AMER. ZOOL., 37:12-22 (1997)
The Role of Cardiac Shunts in the Regulation of Arterial Blood Gases1
TOBIAS WANG*, EGLE H. KROSNIUNASI , AND JAMES W. HICKS|
*Institute of Biology, University of Odense, DK-5230 Odense M, Denmark
^Department of Ecology and Evolutionary Biology,
University of California at Irvine, Irvine CA 92717, USA
The pulmonary and systemic circulations are not completely separated in reptiles and amphibians, so oxygen-rich blood returning from the
lungs can mix with oxygen-poor blood returning from the systemic circuit
(cardiac shunts). In these animals, the arterial blood gas composition is determined by both lung ventilation and the cardiac shunt. Therefore, changes
in cardiac shunting patterns may participate actively in the regulation of arterial blood gases. In turtles the cardiac shunt pattern changes independently
of ventilation and the cardiac R-L shunt (pulmonary bypass of systemic venous blood) is reduced under circumstances where the demands on efficient
gas exchange are high (hypoxia, hypoxemia or exercise). We propose, therefore, that the size of cardiac shunts is regulated independently of ventilation
and hypothesize that there exist at least two groups of peripheral chemoreceptors with different reflex roles.
SYNOPSIS.
arterial systemic blood is a mixture of systemic venous blood and blood returning
from the lungs. Arterial blood gas composition therefore is determined by both lung
gases and the degree of admixture. This is
in contrast to mammals and birds, where arterial blood gases closely resemble those
within the lung and can be regulated exclusively by means of ventilation. The main focus of this chapter is to discuss the possible
role of cardiac shunts on arterial blood gas
regulation. Following a brief review of the
anatomical basis for cardiac shunts and their
effects on blood gases, we will discuss the
possible neural regulations of blood flows.
Although most of this chapter is based on
our own recent data on turtles, we will, albeit selectively, draw comparisons to previous studies on other reptiles and amphibians.
INTRODUCTION
The pulmonary and systemic circulations
of reptiles, amphibians and many airbreathing fish are not completely separated,
and blood flows to the lungs and body can
be altered independently (e.g., Johansen and
Burggren, 1980). As a result, systemic venous blood returning from the body can bypass the pulmonary circulation (right-to-left
shunt), whereas blood returning from the
lungs can recirculate into the pulmonary circulation (left-to-right shunt). Although the
functional significance of this cardiovascular design remains largely unknown (c/.,
Burggren, 1987; Hicks and Wang, 1996),
numerous studies attest that the blood flows
change in a predictable fashion. In particular, large increases in pulmonary blood flow
during ventilation have been characterized
for many different species (e.g., Johansen et
al., 1970; Shelton, 1970; Shelton and Burggren, 1976; West et al., 1992; Wang and
Hicks, 1996a). The underlying control of
these changes is not well understood.
In the presence of central vascular shunts,
THE ANATOMICAL BASIS FOR CARDIAC
SHUNTS IN NON-CROCODILIAN REPTILES
In all non-crocodilian reptiles (and amphibians), central vascular shunts result
from the incomplete anatomical separation
of the pulmonary and systemic circuits
within the ventricle of the heart. These
shunts are consequently referred to as cardiac shunts. The cardiac shunts can be de-
1
From the Symposium Control of Arterial Blood
Gases: Cardiovascular and Ventilatory Perspectives
presented at the Annual Meeting of the Society for Integrative and Comparative Biology, 26-30 December
1995, at Washington, D.C.
12
13
CARDIAC SHUNTS
Pressure
Shunts
"Ill
Washout
Shunts
* Deoxy
II
Systole
FIG. 1. The basic features of the pressure and washout hypotheses for Right-to-Left cardiac shunts in reptiles
(RA,, right atrium; LA,, left atrium; CP, cavum pulmonale; CA, cavum arteriosum; CV, cavum venosum; LAO,
left aortic arch; RAO, right aortic arch; PA, pulmonary artery). See text for further explanation. Modified from
Hicks and Malvin (1995).
fined as right-to-left cardiac shunt (R-L
shunt) and left-to-right cardiac shunt (L-R
shunt), where R-L shunt refers to systemic
blood that bypasses the lungs and L-R shunt
refers to pulmonary venous blood that reenters the pulmonary circulation.
