Summary 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 (CO
2) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final
P
wO
2=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 (
P
aO
2) 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
PCO
2 (
P
aCO
2) whereas arterial PO
2 was unaltered; the elevation of
P
aCO
2 could not be explained by changes in gill ventilation. Pre-treatment of fish with the -adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of
P
aCO
2. Conversely, pre-treatment with the -adrenoceptor antagonist sotalol abolished both the activation of the RBC Na
+/H
+ antiporter and the associated rise in
P
aCO
2, suggesting a causal relationship between the stimulation of RBC Na
+/H
+ exchange and the elevation of
P
aCO
2. To more clearly establish that elevation of plasma catecholamine levels during severe hypoxia was indeed responsible for causing the elevation of
P
aCO
2, fish were exposed to moderate hypoxia (final
P
wO
2=60–80 torr) and then injected intraarterially with a bolus of adrenaline to elicit an estimated circulating level of 400 nmol·l
-1 immediately after the injection. This protocol activated RBC Na
+/H
+ exchange as indicated by abrupt changes in arterial pH (pHa). In all fish examined,
P
aCO
2 increased after injection of exogenous adrenaline. The effects on
P
aO
2 were inconsistent, although a reduction in this variable was the most frequent response. Gill ventilation frequency and amplitude were unaffected by exogenous adrenaline. Therefore, it is unlikely that ventilatory changes contributed to the consistently observed rise in
P
aCO
2. Pretreatment of fish with sotalol did not alter the ventilatory response to adrenaline injection but did prevent the stimulation of RBC Na
+/H
+ exchange and the accompanying increases and decreases in
P
aCO
2 and
P
aO
2, respectively. These results suggest that adrenergic elevation of
P
aCO
2, in addition to the frequently observed reduction of
P
aO
2 are linked to activation of RBC Na
+/H
+ exchange. The physiological significance and the potential mechanisms underlying the changes in blood respiratory status after addition of endogenous or exogenous catecholamines to the circulation of hypoxic rainbow trout are discussed.Abbreviations
P
aCO
2
arterial carbon dioxide tension
-
P
aO
2
arterial oxygen tension
-
P
da
dorsal aortic pressure
-
pHa
arterial pH
-
P
wO
2
water oxygen tension
-
RBC
red blood cell
-
V
f
breathing frequency
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