First published online November 19, 2004
Journal of Experimental Biology 207, 4451-4461 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.01291
Adenosinergic and cholinergic control mechanisms during hypoxia in the epaulette shark (Hemiscyllium ocellatum), with emphasis on branchial circulation
Kåre-Olav Stensløkken*,1,
Lena Sundin2,
Gillian M. C. Renshaw3 and
Göran E. Nilsson1
1 Physiology Programme, Department of Molecular Biosciences, University of
Oslo, PO Box 1041, NO-0316 Oslo Norway
2 Department of Zoophysiology, Göteborg University, SE-405 30
Göteborg, Sweden
3 Hypoxia and Ischemia Research Unit, School of Physiotherapy and Exercise
Science, Griffith University, PMB 50 Gold coast Mail Centre, Queensland, 9726
Australia
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Fig. 4. Frequency distribution of sharks displaying commenced blood flow in the
longitudinal vessels during (A) hypoxia (grey bars; N=12) and (B)
adenosine injection (1 µmol kg–1) (grey bars;
N=8), and after aminophylline treatment during (A) hypoxia (hatched
bars; N=6) and (B) adenosine injections (1 µmol
kg–1) (hatched bars; N=7). Injection of adenosine at
time 0. An asterisk indicates a significant difference between aminophylline
treated and control group (*P<0.05,
**P<0.01) (Fisher's exact test).
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Fig. 2. Effects of (A) hypoxia (N=12) and (B) acetylcholine (ACh; 1
µmol kg–1) injections (N=7) on blood flow
velocity in efferent filament arteries (EFA). •, ACh;  , ACh after
atropine injection. Values are means ± S.E.M. and normalized
to the proportion (%) of pre-hypoxic velocity. The line indicates a time
period significantly different from the last pre-exposure value
[P<0.05; non-parametric ANOVA (Freidmann test) with Dunn
post-test]. The asterisk indicates a significant difference between atropine
treatment and control.
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Fig. 3. Video micrograph of the free tip of a filament showing longitudinal vessel
during hypoxia. The vessel is outlined with a black line, and direction of
blood flow is indicated by black arrows. White arrows point toward anastomoses
where the blood started flowing during hypoxia and adenosine injections. Scale
bar, 100 µm.
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Fig. 5. Effects of (A) hypoxia (N=9) and (B) adenosine injections
(N=7) (1 µmol kg–1) on ventilation frequency.
Line indicates significant time interval different from last normoxic value;
non-parametric ANOVA (Freidman test) with Dunn post-test. Values are mean
± S.E.M.
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Fig. 6. Cardiovascular responses to adenosine (Ado) injections (at time zero) on
(A) heart rate (fH), (B) ventral aortic blood pressure
(PVA) and (C) dorsal aortic blood pressure
(PDA) in control (•, N=7) and
aminophylline-treated (, N=6) sharks. All values are mean
± S.E.M. Time-dependent changes were tested using repeated
measures ANOVA with Dunnet post-test. Lines indicate the time periods that
differ significantly from the last normoxic value (P<0.05). A
significant ANOVA between aminophylline-treated and control sharks in response
to adenosine injections is indicated by an asterisk.
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© The Company of Biologists Ltd 2004
, N=7), atropine-treated (
,
N=7) and tubocurarine-treated (
, N=7) sharks. All
values are means ± S.E.M. Time-dependent changes were tested
using repeated measures ANOVA with Dunnet post-test. Lines indicate the time
periods that differ significantly from the last normoxic value
(P<0.05). Differences in the effects of hypoxia between
aminophylline-treated and control sharks (A) and between hypoxia- and
atropine-treated (D) are indicated by an asterisk.