Adrenergic involvement in blood oxygen transport and acid-base balance during hypercapnic acidosis in the Rainbow Trout,Salmo gairdneri

Abstract

Rainbow trout (Salmo gairdneri) were subjected to 12 h of external hypercapnia (1% CO2 in air) during α- and/or β-adrenoceptor blockade in order to assess the importance of adrenergic responses in modulating blood oxygen transport and acid-base balance during an acute acidotic stress. External hypercapnia caused an elevation of blood carbon dioxide tension and a reciprocal decrease in whole blood pH. A gradual elevation of blood bicarbonate levels caused whole blood pH to increase toward pre-hypercapnic values throughout the hypercapnic period. Pre-treatment of fish with propranolol (a β-adrenoceptor antagonist) or phentolamine (an α-adrenoceptor antagonist) did not affect their ability to regulate extracellular acid-base status during hypercapnia. On the other hand, adrenergic responses were essential in the maintenance of arterial blood oxygen content during hypercapnia despite the severe extracellular acidosis and a marked Root effect in trout blood, in vitro. Important adrenergic responses included pronounced increases in haematocrit (an α-adrenergic effect) and arterial oxygen tension (α- and β-adrenergic effects) as well as partial regulation of red blood cell pH (a β-adrenergic effect). Although pre-treatment of fish with either propranolol or phentolamine caused a reduction in blood oxygen content during hypercapnia, fish died only during complete adrenoceptor blockade, presumably due to severe hypoxemia.