was to investigate cardiac performance and cardiovascular control in two red-blooded nototheniid species of antarctic fishes, Pagothenia bernacchii (a benthic fish) and P. borchgrevinki (a cryopelagic fish), and to make comparisons with existing information on haemoglobin-free antarctic teleosts. In quiescent P. bernacchii at 0 degrees C ventral aortic pressure (PVA) was 3.09 kPa and cardiac output (Q) was 17.6 ml min-1 kg-1, with a heart rate (fH) of 10.5 beats min-1 and stroke volume of 1.56 ml kg-1. Following atropine treatment, Q was maintained but heart rate increased and stroke volume decreased. Resting heart rate resulted from an inhibitory cholinergic tone of 80.4% and an excitatory adrenergic tone of 27.5%. The intrinsic heart rate was 21.7 beats min-1 at 0 degrees C. In quiescent P. borchgrevinki at 0 degrees C, PVA was 3.6 kPa, Q was 29.6 ml min-1 kg-1 and stroke volume was 2.16 ml kg-1. The resting heart rate in P. borchgrevinki of 11.3 beats min-1 resulted from an inhibitory cholinergic tone of 54.5% and an excitatory adrenergic tone of 3.2%. The intrinsic heart rate was 23.3 beats min-1. P. bernacchii maintained Q during a progressive decrease in water oxygen tension from 20 to 6.7 kPa, but fH was increased significantly. Thus, although there is cholinergic control of the heart, no hypoxic bradycardia was observed. Recovery from hypoxia was associated with increases in Q and fH; stroke volume returned to control values. PVA declined in recovery as total vascular resistance decreased. Hypoxic exposure following atropine treatment resulted in progressive increases in PVA, Q and stroke volume; fH decreased during the recovery period. Hypoxic exposure in P. borchgrevinki produced similar cardiovascular responses to those observed in P. bernacchii. During an acute increase in water temperature from 0 to 5 degrees C, P. bernacchii regulated Q and total vascular resistance. Stroke volume decreased as fH increased. The intrinsic heart rate had a Q10 of 1.96 over this temperature range. P. bernacchii maintained chronotropic inhibition up to a temperature of 2.5-3.0 degrees C. However, by 5 degrees C this chronotropic inhibition of the heart rate was lost. Infusion of adrenaline into the ventral aorta of P. bernacchii resulted in significant increases in Q, fH, PVA and total vascular resistance. Infusion of adrenaline after atropine treatment caused similar cardiovascular changes without the change in fH. P. borchgrevinki could sustain swimming in a water tunnel at approximately 1 body length per second for 6-10 min.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究的目的是调查南极鱼类中两种红色血球的南极鱼科鱼类——伯氏南极鱼（一种底栖鱼类）和博氏南极鱼（一种冰栖远洋鱼类）的心脏功能和心血管控制，并与现有的关于无血红蛋白南极硬骨鱼的信息进行比较。在0℃静止状态下的伯氏南极鱼中，腹主动脉压（PVA）为3.09千帕，心输出量（Q）为17.6毫升·分钟⁻¹·千克⁻¹，心率（fH）为10.5次·分钟⁻¹，每搏输出量为1.56毫升·千克⁻¹。阿托品处理后，心输出量得以维持，但心率增加，每搏输出量减少。静息心率由80.4%的抑制性胆碱能张力和27.5%的兴奋性肾上腺素能张力产生。0℃时的固有心率为21.7次·分钟⁻¹。在0℃静止状态下的博氏南极鱼中，PVA为3.6千帕，Q为29.6毫升·分钟⁻¹·千克⁻¹，每搏输出量为2.16毫升·千克⁻¹。博氏南极鱼11.3次·分钟⁻¹的静息心率由54.5%的抑制性胆碱能张力和3.2%的兴奋性肾上腺素能张力产生。固有心率为23.3次·分钟⁻¹。随着水氧张力从20千帕逐渐降至6.7千帕，伯氏南极鱼维持了心输出量，但心率显著增加。因此，尽管心脏存在胆碱能控制，但未观察到低氧性心动过缓。从低氧状态恢复与心输出量和心率增加有关；每搏输出量恢复到对照值。恢复过程中腹主动脉压随着总血管阻力降低而下降。阿托品处理后进行低氧暴露导致腹主动脉压、心输出量和每搏输出量逐渐增加；恢复期心率降低。博氏南极鱼的低氧暴露产生了与伯氏南极鱼中观察到的类似心血管反应。在水温从0℃急剧升至5℃期间，伯氏南极鱼调节了心输出量和总血管阻力。随着心率增加，每搏输出量减少。在此温度范围内，固有心率的Q₁₀为1.96。伯氏南极鱼在高达2.5 - 3.0℃的温度下维持变时抑制。然而，到5℃时，这种对心率的变时抑制消失。向伯氏南极鱼腹主动脉注入肾上腺素导致心输出量、心率、腹主动脉压和总血管阻力显著增加。阿托品处理后注入肾上腺素引起类似的心血管变化，但心率无变化。博氏南极鱼能够在水洞中以约每秒1个体长的速度持续游泳6 - 10分钟。（摘要截选至400字）
