953
The Journal of Experimental Biology 198, 953–959 (1995)
Printed in Great Britain © The Company of Biologists Limited 1995
EFFECTS OF OXYGENATION AND THE STRESS HORMONES
ADRENALINE AND CORTISOL ON THE VISCOSITY OF BLOOD
FROM THE TROUT ONCORHYNCHUS MYKISS
BODIL SØRENSEN AND ROY E. WEBER*
Department of Zoophysiology, Institute of Biological Sciences, Building 131, University of Aarhus, DK 8000
Aarhus C, Denmark
Accepted 10 November 1994
Summary
Although the concentrations of the stress hormones
adrenaline effects were observed. In deoxygenated blood,
adrenaline and cortisol in rainbow trout (Oncorhynchus
addition of cortisol lowered viscosity at all measured shear
mykiss) blood increase upon hypoxic exposure, the
rates compared with blood without cortisol. In oxygenated
combined effects of these hormones and O2 lack upon fish
blood, however, no cortisol effects were observed. The
blood rheology have not been investigated. Deoxygenated
viscosity effects observed in the presence of cortisol could
blood taken by caudal puncture exhibited lower viscosities
not be attributed to concomitant changes in haematological
than oxygenated samples at low shear rates, whereas the
variables, However, the effects in the presence of
opposite was true at high shear rates. However, blood from
adrenaline manifested in deoxygenated ‘cannula’ blood
cannulated trout had similar viscosities in its deoxygenated
and in uncannulated blood without added hormones
and oxygenated states. In the deoxygenated state, addition
appear to result from parallel increases in haematocrit and
of adrenaline lowered viscosity at low shear rates and
cell volume.
increased it at high shear rates, resembling the effects of
deoxygenation observed in blood taken by venepuncture.
Key words: adrenaline, cortisol, fish blood, oxygenation, rheology,
stress hormones, rainbow trout, Oncorhynchus mykiss.
In oxygenated blood on the contrary, no marked
Introduction
It is well known that O2 transport from the gas-exchange
organs to the tissues is proportional to the O2-carrying
capacity, and thus the haematocrit (Hct, volume percentage of
red cells), of the blood and is inversely proportional to flow
resistance, so that the O2 transport potential of blood will
decrease above and below optimal Hct values (Snyder and
Weathers, 1977; Wells and Weber, 1991; Gallaugher et al.
1992). Hct in fish may vary widely, changing in response to
ambient hypoxia (Hughes et al. 1986; Soivo et al. 1974), stress
and exercise (Wells and Weber, 1991), amongst other things
(Weber, 1982). These variations may be mediated by
catecholamines, which may mobilize red cells from the spleen
(Gallaugher et al. 1992) or induce red cell swelling as a result
of fluid shifts into the intracellular compartment.
Catecholamine-induced swelling occurs through activation of
a sodium/proton exchange pump, which decreases plasma pH
and increases intracellular pH, thus raising blood O2-affinity
via the Bohr effect (Nikinmaa, 1992).
Blood is a non-Newtonian fluid, its viscosity (h) increasing
with decreasing shear rate (see Figs 1 and 2) owing to the
*Author for correspondence.
deformability of the red blood cell and changes in aggregation
between cells (Chien, 1975). An increase in cell volume lowers
the shear-dependence of blood viscosity (Wells and Weber,
1991) by decreasing cellular deformability and aggregation
(Chien, 1970, 1975; La Celle and Weed, 1971). Changes in the
shear-dependence also alter the overall resistance to flow and
the resistance ratio between postcapillary and precapillary
segments (Chien, 1969).
The relationships between viscosity, shear rate, oxygenation
state, swelling and stress hormones in fish red cells are still not
clearly understood, and investigations on the rheological
properties of fish blood have primarily focused separately on
the effects of O2 tension and hormones. The present paper
reports the combined effects of adrenaline and cortisol and of
oxygenation state on trout blood viscosity.
