Elliott Nicole M, Andrews Russel D, Jones David R
Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z4.
J Exp Biol. 2002 Dec;205(Pt 23):3757-65. doi: 10.1242/jeb.205.23.3757.
While diving, harbour seals (Phoca vitulina) manage their oxygen stores through cardiovascular adjustments, including bradycardia, a concurrent reduction in cardiac output, and peripheral vasoconstriction. At the surface, post-dive tachycardia facilitates rapid reloading of oxygen stores. Although harbour seals can tolerate >20 min of submergence, the majority of their natural dives are only 2-6 min and are usually followed by surface intervals that are <1 min, so they spend approximately 80% of their time submerged. Given that harbour seals meet their ecological needs through repetitive short aerobic dives, we were interested in the functional role, if any, of the dive response during these short dives. During voluntary diving in an 11 m deep tank, the cardiovascular responses to submergence of five harbour seals were manipulated using specific pharmacological antagonists, and the effects on diving behaviour were observed. Effects of pharmacological blockade on heart rate were also examined to assess the autonomic control of heart rate during voluntary diving. Heart rate was recorded using subcutaneous electrodes and data loggers, while diving behaviour was monitored using a video camera. The muscarinic blocker methoctramine blocked diving bradycardia, the alpha-adrenergic blocker prazosin blocked diving vasoconstriction, and the beta-adrenergic blocker metoprolol blocked post-dive tachycardia. Heart-rate analysis indicated that diving bradycardia is primarily modulated by the vagus, while post-dive tachycardia results from parasympathetic withdrawal as well as increased sympathetic stimulation of the heart. None of the pharmacological blockers had any effect on average dive or surface interval duration. Seals maintained a high percentage of time spent diving in all treatments. Thus, harbour seals do not appear to need the dive response during short dives in order to maintain an efficient dive strategy.
在潜水时，港海豹（Phoca vitulina）通过心血管调节来管理其氧气储备，包括心动过缓、心输出量同时减少以及外周血管收缩。在水面时，潜水后的心动过速有助于氧气储备的快速重新填充。尽管港海豹能够耐受超过20分钟的水下停留，但它们大多数自然潜水仅持续2 - 6分钟，并且之后的水面间隔通常小于1分钟，所以它们大约80%的时间都处于水下。鉴于港海豹通过重复性的短时间有氧潜水来满足其生态需求，我们对这些短潜过程中潜水反应的功能作用（如果有）很感兴趣。在一个11米深的水池中进行自愿潜水时，使用特定的药理学拮抗剂来操控五只港海豹潜水时的心血管反应，并观察对潜水行为的影响。还研究了药理学阻断对心率的影响，以评估自愿潜水期间心率的自主控制。使用皮下电极和数据记录器记录心率，同时使用摄像机监测潜水行为。毒蕈碱阻断剂美索曲明阻断了潜水时的心动过缓，α - 肾上腺素能阻断剂哌唑嗪阻断了潜水时的血管收缩，β - 肾上腺素能阻断剂美托洛尔阻断了潜水后的心动过速。心率分析表明，潜水时的心动过缓主要由迷走神经调节，而潜水后的心动过速是由副交感神经撤离以及心脏交感神经刺激增加所致。没有一种药理学阻断剂对平均潜水或水面间隔时间有任何影响。在所有处理中，海豹保持了较高比例的潜水时间。因此，港海豹在短潜过程中似乎不需要潜水反应来维持高效的潜水策略。
