Department of Biology, Virginia Polytechnic Institute and State University, 24061, Blacksburg, Virginia, USA.
Fish Physiol Biochem. 1988 Jan;4(4):203-19. doi: 10.1007/BF01871746.
Changes in heart rate, ventilatory activity and oxygen consumption were determined in trout (Salmo gairdneri) and brown bullhead catfish (Ictalurus nebulosus) during exposure to a steadily increasing concentration of waterborne cyanide selected to produce death in 8-9 hours for each species. The lethal cyanide concentration for the bullheads was an order of magnitude higher than for trout. Trout developed an immediate and gradually increasing bradycardia throughout the exposure period. Cyanide produced tachycardia in the bullhead followed by a gradual onset of bradycardia as the concentration of cyanide was raised. Pericardial injection of atropine (a muscarinic cholinergic antagonist) indicated that bradycardia in the trout was due initially to increased vagal tone but later due to the direct effect of cyanide on the heart. Hyperventilation in the trout persisted throughout the exposure period, although the rate and amplitude fluctuated and was variable between individual fish. During the last hour of exposure (highest cyanide concentration), ventilation was characterized by rapid, shallow breaths followed by a sudden respiratory arrest. The bullheads exhibited hyperventilation during the first 3 hours of exposure followed by a gradual, linear drop in ventilation rate and amplitude until death occurred. Cardiac and ventilatory responses in both species were attributed to stimulation of central and peripheral chemoreceptors by cyanide. Evidence is presented which suggests the initial response in the bullheads was due, at least in part, to gustatory stimulation by the cyanide. Oxygen consumption of the trout remained above pre-exposure levels for the majority of the test period. Oxygen consumption in the bullhead paralleled the changes in heart and ventilatory rates. Whole-body lactate levels of fingerlings of both species during cyanide exposure were measured to estimate the extent of anaerobiosis. Whole-body lactate levels were much greater in the bullheads than the trout, indicating a higher capacity for anaerobiosis, possibly due to a greater fuel supply. Overall, the trout responded to cyanide in a manner similar to that produced by environmental hypoxia whereas the bullheads experienced a gustatory stimulus which masked the hypoxia-like response.
在暴露于逐渐增加的水基氰化物浓度下,测定了鳟鱼(Salmo gairdneri)和褐鳜(Ictalurus nebulosus)的心率、呼吸活动和耗氧量的变化,该浓度选择为每种鱼类在 8-9 小时内致死。褐鳜的致死氰化物浓度比鳟鱼高一个数量级。鳟鱼在整个暴露期间立即出现并逐渐增加的心动过缓。氰化物在褐鳜中引起心动过速,随后随着氰化物浓度的升高,逐渐出现心动过缓。心脏注射阿托品(一种毒蕈碱型胆碱能拮抗剂)表明,鳟鱼的心动过缓最初是由于迷走神经张力增加,但后来是由于氰化物对心脏的直接作用。鳟鱼的过度通气在整个暴露期间持续存在,尽管呼吸频率和幅度波动,并且在个体鱼之间变化。在暴露的最后 1 小时(氰化物浓度最高),通气的特征是快速、浅的呼吸,随后突然呼吸停止。褐鳜在暴露的前 3 小时表现出过度通气,然后通气率和幅度逐渐线性下降,直到死亡。两种物种的心脏和呼吸反应都归因于氰化物刺激中枢和外周化学感受器。有证据表明,褐鳜的初始反应至少部分是由于氰化物的味觉刺激。鳟鱼的耗氧量在测试期间的大部分时间都保持在暴露前的水平之上。褐鳜的耗氧量与心率和通气率的变化平行。测量两种物种的鱼苗在氰化物暴露期间的全身乳酸水平,以估计无氧代谢的程度。褐鳜的全身乳酸水平比鳟鱼高得多,表明无氧代谢能力更高,这可能是由于燃料供应更多。总的来说,鳟鱼对氰化物的反应方式与环境缺氧产生的反应相似,而褐鳜则经历了味觉刺激,掩盖了类似缺氧的反应。