Materials and methods
Experimental animals
Rainbow trout [Oncorhynchus mykiss (Walbaum)] of both
954
B. SØRENSEN AND R. E. WEBER
sexes, weighing 380±30 g, were obtained from fish farms in
Jutland and kept in aerated tapwater (>90 % air saturation) in
1 m31 m31 m glassfibre tanks at 15±1 ˚C and a 12 h:12 h
light:dark photoperiod. The fish were given maintenance
rations of commercially available trout pellets and were
allowed to acclimate to laboratory conditions for at least 10
days before use.
Blood sampling and surgery
Blood was collected either by venepuncture from the caudal
blood vessels or, to avoid the effects of handling stress, via
implanted cannulae. Blood sampling by caudal venepuncture
was normally carried out within 1 min after lifting the fish out
of the water.
The fish were cannulated in the dorsal aorta after anaesthesia
in tapwater containing 0.1 g l21 4-aminobenzoate, using PE-50
polyethylene tubing (Portex) filled with a 0.9 % NaCl solution
containing 125 i.u. of sodium heparin (Soivio et al. 1972, 1975;
Tetens and Lykkeboe, 1985). The operation was completed
within 15 min from induction of anaesthesia and was carried
out at least 48 h before blood sampling. Blood samples of
6–8 ml were drawn into heparinized syringes and kept on ice
until use.
Viscosity measurements
Viscosity measurements were carried out using whole blood,
since the mechanical properties of red cells may be altered by
removal of plasma proteins, which are implicated in rouleaux
formation and aggregation (Fåhraeus, 1921).
Viscosity measurements were carried out at 15 ˚C using an
LVT-DVII cone/plate viscometer with a 0.8 ˚ cone spindle
(Brookfield Engineering Laboratory, Stoughton, MA), which
has eight rotational speeds ranging from 0.3 to 60 revs min21
(corresponding to shear rates of 2.25–450 s21) and requires a
sample volume of 0.5 ml. Calibration checks were carried out
using two Brookfield viscosity standards (9.2 and 98.3 cP at
25 ˚C) that correspond to the values measured in blood.
Viscosity readings were normally recorded first at the
highest shear rate after a 4 min stabilization period, and
thereafter at successively lower shear rates. This minimises the
effects of aggregation and erythrocyte sedimentation that may
occur if the reverse order is followed (International Committee
for Standardization in Haematology, ISCH, 1986). Viscosity
readings at low shear rates (45 and 22.5 s21) were occasionally
erroneously low, which may be due to the above-mentioned
phenomena or to cohesion between the blood cells. In such
cases, the shear rate was returned to the highest level (450 s21).
If the reading returned to within 5 % of the earlier recorded
value, shear rate was once more reduced to the value where the
anomalous value had been observed; if not, measurements on
the sample in question were discontinued. Care was taken to
avoid trapping air bubbles between the cone and plate, which
may cause erroneously high viscosity readings. In the present
investigations, some measurement series lasted up to 6 h after
blood had been drawn.
Before measuring viscosities, 1.2 ml blood samples were
equilibrated at predetermined gas tensions in Kutofix
tonometers (Eschweiler and Co., Kiel) for 60 min. Gas
mixtures were prepared by two serially coupled Wösthoff
(Bochum, Germany) gas-mixing pumps. Oxygenated and
deoxygenated blood were obtained by mixing 0.5 % CO2 with,
respectively, room air or pure (99.98 %) N2. To observe the
effects of hypoxia, an additional gas mixture of 0.5 % air and
99.5 % N2 was used.
To prevent oxygenation of deoxygenated samples during
measurements, the cup of the viscometer was encased in an
acrylic glove box that was flushed for at least 2 h with N2
before measurements started. This reduced the O2 content in
the glove box to less than 1 % of that in air, as predicted by a
simple exponential equation.
