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-Adrenoreceptor influences on liquid movements by in vitro lungs
from fetal guinea pigs
Departments of Obstetrics and Gynecology and Zoology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z4
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ABSTRACT |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Doe, S., and A. M. Perks. 
-Adrenoreceptor influences
on liquid movements by in vitro lungs from fetal guinea pigs. J. Appl. Physiol. 84(2): 746-753, 1998.
Lungs from near-term fetal guinea pigs (60 ± 2 days of
gestation) were supported in vitro for 3 h; lung liquid production was
monitored by a dye-dilution method. Studies of 30 fetuses showed that
untreated preparations produced fluid at 1.34 ± 0.21 ml · h
1 · kg
body wt1, but epinephrine
at concentrations known at delivery
(108 and
107 M) produced significant
reductions or fluid reabsorption (analysis of variance, regression
analysis); at high levels
(106 and
105 M), epinephrine had no
effect. Maximal responses from
107 M epinephrine involved
-adrenoreceptors, since they were abolished by
106 M phentolamine
(-antagonist) but were unaffected by
106 M propranolol
(
-antagonist; n = 36). Activation
was through 2-adrenoreceptors,
since responses were abolished by
104 M yohimbine
(2-antagonist;
n = 24) but were resistant to
105 M prazosin
(1-antagonist;
n = 24). At high levels of epinephrine (105 M), where responses
did not normally occur, reductions in lung liquid production were large
if prazosin was also present (n = 24),
and increases were significant if yohimbine was included (n = 24). In guinea pigs, epinephrine
appears to activate lung fluid reabsorption through
2-adrenoreceptors; at high
concentrations only, it can also increase production through
1-adrenoreceptors. Therefore,
species differences appear to exist.
epinephrine; prazosin; yohimbine; lung fluid
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INTRODUCTION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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THE FETAL LUNG PRODUCES large quantities of fluid by
means of a
Na+-K+-2Cl
cotransport system, probably in type II alveolar cells (21, 29).
However, this fluid is reabsorbed at birth by activation of an
amiloride-sensitive, Na+-based
reabsorptive system, aided by colloid osmotic effects (21, 29). This
reabsorption may be turned on by a number of factors, but an important
stimulus is probably epinephrine (4, 31). Although epinephrine appears
to act through -adrenoreceptors in sheep and rabbits, there have
been some difficulties in accepting the -receptor system as the only
means of activation (2, 3, 11, 32). First, other systems must exist,
probably outside the field of catecholamines, since irreversible
-antagonists and propranolol have failed to stop fluid clearance at
birth in both species (8, 19). Second, norepinephrine has been shown to
be capable of reducing lung liquid production via -receptors in
fetal sheep (13). Third, initial studies in our laboratory suggested
that epinephrine acted through -, not -, adrenoreceptors in in
vitro lungs from fetal guinea pigs. The studies presented here were
carried out at the concentration of epinephrine with maximal effects
and were extended to the more specific
1- and 2-antagonists prazosin and
yohimbine. This allowed analysis of the nature of the
-adrenoreceptor involved; therefore, the work gave probable reasons
for the failure of the action of epinephrine at higher concentrations.
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MATERIALS AND METHODS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Animals
Pregnant albino guinea pigs of an inbred departmental stock were given food and water ad libitum (Ralston-Purina guinea pig chow supplemented with fresh vegetables and vitamin C). Treatment of the animals was in accordance with the Canadian Council for Animal Care, and conditions were approved by the Animal Care Committee of the University of British Columbia. Studies were performed on fetuses of 60 ± 2 days of gestation (full term = 67 days) and 78.9 ± 13.4 (SD) g body wt.Experimental Procedures
