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Neurochemical mechanisms behind gill microcirculatory responses to hypoxia in trout: in vivo microscopy study

American journal of physiology. Regulatory, integrative and comparative physiology, 1997-02, Vol.272 (2), p.576-R585 [Peer Reviewed Journal]

ISSN: 0363-6119 ;ISSN: 0002-9513 ;EISSN: 1522-1490 ;EISSN: 2163-5773 ;DOI: 10.1152/ajpregu.1997.272.2.r576 ;PMID: 9124481

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  • Title:
    Neurochemical mechanisms behind gill microcirculatory responses to hypoxia in trout: in vivo microscopy study
  • Author: Sundin, L ; Nilsson, G. E
  • Subjects: Acetylcholine - pharmacology ; Animals ; Aorta - physiopathology ; Blood Flow Velocity - drug effects ; Branchial Region - physiopathology ; Female ; Gills - blood supply ; Gills - innervation ; Heart Rate ; Hypoxia - metabolism ; Hypoxia - physiopathology ; Injections ; Male ; Microcirculation - drug effects ; Nervous System - metabolism ; Oncorhynchus mykiss - physiology ; Parasympathetic Nervous System - physiopathology ; Reflex - physiology ; Regional Blood Flow ; Vascular Resistance ; Vasoconstriction - physiology
  • Is Part Of: American journal of physiology. Regulatory, integrative and comparative physiology, 1997-02, Vol.272 (2), p.576-R585
  • Description: L. Sundin and G. E. Nilsson Department of Zoophysiology, University of Goteborg, Sweden. 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 (P(O2) 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, because the gill resistance (R(G)) increased. These effects were mimicked by prebranchial 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 R(G) remained. The latter appeared to be of a nonadrenergic noncholinergic origin, being unaffected by additional treatment with an alpha-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 alpha-adrenoceptor-mediated posthypoxic hypertension. This study demonstrates that hypoxia evoked a cholinergic reflex vasoconstriction located at proximal parts of the efferent filamental vasculature.
  • Publisher: United States
  • Language: English
  • Identifier: ISSN: 0363-6119
    ISSN: 0002-9513
    EISSN: 1522-1490
    EISSN: 2163-5773
    DOI: 10.1152/ajpregu.1997.272.2.r576
    PMID: 9124481
  • Source: MEDLINE
    Alma/SFX Local Collection
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