Signore P E, Jones D R
Department of Zoology, University of British Columbia, Vancouver, Canada.
J Exp Biol. 1995 Nov;198(Pt 11):2307-15. doi: 10.1242/jeb.198.11.2307.
Neural control of free and forced diving bradycardia and peripheral resistance was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine, the alpha-adrenergic blocker phentolamine and the beta-adrenergic blockers nadolol and propranolol. Saline injection was used as a control. Heart rate in control animals increased before voluntary dives and dropped markedly as soon as the animals submerged. Heart rate started increasing towards the end of voluntary dives and reached pre-dive values within the first 5 s of recovery. Pre-dive and post-dive tachycardia were reduced in beta-blocked animals, emphasizing the role of the sympathetic system during the preparatory and recovery periods of voluntary dives. Diving bradycardia and the acceleration in heart rate before surfacing were abolished by atropine and unaffected by nadolol, demonstrating the importance of vagal efferent activity during diving. The results after blockade with nadolol suggest that there is an accentuated antagonism between the two branches of the autonomic nervous system during diving, so that parasympathetic influences on the heart predominate. Propranolol-treated muskrats had a higher diving heart rate than saline- and nadolol-treated animals, which may be due to a sedative effect caused by propranolol crossing the blood-brain barrier, a blockade of central catecholaminergic pathways or a peripheral neural effect, due to the anaesthetic properties of propranolol. Phentolamine did not affect diving bradycardia, indicating that diving bradycardia occurs independently of peripheral vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)
通过使用毒蕈碱阻滞剂阿托品、α-肾上腺素能阻滞剂酚妥拉明以及β-肾上腺素能阻滞剂纳多洛尔和普萘洛尔进行急性药理学阻断,研究了麝鼠(麝鼠属)自由潜水和强迫潜水时心动过缓和外周阻力的神经控制。注射生理盐水作为对照。对照动物在自主潜水前心率增加,动物一旦潜入水中心率就明显下降。在自主潜水接近尾声时心率开始上升,并在恢复的前5秒内达到潜水前的值。β受体阻滞剂处理的动物潜水前和潜水后的心动过速有所减轻,这突出了交感神经系统在自主潜水准备期和恢复期的作用。阿托品消除了潜水心动过缓和浮出水面之前的心率加速,而纳多洛尔对此无影响,这表明潜水期间迷走神经传出活动的重要性。纳多洛尔阻断后的结果表明,潜水期间自主神经系统的两个分支之间存在增强的拮抗作用,因此副交感神经对心脏的影响占主导。普萘洛尔处理的麝鼠潜水心率高于生理盐水和纳多洛尔处理的动物,这可能是由于普萘洛尔穿过血脑屏障引起的镇静作用、对中枢儿茶酚胺能途径的阻断或由于普萘洛尔的麻醉特性导致的外周神经效应。酚妥拉明不影响潜水心动过缓,表明潜水心动过缓独立于外周血管收缩而发生。(摘要截短至250字)