Two dominating hypotheses {pressure
shunt and washout shunt) have been advanced to explain the mechanisms of cardiac shunts in non-crocodilian reptiles.
These hypotheses differ regarding the intraventricular flow patterns during systole
(Heisler and Glass, 1985; Hicks and
Malvin, 1995; Fig. 1). The ventricle is divided into two main chambers (the cavum
pulmonale and a larger dorso-lateral chamber, the cavum dorsale) by a septum-like
structure called the muscular ridge. In most
species, the cavum dorsale is further subdivided into the cavum arteriosum and
the cavum venosum. The pulmonary artery emerges from the cavum pulmonale,
whereas the two aortic arches arise from the
cavum venosum. During diastole, O2 poor
blood from the right atrium enters the cavum venosum and flows to the cavum pulmonale, while O2 rich blood enters the cavum arteriosum directly from the left
atrium. During systole, blood is ejected into
the systemic arteries from the cavum venosum and into the pulmonary arteries from
the cavum pulmonale. The washout hypothesis proposes that the muscular ridge effectively separates the cavum pulmonale
and the cavum venosum at the onset of systole and that the R-L shunt results from the
O 2 poor blood residing in the cavum venosum at the end of diastole. Similarly, the O2
rich blood remaining in the cavum venosum
following systole is washed into the cavum
pulmonale during diastole account for the
L-R shunt. The pressure shunt hypothesis
proposes that the muscular ridge does not
separate the cavum pulmonale and the
14
T. WANG ET AL.
cavum venosum during systole. According
to this view, blood will flow between these
cava if differences exist in the outflow resistances.
The washout shunt hypothesis and the
pressure shunt hypothesis are not mutually
exclusive. Rather, the extent to which one
or the other mechanism can account for the
shunt depends on when the muscular ridge
separates the cavum pulmonale and the cavum venosum during systole. The respective contribution of these two types of
shunts probably varies greatly among species. In the turtle Trachemys scripta, both
pressure and washout shunts contribute, but
because the muscular ridge is poorly developed, most of the shunt is due to pressure
shunting (Hicks et al., 1996). In contrast,
the muscular ridge is well developed in
Varanus and the cavum pulmonale and the
cavum venosum are separated early in systole. Most of the shunt in Varanus can accordingly be ascribed to washout shunt (Heisler et al., 1983; Heisler and Glass, 1985).
To date, the mechanism of shunting remains
largely undescribed for other reptilian genera.
Regulation of cardiac shunts presumably
differs according to the underlying mechanism. In animals with a prominent washout
shunt, the degree of shunting is largely
changed through changes in end-diastolic
and end-systolic volumes of the ventricular
chambers. Whether these volumes indeed
are under active control remains to be experimentally verified. In Varanus niloticus
the size of cardiac shunt does not change
during hypoxia, hypercapnia or prolonged
diving (Millard and Johansen, 1974) suggesting that the washout shunt is not actively regulated. In animals with a dominating pressure shunt, the net direction and
magnitude of the shunt flow is affected by
the resistance of the pulmonary circuit relative to that of the systemic circulation, and
an active regulation of pulmonary arterial
resistance is well documented (Johansen
and Burggren, 1980; Hicks, 1994). In turtles
and lizards, contraction or dilation of
smooth muscle in the extrinsic pulmonary
artery alters pulmonary arterial resistance
(RpUl) (Burggren, 1977a; Milsom et al.,
1977; Berger, 1973), whereas in snakes the
primary site of the resistance appears to be
at a narrow region of the ventricular outflow
tract of the pulmonary artery (Burggren,
19776; Smith and Maclntyre, 1979; Lillywhite and Donald, 1994). In addition,
smooth muscle within the lung may regulate Rpul in snakes (Lillywhite and Donald,
1994), but the contribution at this site appears to be small in lizards and turtles.