O2 saturations measured in the deoxygenated samples before
and after viscosity measurement in the glove box were
0.02±0.04 % (N=10) and 1.44±3.03 % (N=9), respectively. O2
tensions in oxygenated blood samples before and after
viscosity measurement were 138±11 mmHg (18.4±1.5 kPa;
N=8) and 119±7 mmHg (15.9±0.9 kPa; N=7), respectively.
Unless otherwise mentioned, measurements on deoxygenated
subsamples were carried out before those on oxygenated
samples.
Hormonal effects
To investigate hormonal effects, blood from individual fish
was divided into four subsamples, for measuring viscosity in
the oxygenated and deoxygenated states, each in the presence
and absence of hormone. The hormones were obtained from
the dispensary of Aarhus University Hospital. Final
concentrations in blood were: 531027 mol l21 cortisol (Solucortef, hydrocortisone succinate) and 531026 mol l21
adrenaline (adrenaline tartrate). These concentrations, which
exceed physiological values under stress situations, were
chosen to ensure that effects, if present, were detected.
Haematological effects
To examine the effect of haematocrit on viscosity, blood
samples were gently centrifuged [4 min at 1000 revs min21
(350 g) in a Sigma 3 MK centrifuge], plasma was removed or
added and the cells were resuspended. Control experiments
revealed no consistent effect of centrifugation and
resuspension of the cells.
In order to analyse the effects of non-adrenergic swelling,
whole blood was centrifuged and a volume of plasma
corresponding to 25 % of that of the whole blood was removed.
The plasma removed was dialysed against distilled water to
remove salts. The resulting protein suspension was then
concentrated by suspending the dialysis bags in air in a
refrigerator, after which distilled water was added to restore the
original plasma volume. The ion-free ‘plasma’ was then returned
to the blood sample after the blood had been equilibrated for
45 min with an oxygen-rich (air + 0.5 % CO2) gas mixture, and
the whole sample was equilibrated for a further 15 min.
Hct was measured by the standard glass capillary procedure
after 5 min of centrifugation at 10 000 revs min21. No
Trout blood viscosity
correction was made for trapped plasma. [Hb] and mean
cellular haemoglobin concentration, MCHC, were determined
as previously described (Wells and Weber, 1990), except that
the cells were lysed in 0.0025 mol l21 Tris buffer, pH 7.5. Red
blood cell counts were obtained using an improved Neubauer
haemocytometer.
pH and O2 measurements
The pH was measured with a BMS2 Mk2 blood micro
system coupled to a PHM 73 pH meter (Radiometer,
Copenhagen). O2 tensions were measured with a Radiometer
E5046 O2 electrode fitted in a D616 thermostat cell. O2
contents of the blood samples were determined as described by
Tucker (1967). The electrodes were calibrated before each
measurement.
Statistics
Student’s t-test was used for statistical analyses of the data.
Results
As expected, blood viscosity increased with Hct (Fig. 1;
Table 1). In this study, the relationship was linear at the Hct
values measured (0–36 %), but the linear correlation
coefficient decreased with shear rate. Interestingly, the Hctdependence of viscosity tended to be lower in deoxygenated
A
11.3 s−1
22.5 s−1
45 s−1
90 s−1
225 s−1
450 s−1
40
0
0
10
20
30
Table 1. Dependence of viscosity (y) on haematocrit (x) in
oxygenated and deoxygenated cannula blood measured at
different shear rates
Shear
rate (s –1)
Oxygenated blood
Deoxygenated blood
450
225
90
45
22.5
11.3
y=0.083x+2.22, r=0.95
y=0.106x+2.82, r=0.87
y=0.164x+3.72, r=0.86
y=0.264x+4.30, r=0.87
y=0.335x+5.78, r=0.76
y=0.928x+20.74, r=0.79
y=0.082x+2.08, r=0.98
y=0.094x+2.93, r=0.91
y=0.123x+3.98, r=0.87
y=0.164x+5.73, r=0.88
y=0.295x+6.09, r=0.82
y=0.576x+20.86, r=0.66
r, linear regression coefficient.
than in oxygenated blood at low shear rates, but the differences
were not significant (Table 1).