The rate of lung liquid production was measured by an impermeant tracer technique using blue dextran 2000 (Pharmacia, Dorval, PQ, Canada; molecular mass = 2 × 106 Da, Stoke's radius = 270 Å; radius of gyration = 380 Å). The basis of the method and confirmation of its validity have been reported previously (6, 25).Pregnant guinea pigs were anesthetized with halothane (Fluothane, Ayers, Montreal, PQ, Canada) until full inhibition of the corneal reflex; euthanasia was achieved by severing the carotid arteries. The fetuses were removed by cesarean section, with their amniotic sacs intact, and transferred to Krebs-Henseleit saline. Ligatures were placed around the amnion at the level of the neck to maintain a pool of amniotic fluid around the head and prevent inhalation of air; no fetal breathing movements were seen. A midline incision through the thorax exposed the lungs and trachea. The trachea was ligated rostrally and cannulated caudally with 1.5-2.0 cm of polyethylene tubing filled with saline (PE-50, Intramedic, Clay Adams, Parsippany, NJ). The cannula was attached to a 1.0-ml tuberculin reservoir syringe via an 18-gauge hypodermic needle and three-way stopcock (model K75, Pharmaseal). The cannula was tied in place with double ligatures just above the bifurcation of the bronchi; this eliminated the trachea itself from study. The trachea was severed rostral to the cannula, then the lungs were separated from their vascular attachments and from the esophagus. Throughout this time the lungs were kept warm and moist by frequent washes with Krebs-Henseleit saline at 37°C. The lungs, with the heart still attached, were transferred to fresh saline, and the heart was removed. The preparations were then suspended in 100-ml baths of Krebs-Henseleit saline at 37°C, oxygenated, and maintained at pH 7.4 with 95% O2-5% CO2. In all studies of catecholamines, the baths were protected from light with aluminum foil. It was important to set up the preparations rapidly (within 3-4 min). Approximately 0.35 ml of lung liquid was withdrawn into the reservoir syringe, and a 10-µl sample was taken from the upper cup of the stopcock with a gastight fixed-volume syringe (model 1701 NCH, Hamilton, Reno, NV); this was a blank for spectrophotometry. One hundred microliters of blue dextran 2000 (50 mg/ml in 0.9% NaCl) were added to the fluid remaining in the syringe and thoroughly mixed in, and the mixture was passed into the lungs. The preparations equilibrated for 30 min, and ~0.3 ml of lung fluid was withdrawn and returned every 5 min throughout this period to ensure an even distribution of dye throughout the lungs.
After equilibration, experiments continued for 3 h. During this time,
fluid was withdrawn every 10 min, and 10-µl samples were removed as
described above. Fluid was also withdrawn and returned to the lungs
midway between sampling; this ensured proper mixing within the lungs.
Mixing was also aided by the gentle but continuous movements of the
lungs in the bubbled saline. Samples were placed in polyethylene micro
test tubes (250-µl Eppendorf C3515-7, Brinkman Instruments,
Rexdale, ON, Canada), diluted 1:20 with distilled water, sealed, and
vortexed (Vortex-Genie, Fisher Scientific). Samples were then
centrifuged at 250 g for 10 min (clinical centrifuge, model CL, International Equipment, Needham Heights, MA). The supernatants were analyzed for blue dextran by
spectrophotometer (model 250, Gilford, Oberlin, OH or model DU-8,
Beckman Instruments, Mississauga, ON, Canada); spectrophotometry utilized 250-µl quartz microcells (type 10972, NSG Precision Cells, Farmington, NY; wavelength = 620 nm). The experiments followed an ABA
design (control-treatment-control). Samples taken during the 1st h after equilibration gave the resting rate of fluid
production. The lungs, still attached to their reservoir syringe, were
then transferred to fresh Krebs-Henseleit saline, which contained one of the following: 1) epinephrine at
108,
107,
106, or
105 M (Adrenalin,
Parke-Davis, Scarborough, ON, Canada);
2)
107 M epinephrine with
106 M propranolol;
3)
106 M propranolol alone;
4)
107 M epinephrine with
106 M phentolamine;
5)
106 M phentolamine alone;
6)
107 M epinephrine with
105 M prazosin;
7)
105 M epinephrine with
105 prazosin;
8)
105 prazosin alone;
9)
107 M epinephrine with
104 M yohimbine;
10)
105 M epinephrine with
104 M yohimbine;
11)
104 M yohimbine alone; and
12) Krebs-Henseleit saline with no
drugs (untreated controls; these preparations received changes of
saline on each hour, as for experimental preparations). All agents were in the form of their hydrochlorides; all drugs were from Sigma Chemical
(St. Louis, MO). Concentrations of antagonists were based on the work
of Sheppard and Burghardt (26), Starke et al. (27), Dobbs and Mason
(9), Han et al. (12), and Takayanagi et al. (30). In all experiments,
the preparations were returned to Krebs-Henseleit saline for the final
hour.