In all reptiles studied, the regulation of
pulmonary resistance and, thus, pulmonary
blood flow (Qpul) is controlled by the vagus nerve. Electrical stimulation of the efferent vagus or intravenous infusions of
acetylcholine increase Rpul and reduce heart
rate, and these changes are abolished following administration of atropine (Burggren, 1977a; Comeau and Hicks, 1994;
Hicks and Comeau, 1994). The central vascular blood flows are also controlled adrenergically. In turtles, intravenous injection of
epinephrine elicits a tachycardia, a reduction in Rpu, and a L-R shunt (Comeau and
Hicks, 1994). Electrical stimulation of vagal afferents results in similar cardiovascular changes that are blocked by administration of bretylium (Comeau and Hicks,
1994), suggesting that the cardiovascular
changes, often associated with brief periods of ventilation, may have an adrenergic component. Finally, non-adrenergicnon-cholinergic factors seem to be involved
in regulating systemic and pulmonary vascular resistances and may influence cardiac
shunt patterns (Lillywhite and Donald,
1994).
THE IMPACT OF CARDIAC RIGHT-TO-LEFT
SHUNT ON ARTERIAL OXYGEN LEVELS
In the presence of cardiac shunts, the
blood gases of systemic arterial and pulmonary arterial blood are different from the venous blood entering the heart from the pulmonary and systemic circulations. Specifically, L-R shunt elevates the O2 content of
pulmonary arterial blood relative to systemic venous blood, and R-L shunt reduces
the O 2 content of the systemic arterial blood
relative to that entering the heart from the
lung. With the exception of alligators and
crocodiles, R-L and L-R shunt normally occur simultaneously (Hicks, 1994). Nevertheless, because L-R shunt only influences
CARDIAC SHUNTS
15
the blood gas composition of pulmonary arterial blood, only R-L shunt needs to be
considered to evaluate the impact of cardiac
shunts on systemic arterial blood gases.
The reduction in O 2 content caused by
R-L shunt takes place in the equivalent of a
closed system. Arterial PO2 therefore becomes a dependent variable determined by
the resulting arterial HbO2 saturation (O2
content relative to blood O2 carrying capacity) and blood O2 affinity (Wood, 1984).
The impact of R-L shunt on arterial O2 content ([O2]a) can be quantified as the
weighted mean of the O2 content of pulmonary venous and systemic venous blood
([O2]pv and [O2]sv, respectively):
tive to blood oxygen affinity (i.e., P o of the
blood leaving the lung is positioned at the
flat portion of the oxygen dissociation
curve), because increased ventilation, in
that case, only causes a small increases in
O 2 content of blood leaving the lung. Therefore, the cardiorespiratory response that secures O2 delivery seemingly depends on the
conditions of O2 loading in the lungs. For
example, both increased ventilation and reduced R-L shunt improve O2 delivery during hypoxia, but during anemia (reduced
O 2 carrying capacity of the blood) a reduction in R-L shunt is more effective than ventilatory changes in maintaining O2 delivery
(Wang and Hicks, 1996ft).
[OJ« = (QPu. X [O2]pv + QR_L
X [O2]sv)/(Qpul + QR_L),
RECEPTORS FEED-BACK REGULATING
BLOOD FLOWS AND CARDIAC SHUNT
(1)
where Qpul is pulmonary blood flow and
QR-L denotes the R-L shunt blood flow
(Qpui + QR-L = Qsys)- Thus, in the presence
of R-L shunt, arterial P o is a composite
variable depending on any factor that influences O2 content of either pulmonary or
systemic venous blood or the O2 affinity of
the blood (Wood, 1984; Wang and Hicks,
1996ft). Arterial blood gases in reptiles
therefore can change independently of lung
PO2. For example, if systemic oxygen extraction increases (e.g., during increased
metabolic rate) at a constant cardiac R-L
shunt, arterial POz will decrease even if ventilation is matched to metabolic rate. In this
case lung P o would not change, and the reduction in arterial PO2 could not be predicted
from measurements of ventilation or endtidal gas composition. This is never the case
in healthy mammals.
