Abstract
A perfused and ventilated gill preparation is described in which the pO2 of the perfusion medium and the irrigating water is controlled. Dorsal aorta effluent pO2 and flow were measured together with the branchial vascular resistance. Decreasing pO2 in the perfusion fluid caused increased branchial vascular resistance, probably by constriction of efferent lamellar arterioles. α-adrenoceptor stimulation caused constriction of arteriovenous connections and of efferent lamellar arterioles, and enhanced oxygenation of the perfusion fluid. β-adrenoceptor stimulation also increased O2 transfer, but to a lesser extent. It is suggested that both hypoxia and α-adrenoceptor stimulation improved O2 transfer via constriction of efferent lamellar arterioles. Both stimuli may also increase systemic blood flow by constriction of the arterio-venous connections, although such an effect of hypoxia has not been clearly shown. β-stimulation probably increased O2 transfer by dilation of afferent lamellar arterioles, thereby causing recruitment of unperfused lamellae.