Department of Biology, University of Ottawa, 30 Somerset St. E, K1N 6N5, Ottawa, Ontario, Canada.
Fish Physiol Biochem. 1988 Jan;4(4):189-202. doi: 10.1007/BF01871745.
Rainbow trout were infused continuously for 12h with epinephrine in the presence or absence of alpha-and/or beta-adrenergic blockade to characterize the specific adrenergic mechanisms involved in the control of blood acid-base status and oxygen transport capacity. Infusion of epinephrine, alone, produced a transient respiratory acidosis, as indicated by an increase in carbon dioxide tension and a decrease in whole blood pH, yet arterial oxygen tension was elevated. Red blood cell pH increased by approximately 0.2 pH units during epinephrine infusion and this increase as well as the increase in oxygen tension were prevented by pretreatment with propranolol (a beta-adrenergic antagonist). Epinephrine infusion during alpha-adrenergic blockade caused a prolonged elevation of blood carbon dioxide tension and abolished the increases in hematocrit and hemoglobin concentrations observed during epinephrine infusion alone. Infusion of the alpha-adrenergic agonists phenylephrine (an alpha1 agonist) or clonidine (an alpha2 agonist) caused respiratory acidosis (decreased pH, increased CO2 tension) and a reduction in oxygen tension. Infusion of isoprenaline (a non-specific beta agonist) caused delayed increases in carbon dioxide and oxygen tensions. We speculate that the increased carbon dioxide tension observed during epinephrine infusion is a result of beta-adrenoceptor mediated inhibition of red blood cell bicarbonate dehydration and not branchial convective or diffusive adjustments. The effects of epinephrine on blood O2 tension, content and carrying capacity are discussed with reference to the participation of alpha- and beta-adrenergic mechanisms at the gill, spleen and red blood cell.
虹鳟鱼连续输注肾上腺素 12 小时，同时存在或不存在α-和/或β-肾上腺素能阻断，以描述参与控制血液酸碱状态和氧运输能力的特定肾上腺素能机制。单独输注肾上腺素会导致短暂的呼吸性酸中毒，表现为二氧化碳分压升高和全血 pH 值降低，但动脉氧分压升高。红细胞 pH 值在肾上腺素输注期间增加了约 0.2 pH 单位，这种增加以及氧分压的增加被普萘洛尔（β-肾上腺素能拮抗剂）预处理所预防。在α-肾上腺素能阻断期间输注肾上腺素会导致长时间的血液二氧化碳分压升高，并消除单独输注肾上腺素时观察到的红细胞比容和血红蛋白浓度的增加。输注α-肾上腺素能激动剂苯肾上腺素（α1 激动剂）或可乐定（α2 激动剂）会导致呼吸性酸中毒（pH 值降低，CO2 张力增加）和氧分压降低。异丙肾上腺素（非特异性β激动剂）的输注会导致二氧化碳和氧分压的延迟增加。我们推测，在肾上腺素输注期间观察到的二氧化碳分压升高是由于红细胞碳酸氢盐脱水的β-肾上腺素能受体介导的抑制所致，而不是鳃的对流或扩散调节。本文还讨论了肾上腺素对血液 O2 张力、含量和携带能力的影响，参考了在鳃、脾脏和红细胞中α-和β-肾上腺素能机制的参与。
