Neurochemical mechanisms behind gill microcirculatory responses to
hypoxia in trout: an in-vivo microscopy study.
Sundin, Lena, and G divided by ran E. Nilsson.
Department of Zoophysiology, University of G divided by teborg, S
-413 90 G divided by teborg, Sweden
APStracts 3:0367R, 1996.
In vivo microscopy combined with systemic blood flow and pressure
measurements were used to examine the hemodynamic and
microcirculatory responses to hypoxia in gills of rainbow trout, and
to clarify if the underlying mechanisms are adrenergic, cholinergic,
serotonergic or adenosinergic. Hypoxia (PO2 1.07-1.33 kPa) reduced,
halted or reversed the blood flow in the distal portion of the
efferent filamental artery (EFA). Simultaneously a large overflow to
the central venous system appeared, allowing a continuous flow
through many of the secondary lamellae. No vasoconstriction could be
observed in this portion of the filament, showing that a
vasoconstriction occurred elsewhere, possibly at the EFA sphincter,
since the gill resistance (RG) increased. These effects were mimicked
by pre-branchial injection of acetylcholine, a treatment that also
strongly constricted the distal efferent filamental vasculature.
Atropine blocked most of the hypoxia induced hemodynamic changes,
although a minor increase in RG remained. The latter appeared to be
of a non-adrenergic non-cholinergic origin, being unaffected by
additional treatment with an a-adrenoreceptor antagonist. It was also
unaffected by blockers of serotonin and adenosine-A1 receptors. Other
responses seen included a cholinergic maintenance of the systemic
resistance during hypoxia and an a-adrenoceptor-mediated post-hypoxic
hypertension. This study demonstrates that hypoxia evoked a
cholinergic reflex vasoconstriction located at proximal parts of the
efferent filamental vasculature.
Received 9 February 1996; accepted in final form 27 August 1996.
APS Manuscript Number R86-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996