The viscosity of trout blood taken by caudal venepuncture
(Fig. 2) increased with decreasing shear rate. As indicated for
a single series of measurements (Fig. 2) shear-dependence was
lower in deoxygenated blood than in oxygenated blood. No
consistent variations in blood viscosity with season were
observed.
Since individual differences in blood properties, e.g. Hct,
could mask the effects of oxygenation or hormones, blood
viscosity effects were assessed from viscosity ratios obtained
for the same blood sample under different conditions (see
Figs 3–6).
For trout blood taken by venepuncture, the
deoxygenated/oxygenated viscosity ratios were below 1 at low
shear rates (below 100 s21), but increased to values greater
than 1 at high shear rates (225 and 450 s21, Fig. 3A). For blood
taken by venepuncture, hypoxygenated/oxygenated ratios (data
not shown) were similar to deoxygenated/oxygenated ratios. In
contrast, blood from the cannulated specimens had similar
viscosities in the deoxygenated and oxygenated states, giving
ratios of approximately 1 (Fig. 3B).
25
40
Oxygenated
Deoxygenated
20
B
Viscosity (cP)
Viscosity (cP)
20
955
40
15
10
20
5
0
0
0
10
20
30
Haematocrit (%)
40
Fig. 1. Effects of haematocrit and shear rate on viscosity in (A)
oxygenated and (B) deoxygenated trout cannula blood.
0
100
200
300
400
500
Shear rate (s−1)
Fig. 2. Blood viscosity at different shear rates in oxygenated and
deoxygenated trout blood obtained by caudal venepuncture.
956
B. SØRENSEN AND R. E. WEBER
1.5
1.5
A
A
**
†
†
*
1.0
0.5
0.5
0
100
200
300
400
500
1.5
B
ηadr/η−adr
ηdeoxy/ηoxy
1.0
0
100
200
300
400
1.5
†
†
†
†
B
*
*
†
1.0
500
1.0
0.5
0
100
200
300
400
500
Shear rate (s−1)
Fig. 3. Ratio of viscosities in deoxygenated and oxygenated blood
(hdeoxy/hoxy) taken by (A) venepuncture (N=10) and (B) implanted
cannula (N=7), as a function of shear rate. In this and later figures,
the daggers and asterisks denote significance of difference: †P<0.1;
*P<0.05; ††P<0.01; **P<0.005; †††P<0.001; ***P<0.0005;
††††P<0.0001.
Addition of adrenaline had no effect or only a slight effect
on the viscosity of oxygenated cannula blood, the values of
hadr/h2adr tending to be below 1 at low shear rates and above
1 at high shear rates (Fig. 4A). In the deoxygenated cannula
blood (Fig. 4B), these effects were more pronounced,
resembling the deoxygenated/oxygenated pattern found in
blood from uncannulated trout (cf. Fig. 3A).
In oxygenated cannula blood, cortisol exerted no effect on
viscosity compared with values in blood without cortisol
(Fig. 5A). In deoxygenated blood, however, cortisol lowered
viscosity at all measured shear rates (Fig. 5B).
Besides possible direct effects, hormones may influence the
rheological properties of blood through changes in secondary
variables, e.g. Hct, MCHC, mean cell volume, MCV (Trevan,
1918; Nygaard et al. 1935; Chien, 1975; Fletcher and
Haedrich, 1987; Chiocchia and Motais, 1989), blood pH
(Wells et al. 1963; Rand et al. 1968; Giombi and Burnard,
1970) and ATP concentrations (Nakao et al. 1960; Weed et al.
1969; La Celle and Weed, 1971). The haematological data for
the blood samples used to study the effects of hormones are
shown in Tables 2 and 3.