The effects of R-L shunt on arterial
PO2 can be quantified theoretically using
the two-compartment model (e.g., Wood,
1984). Recently, we used this model to
evaluate the impact of increasing ventilation
or eliminating R-L shunt on arterial P o
(Wang and Hicks, 1996ft). Based on published values for ventilation, oxygen uptake,
and degree of R-L shunt, we found that
changes in the R-L shunt are as important
as realistic changes in ventilation in determining arterial P o in turtles (Wang and
Hicks, 1996ft). The relative effect of R-L
shunt is largest when lung P o is high rela-
The cardiovascular system is regulated, in
part, by a number of chemo- and mechanoreceptors. In mammals, the majority of afferent input from these receptors projects to
the nucleus of the tractus solitarius of the
medulla, but the final integration of receptor feedback involves multiple brain centers
with interaction of afferent input from different receptor groups (Daly, 1983; Dampney, 1994; Marshall, 1994). The anatomical
structures and the physiological basis responsible for the integration of afferent receptor feed-back have not been investigated
in reptiles or amphibians.
Trigeminal, nasal and upper airway
receptors
Stimulation of trigeminal receptors of the
face and receptors in the upper airways
evokes bradycardia and systemic vasoconstriction in most mammals and birds (Butler and Jones, 1982), but the role of these
receptors is not well known in reptiles or
amphibians. During forced dives in snakes,
bradycardia only develops if the nose is wet
(Johansen, 1959; Murdaugh and Jackson,
1962), and immersion may be important for
the development of bradycardia in alligators
(Andersen, 1962). Nevertheless, in turtles
the bradycardia and the increase in R-L
shunt associated with breath hold develops
regardless of whether or not the face is immersed (Burggren, 1975; T. Wang unpublished). However, these observations do not
16
T. WANG ET AL.
exclude the possibility that these receptors
participate in the regulation of QpuJ and/or
cardiac shunts. The CO2 sensitive chemoreceptors located in the upper airways
and/or lungs of most amphibians and reptiles are important for ventilatory control,
but their effect on the cardiovascular system has not been investigated.
Pulmonary stretch receptors (PSR)
As in other air-breathing vertebrates, reptiles and amphibians possess pulmonary
stretch receptors (PSR) that convey information regarding lung pressure and volume
to the central nervous system (Milsom,
1997). Stimulation of PSR during breathing
could provide a stimulus to increase Qpu,
and heart rate, but the contribution of PSRs
to the cardiorespiratory interactions is not
resolved (see West and Van Vliet [1992] for
a review on amphibians). In turtles, artificial tidal ventilations via a chronically implanted lung catheter elicited increases in
heart rate and Qpul that closely resembled
those occurring during voluntary breathing
(Johansen et al., 1978). We have, however,
not been able to reproduce this response in
the turtle, Trachemys scripta (Wang and
Hicks, unpublished). In our experiments,
turtles were equipped with blood flow
probes (Transonic, 2R) around the left aortic arch and the left pulmonary artery. In addition, a catheter (PE 160) was placed in
each lung and connected to a T-piece allowing simultaneous inflation or deflation of
both lungs and measurements of lung pressure. Three to ten days after surgery, the
turtles were placed in an experimental
set-up in which they could dive freely but
were constrained to breathe in a small funnel connected to a pneumotachograph for
measurements of ventilation. Figure 2
shows the pronounced increase in Qpul during ventilation and that withdrawal of lung
gas (marked as A and C) and injection of
air into the lungs (B) did not affect Qpul. In
all experiments (n = 5), artificial manipulation of lung volume/pressure had absolutely no effect on blood flows or heart rate.