Quantification of Results and Statistical Methods
The rates of fluid production were calculated from the fall in concentration of blue dextran, as described previously (6, 25). Rates were estimated from plots of the total volume of fluid against time, with readings recorded every 10 min; the total volume of fluid was the sum of that within the lungs and that removed for study. Appropriate sequential adjustments were made every 10 min for the removal of fluid and dextran during incubation. The rates of production of fluid over 1-h intervals were calculated from the volume plots, using the slopes of their regressions, fitted by the method of least squares (28) (Hewlett-Packard program SD-O3A or Apple II Plus computer). In groups of similar experiments, differences in rates in successive hours were analyzed by analysis of variance (ANOVA) and Newman-Keuls test (33). When plots from similar experiments were combined, the volumes were expressed as a percentage of the volume present at the end of the 1st h, just before transfer to test solutions or fresh saline; the values were then averaged (6, 24, 25). The significance of changes in rate was also assessed from the combined graphs by submitting the changes in slope to a test for differences between two regressions (regression analysis) (6, 25); this test utilized all values for volumes from all experiments in the group. Although ANOVA and regression analysis considered the magnitude of the changes seen, ANOVA took into consideration the repeatability of the responses, and regression analysis allowed for scatter around the lines of best fit, a variability not included in ANOVA. All mean values are given with their standard errors, unless otherwise stated. Statistical significance was accepted at or below P < 0.05.| |
RESULTS |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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Effect of Epinephrine on Lung Liquid Production
Studies were carried out on 30 fetuses of 61 ± 2 days of gestation and 80.7 ± 12.8 (SD) g body wt. Results are shown in Fig. 1. Untreated controls produced fluid with no significant change (Fig. 1A; n = 6). All preparations treated with 108 M epinephrine during
the middle hour showed significantly reduced production during
treatment (P < 0.001-0.0005;
ANOVA, regression analysis), and one showed reabsorption (74.8 ± 11.7% reduction; Fig. 1B;
n = 6). In those treated with
107 M epinephrine,
production was reduced, and two turned to reabsorption (P < 0.001-0.0005, ANOVA,
regression analysis; 91.6 ± 9.8% reduction; Fig.
1C; n = 6). In contrast, preparations treated with epinephrine above
physiological levels (106 M
and 105 M) showed no
significant change (same tests; Fig. 1,
D and
E). This establishes the
disappearance of responses at high concentrations of epinephrine.
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Effects of General - and
-Adrenoreceptor Antagonists on Maximal Responses to
Epinephrine (107 M)
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The significant reductions in fluid production by
107 M epinephrine (Fig.
2A; n = 6; 2 reabsorptions) were not abolished by incubation with the
-antagonist propranolol
(106 M; Fig.
2B; n = 6; 1 reabsorption). ANOVA showed no significant differences in
responses with or without propranolol. Preparations treated with
106 M propranolol alone and
untreated controls showed no significant changes (ANOVA, regression
analysis; Fig. 2, C and
D; n = 6). There was no evidence for -receptor activation. In contrast, the effects of 107 M
epinephrine (Fig. 3A;
n = 6) were abolished by the
-antagonist phentolamine
(106 M; Fig.
3B; n = 6). Preparations treated with
106 M phentolamine alone
and untreated controls showed no significant changes (ANOVA, regression
analysis; Fig. 3, C and
D; n = 6). Therefore, -receptor blockade appeared to eliminate responses to epinephrine.
The data suggest that epinephrine reduces lung liquid production in
fetal guinea pigs by activation of -, not -, receptors.
Effects of 1- and
2-Adrenoreceptor Antagonists
on Maximal Responses to 107 M
Epinephrine
-receptor antagonists.
1-Receptor blockade by
prazosin.
Studies were carried out on 24 fetuses of 60 ± 2 days of gestation
and 79.4 ± 18.4 (SD) g body wt. Results are shown in Fig. 4. The significant reductions in fluid
production produced by 107
M epinephrine (Fig. 4A;
n = 6; 2 reabsorptions) were not
blocked by the 1-antagonist
prazosin (105 M; Fig.
4B; n = 6; 1 reabsorption). ANOVA showed no significant differences in
responses with or without prazosin. Preparations treated with
105 M prazosin alone and
untreated controls showed no significant changes (ANOVA, regression
analysis; Fig. 4, C and
D; n = 6). Therefore, there was no evidence for
1-receptor activation by 107 M epinephrine.
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2-Receptor blockade by
yohimbine.
Studies were carried out on 24 fetuses of 60 ± 2 days of gestation
and 80.5 ± 13.5 (SD) g body wt. Results are shown in Fig. 5. The marked reductions in fluid
production produced by 107
M epinephrine (Fig. 5A;
n = 6) were completely abolished by
the 2-antagonist yohimbine
(104 M; Fig.
5B, n = 6); in fact, a small but nonsignificant increase in production was
seen (see below). Preparations treated with 104 M yohimbine alone and
untreated controls showed no significant changes (ANOVA, regression
analysis; Fig. 5, C and
D; n = 6). Yohimbine appeared to be an effective antagonist of the effects of epinephrine; therefore, activation appeared to be through the 2-adrenoreceptor in the guinea
pig.