Viscosity ratios for osmotically swollen compared with
control cells (where Hct values were 21.15±2.23 and
14.58±0.85, respectively; Fig. 6) showed similar variation with
shear rate to the the deoxygenated/oxygenated ratios in blood
0.5
0
100
200
300
Shear rate
(s−1)
400
500
Fig. 4. Ratio of viscosity in the presence and absence of
531026 mol l21 adrenaline (hadr/h2adr) for (A) oxygenated samples
(N=5) and (B) deoxygenated samples (N=7) of blood taken by
cannula. Other details as in Fig. 3.
taken by venepuncture (Fig. 3A; Table 2) and the
deoxygenated viscosity ratios in the presence and absence of
adrenaline (Fig. 4B; Table 3), i.e. higher ratios at high shear
rates than at low shear rates. This reflects the lower sheardependence in swollen cells (as previously observed by Wells
et al. 1991).
The possibility that the viscosity of drawn blood may change
with time was investigated by repeating viscosity
measurements under the same conditions or by changing the
sequence of measurements carried out on subsamples
(oxygenated and deoxygenated samples, with and without
hormones). These results showed unchanged viscosity ratios in
blood from the same pool within the measurement period,
although the absolute viscosity readings showed small
increases after 4–6 h.
Discussion
This study appears to be the first focusing on the combined
effects of stress hormones and oxygenation on the viscosity of
fish blood.
Handling stress (caudal blood sampling) and in vitro
adrenaline administration markedly increased Hct in
deoxygenated trout blood (Tables 2 and 3). The change was
correlated with decreased MCHC, increased MCV and
Trout blood viscosity
1.5
1.5
A
†
ηswollen/ηcontrol
1.0
ηcort/n−cort
0.5
0
100
200
300
400
**
*
1.0
500
0.5
1.5
B
1.0
†
†
†
** ††
* †
957
*
†
0
100
200
300
Shear rate
(s−1)
400
300
400
500
(s−1)
Fig. 6. Ratio of viscosities in oxygenated osmotically swollen and
control cells (hswollen/hcontrol) from blood taken by cannula (N=3).
Other details as in Fig. 3.
0.5
0
200
Shear rate
**
*
*
100
500
Fig. 5. Ratio of viscosities in the presence and absence of 531027 mol
l21 cortisol (hcort/h2cort) for (A) oxygenated samples (N=5) and (B)
deoxygenated samples (N=6) of trout blood taken by cannula. Other
details as in Fig. 3.
unchanged blood [Hb], which reflect the red cell swelling
associated with adrenergic stimulation of trout red cells by
activation of the Na+/H+ exchanger (Nikinmaa, 1992).
Adrenaline decreased the viscosity at low shear rates, but
increased it at high shear rates in deoxygenated blood, without
exerting pronounced effects in oxygenated blood (Fig. 4).
Cortisol lowered the viscosity of deoxygenated blood at all
shear rates, without affecting viscosity in oxygenated blood
(Fig. 5). As noted previously (Wells et al. 1991), it is not
known whether the adrenergic effects on the viscous properties
of blood are a direct result of hormonal stimulation or whether
they result from changes in haematological variables.
Blood viscosity increased with Hct (Fig. 1; Table 1). At all
shear rates measured in this study where Hct values were
below 40 %, the relationship was linear, as previously observed
at low Hct (Trevan, 1918; Nygaard et al. 1935; Snyder and
Weathers, 1977; Pankhurst et al. 1992), but the linear
correlation coefficient decreased at low shear rates (Table 1).
Since increased Hct raises viscosity at all shear rates, the
adrenaline-induced decrease in viscosity observed at low shear
rates (Fig. 3) cannot be attributed to an associated increase in
Hct. Instead, the data indicate that the adrenergic effect on
viscosity is due to red cell swelling per se. The effects of
adrenaline on the viscosity of deoxygenated cannula blood
(Fig. 4B) correlate with increases in Hct and MCV (Table 3).
This reflects cell swelling, which is known to decrease
aggregation, deformability and shear-dependence (Chien,
1975;
La
Celle
and
Weed,
1971).
