Kinkead R, Perry S F
Department of Biology, University of Ottawa, Ontario, Canada.
Respir Physiol. 1991 Apr;84(1):77-92. doi: 10.1016/0034-5687(91)90020-j.
This study assessed the effects of experimentally elevated plasma catecholamine levels on gill ventilation in rainbow trout (Oncorhyncus mykiss) exposed to various external ventilatory stimulants. Trout were exposed to hypoxia (water PO2 (PwO2) = 90 Torr) or hypercapnia (water PCO2 (PwCO2) = 4.5 Torr) for 30 min. These conditions caused gill ventilation volume (Vw) to increase by 2.3- and 1.5-fold, respectively, but did not stimulate release of catecholamines into the blood. While the stimulus (hypoxia or hypercapnia) was maintained, fish were given a bolus injection (0.3 ml), followed by intra-arterial infusion (0.6 ml.h-1), of a catecholamine mixture (2 x 10(-5) mol.l-1 adrenaline + 5 x 10(-6) mol.l-1 noradrenaline) to mimic the physiological concentrations and ratios of these catecholamines observed under more severe hypoxic or hypercapnic conditions. In hypoxic fish, this treatment caused a significant, but transient (5 min) depression of ventilation while during hypercapnia, the administration of exogenous catecholamines caused a more prolonged hypoventilatory response. These hypoventilatory responses occurred despite a catecholamine-induced blood acidosis (a potential ventilatory stimulant). To assess the importance of initial Vw and/or blood respiratory status on catecholamine-mediated hypoventilation, these experiments were repeated under hyperoxic (PwO2 = 640 Torr) hyperoxic hypercapnic (PwO2 = 510 Torr, PwCO2 = 4.8 Torr) or normoxic (PwO2 = 151 Torr) conditions in which Vw was either depressed (3.9-fold during hyperoxia) or unaffected. Intra-arterial infusion of catecholamines did not affect Vw under either of these experimental conditions. These results demonstrate that during a respiratory challenge, such as hypoxia or hypercapnia, physiologically relevant levels of circulating catecholamines can depress Vw and therefore do not support a stimulatory role for circulating catecholamines in the control of ventilation in fish.
本研究评估了实验性升高血浆儿茶酚胺水平对暴露于各种外部通气刺激物的虹鳟(Oncorhyncus mykiss)鳃通气的影响。将虹鳟暴露于低氧(水体氧分压(PwO2)= 90托)或高碳酸血症(水体二氧化碳分压(PwCO2)= 4.5托)环境中30分钟。这些条件分别使鳃通气量(Vw)增加了2.3倍和1.5倍,但并未刺激儿茶酚胺释放到血液中。在维持刺激(低氧或高碳酸血症)的同时,给鱼静脉推注(0.3毫升),随后进行动脉内输注(0.6毫升·小时-1)儿茶酚胺混合物(2×10(-5)摩尔·升-1肾上腺素 + 5×10(-6)摩尔·升-1去甲肾上腺素),以模拟在更严重的低氧或高碳酸血症条件下观察到的这些儿茶酚胺的生理浓度和比例。在低氧的鱼中,这种处理导致通气量显著但短暂(5分钟)下降,而在高碳酸血症期间,给予外源性儿茶酚胺会导致更持久的通气不足反应。尽管儿茶酚胺会引起血液酸中毒(一种潜在的通气刺激物),但这些通气不足反应仍会发生。为了评估初始Vw和/或血液呼吸状态对儿茶酚胺介导的通气不足的重要性,在高氧(PwO2 = 640托)、高氧高碳酸血症(PwO2 = 510托,PwCO2 = 4.8托)或常氧(PwO2 = 151托)条件下重复这些实验,在这些条件下Vw要么下降(高氧期间下降3.9倍)要么未受影响。在这些实验条件中的任何一种下,动脉内输注儿茶酚胺均未影响Vw。这些结果表明,在呼吸挑战(如低氧或高碳酸血症)期间,生理相关水平的循环儿茶酚胺可降低Vw,因此不支持循环儿茶酚胺在鱼类通气控制中起刺激作用。