When many fish experience environmental hypoxia (a drop in oxygen availability) or hypercarbia (an increase in environmental carbon dioxide levels) their heart rate decreases and their systemic vasculature constricts resulting in an increase in arterial blood pressure. Much previous theoretical and empirical data has lead to the suggestion that these cardiovascular adjustments should enhance gas transfer across the gills enhancing O2 uptake and CO2 excretion. However, direct measurements of the consequences of a reduced heart rate, known as bradycardia, and increased blood pressure, known as hypertension, on branchial gas transfer in fish gills are extremely sparse, and the few studies that exist have so far yielded conflicting results as to the effects of bradycardia and hypertension on gas exchange. Steven Perry and Patrick Desforges of the Department of Biology at the University of Ottawa decided to rectify this situation by quantifying exactly how reduced heart rate and raised blood pressure affect branchial gas transfer during hypoxia and hypercarbia in the rainbow trout (Oncorhynchus mykiss).
The team first monitored heart rate, cardiac output (the amount of blood pumped by the heart), arterial blood pressure and arterial blood O2and CO2 tensions in untreated rainbow trout exposed to either 40 min of hypoxia or 30 min of hypercarbia. Next, they tested the effects of bradycardia and hypertension on the fishes' physiology during hypoxia or hypercarbia by treating groups of fish either with atropine (to abolish bradycardia) or prazosin (to eliminate hypertension), before exposing the fish to hypoxia or hypercapnia and measuring their cardiovascular and blood gas responses. The expectation was that differences in blood gas tensions between the treated and untreated fish would indicate if and how bradycardia and hypertension affects branchial gas transfer.
Surprisingly, in contrast with current beliefs, the team found that bradycardia did not enhance branchial gas transfer efficiency in the rainbow trout during hypoxia or hypercarbia. No differences in blood gas O2or CO2 tensions existed between untreated trout, which exhibited bradycardia, and atropine treated fish, which did not exhibit a decrease in heart rate. The team argues that this lack of difference in blood gas tensions indicates that reducing heart rate during hypoxia or hypercarbia does not have any beneficial effects on gas exchange.
Similarly, the team found no beneficial effect of hypertension on blood gas tensions during exposure to increased environmental CO2. There were no differences in the blood gas levels between untreated fish and hypertension-inhibited fish. Perry and Desforges argue that this suggests that increased blood pressure does not increase gas transfer during hypercarbia.
The team did find that gas transfer across the gills was impaired in hypertension-inhibited fish during hypoxic exposure. Arterial blood O2 tension was lower, and CO2 tension was higher in fish treated with prazosin compared to untreated fish. However, Perry and Desforges suspect that this reduction was not caused by inhibition of the fish's hypertensive response. Rather, they suggest that it was probably caused by prazosin impairing the normal ventilatory responses to hypoxia, resulting in reduced gas transfer across the gills.
Thus, in contrast to current models of gas transfer in fishes, it appears that neither bradycardia nor hypertension enhances branchial gas transfer in rainbow trout during hypoxia or hypercarbia. It remains to be determined whether this finding can be extended to other fish species.