The
deoxygenated/oxygenated viscosity ratio in uncannulated trout
blood (Fig. 3A) may similarly result from adrenaline release
Table 2. Haematological data for trout blood obtained either by caudal puncture or by cannula
Caudal puncture
Haematocrit (%)
[Haemoglobin] (mmol l–1)
10–6 × red blood cell count (ml–1)
MCHC (mmol l−1)
Mean cell volume (nm3)
pH
Cannula
Deoxygenated
Oxygenated
P
Deoxygenated
Oxygenated
28.34±3.13 (10)
1.15±0.32 (6)
0.85±0.13 (5)
4.33±0.73 (6)
327±31 (5)
7.67±0.06 (4)
22.68±2.06 (9)
1.23±0.45 (6)
0.85±0.13 (5)
5.39±1.45 (6)
265±34 (5)
7.68±0.09 (4)
<0.0001
16.92±5.05 (8)
0.92±0.30 (8)
0.57±0.17 (8)
5.51±1.39 (8)
306±43 (8)
7.79±0.10 (8)
16.14±4.73 (8)
0.92±0.30 (8)
0.56±0.17 (8)
5.70±1.40 (8)
291±37 (8)
7.69±0.15 (8)
<0.05
<0.0005
Data are means ± S.D. (N).
Blood samples were equilibrated with 0.5 % CO 2 in either air (oxygenated blood) or pure (99.98 %) N 2 (deoxygenated blood).
MCHC, mean cellular haemoglobin concentration.
P
<0.005
<0.005
958
B. SØRENSEN AND R. E. WEBER
Table 3. Haematological data for blood from cannulated trout in the absence and presence of added adrenaline and cortisol
Oxygenated
Control
Treated
Adrenaline
Haematocrit (%)
[Haemoglobin] (mmol l–1)
10–6 × red blood cell count (ml–1)
MCHC (mmol l–1)
MCV (nm 3)
pH
18.96±3.00 (4)
1.16±0.25 (5)
0.56±0.17 (5)
7.10±1.72 (4)
298±43 (4)
7.79±0.14 (5)
18.67±5.12 (5)
1.16±0.25 (5)
0.59±0.16 (5)
6.21±1.50 (5)
318±53 (5)
7.67±0.14 (5)
Cortisol
Haematocrit (%)
[Haemoglobin] (mmol l–1)
10–6 × red blood cell count (ml–1)
MCHC (mmol l–1)
MCV (nm 3)
pH
16.35±1.97 (5)
0.93±0.25 (5)
0.60±0.11 (5)
5.67±1.47 (5)
281±66 (5)
7.66±0.05 (5)
16.24±2.05 (5)
0.93±0.25 (5)
0.63±0.07 (5)
5.73±1.54 (5)
257±21 (5)
7.71±0.08 (5)
Deoxygenated
P
Control
Treated
P
26.70±3.96 (7)
1.25±0.19 (7)
0.73±0.14 (7)
4.68±1.19 (7)
370±46 (7)
7.78±0.13 (7)
<0.0001
<0.05
<0.05
<0.01
21.28±3.01 (7)
1.25±0.33 (7)
0.74±0.17 (7)
5.87±1.54 (7)
295±18 (6)
7.88±0.10 (7)
<0.01
16.58±1.95 (6)
0.96±0.24 (6)
0.60±0.10 (6)
5.82±1.56 (6)
276±21 (6)
7.78±0.05 (6)
16.40±1.88 (6)
0.96±0.24 (6)
0.60±0.10 (6)
5.85±1.50 (6)
275±29 (6)
7.80±0.03 (6)
<0.0005
<0.05
<0.05
Other details as in Table 2.
during the stressful blood-sampling procedure, which increases
Hct and MCV more in deoxygenated than in oxygenated blood
(Table 2). This is supported by the observation that the same
responses (increased viscosity ratio at high shear rates) were
seen upon administration of adrenaline to deoxygenated
cannula blood and in osmotically swollen cells (compare
Figs 4B and 6). The effects of osmotic swelling (Fig. 6) agree
with the concept that swelling reduces aggregation, and thus
viscosity, at low shear rates, but increases viscosity at high
shear rates, because of the lower deformability of swollen red
cells (Chien, 1970, 1975; La Celle and Weed, 1971).
