NEUROCHEMICAL MECHANISMS BEHIND GILL MICROCIRCULATORY RESPONSES TO HYPOXIA IN TROUT - IN-VIVO MICROSCOPY STUDY

In vivo microscopy combined with systemic blood flow and pressure meas urements were used to examine the hemodynamic and microcirculatory res ponses to hypoxia in gills of rainbow trout and to clarify if the unde rlying mechanisms are adrenergic, cholinergic, serotonergic, or adenos inergic. Hypoxia (PO2 1.07-1.33 kPa) reduced, halted, or reversed the blood flow in the distal portion of the efferent filamental artery (EF A). Simultaneously, a large overflow to the central venous system appe ared, allowing a continuous flow through many of the secondary lamella e. No vasoconstriction could be observed in this portion of the filame nt, showing that a vasoconstriction occurred elsewhere, possibly at th e EFA sphincter, because the gill resistance (R(G)) increased. These e ffects were mimicked by prebranchial injection of acetylcholine, a tre atment that also strongly constricted the distal efferent filamental v asculature. Atropine blocked most of the hypoxia-induced hemodynamic c hanges, although a minor increase in R(G) remained. The latter appeare d to be of a nonadrenergic noncholinergic origin, being unaffected by additional treatment with an alpha-adrenoreceptor antagonist. It was a lso unaffected by blockers of serotonin and adenosine-A(1) receptors. Other responses seen included a cholinergic maintenance of the systemi c resistance during hypoxia and an alpha-adrenoceptor-mediated posthyp oxic hypertension. This study demonstrates that hypoxia evoked a choli nergic reflex vasoconstriction located at proximal parts of the effere nt filamental vasculature.