The effects of endogenous or exogenous catecholamines on blood respiratory status during acute hypoxia in rainbow trout (Oncorhynchus mykiss).

An extracorporeal circulation of rainbow trout (Oncorhynchus mykiss) was utilized to continuously monitor the rapid and progressive effects of endogenous or exogenous catecholamines on blood respiratory/acid-base status, and to provide in vivo evidence for adrenergic retention of carbon dioxide (CO2) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final PwO2 = 40-60 torr; reached within 10-20 min) elicited an initial respiratory alkalosis resulting from hypoxia-induced hyperventilation. However, at a critical arterial oxygen tension (PaO2) between 15 and 25 torr, fish became agitated for approximately 5 s and a marked (0.2-0.4 pH unit) but transient arterial blood acidosis ensued. This response is characteristic of abrupt catecholamine mobilization into the circulation and subsequent adrenergic activation of red blood cell (RBC) Na+/H+ exchange (Fievet et al. 1987). Within approximately 1-2 min after the activation of RBC Na+/H+ exchange by endogenous catecholamines, there was a significant rise in arterial PCO2 (PaCO2) whereas arterial PO2 was unaltered; the elevation of PaCO2 could not be explained by changes in gill ventilation. Pre-treatment of fish with the alpha-adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of PaCO2. Conversely, pre-treatment with the beta-adrenoceptor antagonist sotalol abolished both the activation of the RBC Na+/H+ antiporter and the associated rise in PaCO2, suggesting a causal relationship between the stimulation of RBC Na+/H+ exchange and the elevation of PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)