The effects of adrenaline on rheology are varied and appear
to depend on species and on the exact measurement conditions.
For trout, Wells et al. (1991) found that adrenaline decreased
blood viscosity, particularly at low shear rate where the
hadr/h2adr ratio was 0.65, although it increased to
approximately 1 at 450 s21, and Wells and Weber (1991)
observed a decrease in shear-dependence in blood from
exercised and anaesthetised specimens where the cells were
swollen. Chiocchia and Motais (1989) found that in vitro
adrenergic stimulation increased the deformability of washed
trout red cells. However, Hughes and Albers (1988) found that
adrenaline decreased the filtration rate of whole blood
equilibrated with low O2 and high CO2 tensions in carp blood.
In washed rat and human red cells, adrenaline similarly
lowered the filterability (Rasmussen et al. 1975), which
accords with the results of Pfafferott et al. (1986), who showed
that noradrenaline decreased the deformability of human
washed cells. Rasmussen et al. (1975) consider that the effects
of adrenaline may be mediated by changes in the cell
membrane, in cell shape or in cell volume. It should, however,
be borne in mind that mammalian red cells do not exhibit
catecholamine-induced alkalization and swelling (Nikinmaa,
1992).
In contrast to the red cell swelling induced by
catecholamines (Nikinmaa, 1992), swelling and MCV changes
were not observed with cortisol (Table 3). Since cortisol had
no major influence on the haematological variables measured
in either oxygenated or deoxygenated blood (Table 3), its
viscosity effects cannot be attributed to concomitant changes
in Hct, MCHC, MCV or blood pH. The slight increase in the
pH of deoxygenated blood observed in the presence of cortisol
(from 7.78 to 7.80) is unlikely to have had a significant effect
since a greater pH increase in oxygenated blood induced by
cortisol (from 7.66 to 7.71) was not associated with a lower
viscosity (Table 3; Fig. 5A).
The decreased viscosity after cortisol administration may be
due to changes in the red cell membranes or to a lowered
cellular ATP concentration, which has been observed in
cortisol-stimulated blood from the fish Pagrus auratus
(Bollard et al. 1993) and in deoxygenated trout blood (O. B.
Nielsen and G. Lykkeboe, unpublished data). Lowering the
ATP concentration decreases the deformability of human red
cells (Weed et al. 1969). However, Wells and Weber (1991)
found no evidence for effects of lowered ATP concentrations
on the viscosity of trout blood.
The present results indicate that, in rainbow trout, red blood
cell swelling in the presence of adrenaline reduces the viscosity
of deoxygenated blood at low shear rates. Physiologically, this
effect may be more important than the accompanying increase
in viscosity of hypoxic blood at high shear rates, given the low
flow rates of blood in the veins and the small blood vessels (La
Celle and Weed, 1971). Sirs (1993) suggests that fish with low
blood pressures have an improved blood flow with less flexible
cells caused by a reduction in the Fåhreaus Lindqvist
phenomenon, i.e. decreasing viscosity with decreasing vessel
diameter, since less flexible cells do not move towards the
central core to the same degree as flexible ones. The present
results suggest that viscosity changes continuously in parallel
with arterio-venous changes in oxygenation and red cell volume.
Trout blood viscosity
We thank the Danish Natural Science Research Council and
the E. and K. Petersen Fund for financial support.
References
BOLLARD, B. A., PANKHURST, N. W. AND WELLS, R. M. G. (1993).
Effects of artificially elevated plasma cortisol levels in the teleost
fish Pagrus auratus (Sparidae). Comp. Biochem. Physiol. 106A,
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