In several instances, manipulations of lung
volume initiated breathing which was associated with the normal increase in Qpul during voluntary ventilation. Johansen et al.
(1978) did not measure ventilation, so the
manipulation of lung volume in their experiments may also have elicited voluntary
breathing, which could explain the observed
changes in blood flows.
Given the conflicting results obtained in
different studies, it is difficult to construct
a simple model to explain the role of PSR's
in the regulation of central vascular blood
flows. Our experiments on turtles described
above indicate that afferent input arising
from PSRs alone is not sufficient to elicit
cardiovascular changes. Increase in Qpul
during ventilation may therefore be due to
a feed-forward mechanism acting simultaneously on both the respiratory and vagal
motor neurons (see also, West et al., 1992).
This hypothesis does not preclude the possibility that PSRs contribute to the final expression of the cardio-respiratory interactions.
Effects of altering blood Po2 and O2
content: Possible roles of peripheral
chemoreceptors
Because many reptiles and amphibians
display pronounced cardiorespiratory interactions (tachycardia, increased Q pu | and a
reduction in R-L shunt during breathing),
distinguishing the direct effects of a given
stimulus on the cardiovascular performance
from a secondary effect arising from
changes in ventilation is difficult. For example, during hypoxia, an increase in mean
Qpui is to be expected, simply because the
animal spends more time breathing. Indeed,
in three species of turtles (Testudo pardalis, Pelomedusa subrufa and Chelonia mydas), mean Q pu | increases during hypoxia,
but the attained flows resemble those occurring during ventilation (Burggren et al.,
1977; West et al., 1992). It may, therefore,
be more informative to describe the cardiovascular parameters during a defined period
of either ventilation or breath hold. Figure
3 shows Qpul and Q sys during breath hold
(longer than 180 sec) or a ventilatory period (2—4 breaths) at four levels of inspired
oxygen fractions (FjO2) in six turtles. At any
given F ; o 2 , Qpu) is higher during ventilation
than during breath hold, which reflects the
cardiorespiratory interaction. However, the
blood flows during breath holds or ventilatory periods were not affected by hypoxia
per se. Therefore, although mean blood
CARDIAC SHUNTS
17
1 minute
FIG. 2. The effect of manipulating lung volume and pressure (P|ung) on pulmonary (Qpul; 2 X QLPA) and left
aortic blood (QLAo) flows in a 1.3 kg turtle. At the marked events lung gas was withdrawn (A and C) or air was
injected (B) through catheters placed in the lungs (T. Wang and J. W. Hicks, unpublished).
flows and heart rate were elevated during
hypoxia (data not shown), no selective effect of hypoxia on the cardiovascular system is indicated.
Based on the theoretical prediction that a
reduction in cardiac R-L shunt is particu-
larly beneficial for gas exchange when
blood O 2 carrying capacity is reduced
(Wang and Hicks, 1996a), we investigated
the effect of experimental reductions in
haematocrit on blood flows in turtles. Figure 4 show QpU), Q sys and the net shunt flow
18
T. WANG ET AL.
VP (2-4 breaths)
NVP> 180 sec
120
1
c
pul
(ml
E
o
E
1^
100
80
60
40
20
0
140
120
100
80
60
40
20
0
0.05 0.10 0.15 0.20
0.05 0.10 0.15 0.20
FIG. 3. Pulmonary and systemic blood flows (Qpu! and Qsys) in six turtles at normoxia and during inhalation of
three different hypoxic gas mixtures at 25°C. Turtles were instrumented with a flow probes around the left pulmonary artery (Q pu | = 2 X QLPA) and flow probes around the left aortic arch (LAo), the right branch of the
right aortic arch (RRAo) and a probe around the right subclavian and carotid arteries (Rsub and Rca) for calculation of Q sys (Qsys = Q LAo + QR
QRC»)- Each data point represents a mean value for an
individual turtle during non-ventilatory periods (NVP) lasting longer than 180 second and during ventilatory
periods (VP) consisting of 2-4 breaths. Note that several animals did not exhibit any long lasting non-ventilatory
periods during severe hypoxia (T. Wang and J. W. Hicks, unpublished).
