Hicks J M, Farrell A P
Department of Biological Sciences, Simon Fraser University, Burnaby, British Columbia, Canada V5A 1S6.
J Exp Biol. 2000 Dec;203(Pt 24):3775-84. doi: 10.1242/jeb.203.24.3775.
Cardiovascular control in cold-acclimated freshwater turtles during chronic anoxic exposure is not well understood. We tested the hypothesis that the observed bradycardia in Trachemys scripta results from increased cholinergic inhibitory tone and reduced sympathetic activity. Cardiovascular status was measured in vivo in turtles acclimated to either 22 degrees C or 5 degrees C and either acutely exposed (6 h) to anoxia at 22 degrees C or chronically exposed (22 days) to anoxia at 5 degrees C. In 22 degrees C-acclimated turtles, injection of the cholinergic antagonist atropine induced a significant tachycardia under both normoxic and anoxic conditions. However, in 5 degrees C-acclimated turtles, atropine injection had little effect on heart rate. Therefore, cholinergic control of heart rate was suppressed during cold acclimation; instead, temperature effects are more important in bringing about bradycardia, while the intrinsic effects of anoxia and acidosis are probably important during chronic anoxia. Injection of adrenaline caused a pressor response through increased systemic resistance at both acclimation temperatures. This response was blunted by acute and chronic anoxic exposure, suggesting that systemic vasomotor control was altered independently of acclimation temperature. This anoxic blunting may be related in part to the anoxia-induced increase in systemic resistance. Injection of nadolol after atropine decreased systemic cardiac output. The tonic beta-adrenergic cardiac stimulation was attenuated by acute and chronic anoxic exposure. Some of this attenuation of beta-adrenergic control could be attributed to the 39-40 % reduction in cell surface beta-adrenoreceptor density in the ventricles of these turtles that accompanied acute and chronic anoxic exposure. In conclusion and contrary to our original hypothesis, cholinergic and adrenergic control of the cardiovascular system in turtles was attenuated under cold anoxic conditions, perhaps assisting in the depressed physiological state of these animals.
在长期缺氧暴露期间，冷适应淡水龟的心血管控制机制尚未完全明确。我们验证了一个假设，即红耳龟（Trachemys scripta）中观察到的心动过缓是由于胆碱能抑制作用增强和交感神经活动减少所致。我们对适应22摄氏度或5摄氏度环境的海龟进行体内心血管状态测量，这些海龟要么在22摄氏度下急性暴露于缺氧环境（6小时），要么在5摄氏度下长期暴露于缺氧环境（22天）。在适应22摄氏度的海龟中，注射胆碱能拮抗剂阿托品在常氧和缺氧条件下均能引起显著的心动过速。然而，在适应5摄氏度的海龟中，注射阿托品对心率几乎没有影响。因此，在冷适应过程中，心率的胆碱能控制受到抑制；相反，温度效应在导致心动过缓方面更为重要，而缺氧和酸中毒的内在效应在慢性缺氧期间可能很重要。注射肾上腺素通过增加两个适应温度下的全身阻力引起升压反应。急性和慢性缺氧暴露使这种反应减弱，表明全身血管运动控制独立于适应温度而发生改变。这种缺氧减弱可能部分与缺氧引起的全身阻力增加有关。在注射阿托品后注射纳多洛尔会降低全身心输出量。急性和慢性缺氧暴露会减弱β-肾上腺素能对心脏的张力性刺激。这种β-肾上腺素能控制的减弱部分可归因于这些海龟心室中细胞表面β-肾上腺素能受体密度伴随急性和慢性缺氧暴露而降低39 - 40%。总之，与我们最初的假设相反，在冷缺氧条件下，海龟心血管系统的胆碱能和肾上腺素能控制减弱，这可能有助于这些动物处于生理抑制状态。