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Effects of 1- and
2-Adrenoreceptor Antagonists
on Responses to High Concentrations of Epinephrine
(105 M)
1-Blockade by prazosin.
Studies were based on 24 fetuses of 60 ± 1 day of gestation and
75.4 ± 11.3 (SD) g body wt, and the results are given in Fig. 6. As shown earlier,
105 M epinephrine was
without effect (Fig. 6A;
n = 6), but in the presence of the
1-antagonist prazosin
(105 M) there were strong
and significant declines in production
(P < 0.005-0.0005; ANOVA,
regression analysis), and two preparations showed reabsorption (Fig.
6B; n = 6). Preparations treated with 105 M prazosin alone and
untreated controls showed no significant changes (same tests; Fig. 6,
C and
D; n = 6). Therefore, blockade of
1-receptors appeared to allow
high concentrations of epinephrine to reduce fluid production or cause
reabsorption, as at lower concentrations of the hormone.
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2-Blockade by yohimbine.
Studies were based on 24 fetuses of 61 ± 2 days of gestation and
81.9 ± 14.2 (SD) g body wt. Results are shown in Fig.
7. As shown previously,
105 M epinephrine was
without effect (Fig. 7A;
n = 6), but in the presence of the
2-receptor antagonist yohimbine
(104 M) it produced
significant increases in fluid production in every experiment
(P < 0.05-0.025; ANOVA,
regression analysis; Fig. 7B, n = 6). Preparations treated with
104 M yohimbine alone and
untreated controls showed no significant changes (same tests; Fig. 7,
C and
D; n = 6). It appeared that blockade of
2-receptors allowed high
concentrations of epinephrine to activate
1-receptors and increase fluid
production.
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1- and
2-adrenoreceptors: stimulation of 1-receptors can increase
fluid production, whereas activation of
2-receptors can inhibit it; the
final result is no apparent change.
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DISCUSSION |
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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The results presented here show that
108 and
107 M epinephrine
reduce lung liquid production or produce reabsorption in in vitro lungs
from fetal guinea pigs (P < 0.001-0.0005) but are ineffective at high, unphysiological
concentrations (106 and
105 M). Responses at the
most effective concentration
(107 M) appeared to be
through -adrenoreceptors, since the general -receptor antagonist
phentolamine abolished responses, but the general -adrenoreceptor
antagonist propranolol was without effect. This was confirmed by use of
more specific blockers. The
2-antagonist yohimbine
eliminated responses to 107
M epinephrine, but the
1-antagonist prazosin was
without effect; therefore, activation appeared to be through
2-adrenoreceptors. At high,
ineffective concentrations of epinephrine
(105 M), responses could be
produced if these antagonists were used together with the hormone. In
the presence of prazosin, the inhibition of fluid production seen at
lower concentrations of epinephrine reappeared; in the presence of
yohimbine, production of fluid was stimulated. This suggests that the
disappearance of responses at high, unphysiological concentrations of
epinephrine was the result of two opposing processes:
1) reduction of production by activation of 2-adrenoreceptors
(as at lower concentrations) and 2)
simultaneous increases of production through activation of
1-adrenoreceptors.
The ability of 108 and
107 M epinephrine to reduce
lung liquid production or produce reabsorption is in agreement with
earlier work on fetal sheep and goats and with studies of
catecholamine-related drugs in fetal rabbits (4, 17, 24, 31). The
effect is generally considered physiological, since it occurs at
plasma levels seen at birth, but it is unlikely to be long lasting,
since it reverses readily after infusion (4). In general, the situation is similar in the in vitro preparations studied here.
The antagonist studies reported here utilized
107 M epinephrine, rather
than 108 M epinephrine used
in our pilot experiments. These two concentrations span the probable
levels in fetal plasma during delivery. In sheep, plasma levels reach
3.8 × 108 M in the
early neonate (4), and after normal vaginal deliveries in humans the
average plasma level in the umbilical artery is 1.0 ± 2.0 × 108 M, with some values as
high as 6.1 × 108 M
(based on 13 independent studies, adapted from Refs. 20 and 22). Values
during delivery are not known in fetal guinea pigs, but during asphyxia
concentrations in these fetuses are
~107 M, with some
measurements as high as 1.4 × 107 M (14). Therefore,
107 M epinephrine probably
represents the upper limit of physiological concentrations. Because
107 M epinephrine produced
maximal effects on lung liquid production, this concentration seemed
appropriate for this more extended study of antagonists. Nevertheless,
the effects of propranolol and phentolamine were the same at
108 M epinephrine used in
pilot studies and at 107 M
epinephrine reported here.