(Qpui ~~ Qsys) during breath holds and ventilation as a function of haematocrit. In anemic turtles, Qpu| remained high during
breath holding, whereas Q sys was not affected by reductions of haematocrit. As a result, the net R-L shunt which normally prevails during breath hold is greatly reduced
in turtles with low blood O 2 content and
even reversed to a net L-R shunt in severely
anemic turtles (Figure 4). Because reductions in blood O2 content by inhalation of
CO or by nitrite (NaNO2) infusions elicit
similar responses (Wang et al., 1996), un-
intentional changes in blood volume are unlikely causes for the increase in Qpul. In
none of the experiments did the reduction
in blood O2 content affect ventilation or the
ventilatory response to hypoxia. Similarly,
reductions in blood O 2 content by bleeding
does not affect the hypoxic ventilatory response in toads, but elicits large increases
in heart rate (Wang et al., 1994).
The finding that blood O2 content appears
to alter Qpu, and net shunt flows in the absence of changes in P a o 2 could be explained
by the existence of an O 2 content sensitive
CARDIAC SHUNTS
19
NVP > 180 sec
VP (2-4 breaths)
'c
E
1
"5
CL
o
o
o
i
"E
o
1
U(
}
o
o
°o
6
o
0
c o
V)
•o
60
40
'c
20
E
0
-20
-40
-60
•O
-80
o
oo
\
o
o
o
^
o
%
u
o o
o
o
o
°o
o
o
1
0
1
i
i
1
5 10 15 20 25 30 0
Haematocrit
1
1
1
1
0
o1
5 10 15 20 25 30
Haematocrit
FIG. 4. Pulmonary and systemic blood flows in turtles with varying haematocrit during normoxia at 25°C (see
Figure 3 for calculation of blood flows). Each data point represents a mean value for an individual turtle during
non-ventilatory periods lasting (NVP) longer than 180 second and during ventilatory periods (VP) consisting of
2^4 breaths. Haematocrit was artificially reduced by bleeding and blood volume was maintained constant by
reinfusion of plasma and dextran. Linear regression are included when the correlation between haematocrit and
blood flow was a significant (P s 0.05) (T. Wang and J. W. Hicks, unpublished).
20
T. WANG ET AL.
Exercise
30 -
Rest
I air
30
submerged
20
Rest in
air
Submerged
rest
_L
a>
L-R shunt
10
0
R-L shunt
-10
- -20
- -30
FIG. 5. Net cardiac shunt (Qpu, - Qsys) during different types of voluntary behavior in Trachemys scripta (mean
± 1 s.e.m.; N = 7 - 12; Tb = 20 ± 2°C). All values were obtained for bouts of behavior one minute or longer
in duration (E. Krosniunas and J. W. Hicks, unpublished).
chemoreceptor that selectively influences
the cardiovascular system. In mammals, the
aortic bodies respond to changes in arterial
O 2 content and predominantly influence the
cardiovascular system {e.g., Lahiri et al.,
1981), while ventilatory responses are controlled by the Po2 sensitive carotid bodies.
The aortic bodies are believed to be sensitive to O 2 content because they are supplied
with a low perfusion relative to O 2 uptake.
This could also be the case in reptiles and
amphibians, but O2 content sensitive receptors have not been identified in these animals so far. In fact, the O 2 sensitivity of the
chemoreceptors in the carotid labyrinth in
toads is not affected by blood O 2 content,
indicating that Po2 rather than O 2 content
exerts the primary stimulus for these receptors (Van Vliet and West, 1992). Alternatively, the cardiovascular response to reductions in arterial O2 content can be explained
by the existence of Po 2 sensitive chemoreceptors in the venous circulation. Venous
O 2 levels (O 2 content and Po2) are determined by systemic O 2 delivery (Q sys * arterial O 2 content) relative to metabolic rate.
