Signore P E, Jones D R
Department of Zoology, University of British Columbia, Vancouver, Canada.
J Exp Biol. 1996 Jul;199(Pt 7):1563-8. doi: 10.1242/jeb.199.7.1563.
Neural control of the cardiac responses to exercise in air (running) and under water (diving) was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine and the beta-adrenergic blocker nadolol. Saline injection was used as a control. Controls running on a treadmill showed a marked increase in heart rate with exercise. Atropine-treated animals had a higher resting heart rate than controls, but heart rate still increased with running. Nadolol-treated animals had a lower resting heart rate than controls and displayed a less pronounced increase in heart rate with running than controls. Animals treated with a combination of atropine and nadolol had a resting heart rate similar to that of controls but their heart rate was unaffected by running. Thus, exercise tachycardia in muskrats is due to activation of the sympathetic system and also to a reduction in parasympathetic tone. Heart rate decreased markedly during voluntary submergence in controls but rose as muskrats swam submerged against increasing water flows. Nevertheless, diving bradycardia was still present. Free-diving bradycardia and the relative increase in heart rate with underwater exercise were abolished by atropine and unaffected by nadolol. Hence, unlike the cardiac response to exercise in air, the cardiac response to underwater exercise is due only to a reduction in parasympathetic tone. Injection of the beta-adrenergic agonist isoproterenol markedly increased heart rate in air but had little effect during voluntary and forced dives, indicating a marked decrease in the sensitivity of cardiac cells to adrenergic stimulation during submergence. These results strongly suggest that accentuated antagonism between the two branches of the autonomic nervous system occurs during diving so that parasympathetic influences on the heart predominate and inhibit any chronotropic response to adrenergic stimulation.
通过使用毒蕈碱阻滞剂阿托品和β-肾上腺素能阻滞剂纳多洛尔进行急性药理学阻断，研究了麝鼠（麝鼠属）在空气中（奔跑）和水下（潜水）运动时心脏反应的神经控制。注射生理盐水作为对照。在跑步机上奔跑的对照动物随着运动心率显著增加。用阿托品处理的动物静息心率高于对照，但心率仍随奔跑而增加。用纳多洛尔处理的动物静息心率低于对照，且与对照相比，奔跑时心率增加不明显。用阿托品和纳多洛尔联合处理的动物静息心率与对照相似，但它们的心率不受奔跑影响。因此，麝鼠运动性心动过速是由于交感神经系统的激活以及副交感神经张力的降低。在对照动物中，自愿潜水时心率显著下降，但当麝鼠逆着不断增加的水流在水下游泳时心率上升。然而，潜水性心动过缓仍然存在。自由潜水性心动过缓和水下运动时心率的相对增加被阿托品消除，且不受纳多洛尔影响。因此，与在空气中运动时的心脏反应不同，水下运动时的心脏反应仅由于副交感神经张力的降低。注射β-肾上腺素能激动剂异丙肾上腺素在空气中显著增加心率，但在自愿和强制潜水时影响不大，表明潜水时心脏细胞对肾上腺素能刺激的敏感性显著降低。这些结果强烈表明，自主神经系统的两个分支在潜水时发生明显的拮抗作用，使得副交感神经对心脏的影响占主导，并抑制对肾上腺素能刺激的任何变时反应。