The activation of -adrenoreceptors was entirely unexpected. Although
only a limited number of species have been investigated, studies with
epinephrine, propranolol, and various catecholamine-related drugs have
suggested that fluid reabsorption depends on -activation in sheep,
rabbits, and rats (8, 11, 16, 31, 32). However, norepinephrine is known
to be capable of reducing production through -adrenoreceptors in
fetal sheep (13), and failure of various -receptor antagonists to
prevent clearance of fluid at delivery in sheep and rabbits showed that
mechanisms outside the -receptor system must exist (8, 19).
The work reported here suggests that species differences may be
important.
The work with the more specific -antagonists supported these
conclusions. Although there is some overlap, prazosin is far more
potent at inhibiting
1-receptors and yohimbine is
more potent at blocking
2-receptors; in fact, this has
been the basis for -receptor classification (5). Therefore, the
results given here suggested that the
2-adrenoreceptor was involved
in fluid reabsorption, and the
1-receptor had no influence at
physiological levels of epinephrine.
2-Receptors are known to exist
in guinea pig lungs, at least in airways, where they predominate (30). In general, these receptors mediate their effects through
Gi protein and the adenyl cyclase
system (5), and this system is known to influence fluid reabsorption
(15). However, there is a problem. Adenosine 3
,5-cyclic
monophosphate (cAMP) stimulates reabsorption (15), but the usual action
of the 2-receptor is to
inhibit, not stimulate, release of cAMP (5). Therefore, it is possible that the receptor is acting through its other effects, such as modulation of ion channels (5). However, there is a more interesting possibility. The 2-receptor
might act through the usual adenyl cyclase system, but to stimulate its
activity. Although not the general rule, this has been seen in a number
of tissues from different species (23). Therefore, it may be
particularly significant that epinephrine has been shown to generate
cAMP through -receptor activation in the lungs of adult guinea pigs,
an action blocked by phentolamine (23). In addition, generation of cAMP
through 2-receptor activation
has been seen in isolated tracheal cells from rabbits, so such
mechanisms are not unreasonable in the pulmonary system (18). The final
response is also reasonable. Activation of
2-receptors has been shown to
produce reabsorption of Na+ and
Cl in the intestine, and
the lungs, like the intestines, are modifications of the alimentary
tract (7, 10).
The work also suggested that
1-receptors could have effects,
but to stimulate secretion, and only at high, unphysiological concentrations of epinephrine. Again,
1-receptors have been
demonstrated in the lungs and trachea of guinea pigs, but in lower
numbers than 2-receptors (1,
30). In other tissues,
1-receptors act through the
polyinositol system and elevate intracellular Ca2+ (5, 12). However, the
mechanisms used here and the way in which fluid production is increased
are not clear. Perhaps the most remarkable aspect was the consistency
of the responses, since factors that consistently raise fluid
production have been difficult to find (21). However, the opposing
effects of 1-receptors, which
stimulate fluid production, and
2-receptors, which inhibit it,
can explain the unusual disappearance of effects of epinephrine at high
unphysiological concentrations. At this time, stimulation of production
must be regarded as an interesting pharmacological effect; however,
there must be some reservation, since there was also an increase in
production at physiological levels of epinephrine, although this
increase could not be shown to be statistically significant.
Nevertheless, this study shows more clearly than most that stimulation
of production is a possibility.
It must be remembered that any in vitro method, whether by tissue culture or isolated organ, is never entirely physiological and needs to be extended to the intact animal. Nevertheless, this in vitro model gives a good basis for further investigation and has many assets. It allows elimination of external influences, such as reflexes, and a reduction in the variables in a complex situation, such as elimination of vascular and colloid osmotic effects. It allows the use of hormones and antagonists at precise concentrations, uninfluenced by placental destruction or loss, and the use of agents that are toxic or have widespread effects in the whole animal. These factors were an asset here. The results suggest that there can be species differences in the mechanisms that help drain the lungs at birth, so those that operate in the human may be more complex than we believe.
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ACKNOWLEDGEMENTS |
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We thank the Dept. of Zoology for financial assistance and the National Research Council of Canada for Operating Grant NSERC-582584 (A. M. Perks).
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FOOTNOTES |
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Address for reprint requests: A. M. Perks, Dept. of Zoology, University of British Columbia, 6270 University Bl., Vancouver, BC, Canada V6T 1Z4.
Received 13 November 1996; accepted in final form 29 October 1997.
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Top
Abstract
Introduction
Materials & Methods
Results
Discussion
References
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