Therefore, if Qsys and metabolic rate remain
constant, a reduction of arterial O 2 content
will reduce venous PO2 and O 2 content. The
existence of chemoreceptors within the venous circulation has not been identified in
any vertebrate group. However, Ishii et al.
(1985) described O 2 sensitive chemorecep-
tors on the pulmonary artery in turtles. The
blood in this vessel is perfused predominantly by venous systemic blood, although
the exact composition depends on the level
of L-R shunt. Perhaps O2 sensitive chemoreceptors on the pulmonary artery are responsible for cardiovascular control while
the arterial chemoreceptors are responsible
for ventilatory control. Clearly this hypothesis needs to be verified experimentally
through direct recording of the peripheral
chemoreceptors to determine the exact receptor modalities, as well as by establishing the reflex roles of the different receptor
groups.
CARDIAC SHUNTS DURING EXERCISE AND
DIFFERENT TYPES OF BEHAVIOUR
In most animals, different types of behavior are associated with changes in central
vascular blood flows. For example, during
swimming and terrestrial locomotion, Qpul
increases 2-3 fold over resting values in
turtles (Shelton and Burggren, 1976; West
et al., 1992; Krosniunas and Hicks, 1995)
and similar changes have been reported in
frogs (Johansen et al., 1970). Recently,
Jones and Shelton (1993) showed that alligators eliminate the R-L shunt if disturbed.
Recently, Krosniunas and Hicks (1995)
assessed the effects of behavioral state on
blood flows Trachemys scripta. In these experiments, turtles were instrumented with
21
CARDIAC SHUNTS
flow probes and followed for several
months in an enriched laboratory setting.
There the animals performed a range of
spontaneous activities in either an aquatic or
terrestrial environment. The behavior was
divided into six categories: walking, rest in
air, rest in water, active diving (movement
into water from air), feeding and swimming.
The latter four types of behavior were operationally defined as those in which turtles
were completely submerged and therefore
unable to breathe. The cardiac shunt pattern
during voluntary behavior in turtles is primarily associated with activity level (Fig.
5). Activity leads to an increase in Qpu] and
reduction or elimination of the net R-L cardiac shunt, both in the presence or absence
of pulmonary ventilation. Longer bouts of
exercise, those lasting one minute or more,
resulted in the development of a net L-R
shunt, irrespective of submergence (Fig. 5).
These findings point to an independent
feed-forward regulation of blood flows, because Qpu, increased before or quickly after
the onset of exercise.
CONCLUSIONS
The cardiac shunt in amphibians and reptiles is actively regulated and has important
implications for arterial blood gas composition. The development of a comprehensive
model to explain blood gas control in these
animals must encompass both ventilatory
and cardiovascular control. The neural aspects of cardiovascular control is poorly understood, but cardiac shunt patterns appear
to be controlled by centrally generated feedforward mechanisms and feed-back from
peripheral receptors. Large interspecific differences apparently exist in the relative importance of the different receptors. In addition, the effects of some receptors are entirely unknown; for example the role of central chemoreceptors in cardiovascular
control has not been studied.
Based on studies to date, large net R-L
cardiac shunts in amphibians and reptiles
are only apparent at rest. When the demands
on gas exchange are increased (hypoxia,
hypoxemia, exercise) the R-L shunt is reduced and may be reversed to a net L-R
shunt. This pattern seems advantageous
with respect to the systemic O 2 delivery, as
elimination of R-L shunt increases arterial
O2 content.
ACKNOWLEDGEMENTS
We thank Drs. N. H. West, S. Reid and
E. W. Taylor for providing critical comments and numerous suggestions on an
early version of the manuscript. TW was
supported by a NSERC international post
doctoral fellowship and JWH was supported
by NSF (IBN-9218936).
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