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Division of Cardiology, The Milton S. Hershey Medical Center, The Pennsylvania State University, Hershey 17033; and Lebanon Veterans Affairs Medical Center, Lebanon, Pennsylvania 17042
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway. Effects of supplemental oxygen on forearm vasodilation in humans.
J. Appl. Physiol. 82(5):
1601-1606, 1997.
Supplemental O2 reduces cardiac output and
raises systemic vascular resistance in congestive heart failure. In
this study, 100% O2 was given to
normal subjects and peak forearm flow was measured. In
experiment 1, 100%
O2 reduced blood flow and
increased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml · min
1 · 100 ml1;
P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg · min · 100 ml · ml1;
P < 0.03). In
experiment 2, lower body negative
pressure (LBNP; 
30 mmHg) and venous congestion (VC) simulated
the high sympathetic tone and edema of congestive heart failure.
Postischemic forearm flow and resistance were measured under four
conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100%
O2+LBNP+VC. LBNP and VC did not
lower peak flow. However, O2
raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC,
P < 0.04). When O2 alone
(experiment 1) was compared with
O2+LBNP+VC
(experiment 2), no effect of LBNP+VC
on peak flow or minimum resistance was noted, although the return rate
of flow and resistance toward baseline was increased.
O2 reduces peak forearm flow even
in the presence of LBNP and VC.
vascular resistance; lower body negative pressure; venous
congestion
INTRODUCTION PREVIOUS WORK in normal subjects suggests that
supplemental O2 increases
peripheral vascular resistance (4, 6). This response, in part, seems to
be due to a reduction in cardiac output, which in turn is due to a
reduction in heart rate and stroke volume (4, 6). This effect is not
due to an increase in sympathetic drive because prior reports suggest
that supplemental O2 lowers or
does not change muscle sympathetic nerve activity in humans (8, 20).
These findings may be pathophysiologically important; a recent report
indicated that supplemental O2
lowered cardiac output and raised peripheral vascular resistance and
pulmonary capillary wedge pressure in patients with end-stage heart
failure (7).
In addition to potential cardiac effects of
O2, preliminary observations in
humans with left ventricular-assist devices suggest that, even when
cardiac output remains fixed, vascular resistance rises (7). This
suggests that hyperoxia may act as a peripheral vasoconstrictor.
However, there has been very little prior work in humans directly
examining the effects of supplemental
O2 on peripheral vascular
function. O2 can inactivate nitric
oxide (19) and also interfere with prostaglandin-mediated vasodilator
mechanisms (24); both systems may be operative in mediating peripheral dilator function in humans (2, 3, 5, 12).
In the present study, we had two goals. First, we wanted to examine the
effects of supplemental O2 on the
peak forearm reactive hyperemic blood flow (RHBF) response in normal
humans. The forearm RHBF response is independent of changes in cardiac
output (27) and is therefore a specific index of peripheral vascular
function. Accordingly, any effect of
O2 on the RHBF response would
provide support for the concept that
O2 has direct effects on the
peripheral vasculature.
Second, we wished to examine whether acute limb congestion and
heightened sympathetic tone would modify the vascular effects of
O2 on the peripheral circulation.
Peripheral edema and heightened sympathetic tone are commonly seen in
subjects with heart failure who receive supplemental
O2.
METHODS We performed 2 groups of experiments in 15 healthy adults. All subjects
were studied in our human investigation laboratory. Informed consent
was obtained from each subject before he or she was studied.
In experiment 1 [n = 8 (7 men and 1 woman); mean
age 26 ± 3 yr], we measured forearm blood flow and
vascular resistance (FVR) after 10 min of forearm circulatory arrest in
subjects breathing room air (RA) and after breathing 100% supplemental
O2 delivered for 15 min;
supplemental O2 was begun 5 min
before forearm circulatory arrest was begun. On the basis of results of
experiment 1, we performed
experiment 2 (n = 7 men; mean age 27 ± 3 yr).
In this study, we measured the peak forearm flow parameters under four study conditions: 1) breathing RA;
2) breathing RA during the application of lower body negative pressure (LBNP) at Experiment 1
30 mmHg (RA+LBNP); 3) breathing RA during
LBNP and after acutely venous congesting (VC) the forearm (RA+LBNP+VC);
and 4) during LBNP with associated
forearm VC as the subjects breathed 100%
O2
(O2+LBNP+VC).
1 · 100 ml1 of tissue. Arterial
blood pressures were measured on the opposite arm by an automated cuff
(model 1846SX, Dinamap, Tampa, FL). FVR (mmHg · ml1 · min · 100 ml tissue) was calculated by dividing the mean arterial pressures (MAP)
by the forearm flow.
Experiment 2
Effect of LBNP, VC, and 100% O2 on forearm dilator capacity. Postischemic flow measurements were performed under four experimental conditions in each subject. Ten- to fifteen-min rest periods were allowed between each trial. The RA intervention was always performed first and was identical to the control portion in experiment 1. The LBNP trial was always performed as the second intervention. This paradigm was included to examine the effects of isolated heightened sympathetic activity on limb flow. LBNP of30 mmHg was used because it is a relatively
potent sympathoexcitatory stimulant that disengages both low- and
high-pressure baroreceptors (13). LBNP was begun during the sixth
minute of forearm circulatory arrest and was continued until the 3 min
of postischemic forearm flow measurements were completed. During the
RA+LBNP+VC portion of the study, forearm VC was initiated 5 min before
forearm circulatory arrest was initiated. VC was achieved by inflating
the upper arm cuff to 90 mmHg. VC increases forearm volume by ~5%
(14). In the final portion of this study, supplemental
O2 was added to LBNP+VC.
O2 (100%) was delivered by
non-rebreathing face mask beginning 5 min before forearm circulatory
arrest was initiated and was continued for the 3 min of postischemic
forearm flow measurements.
Statistics
In experiment 1, a repeated-measures analysis of variance was used to examine the effects of O2. The two main effects examined were the presence or absence of O2 (2 levels of the variable) and flow (or resistance) at each time point after the release of circulatory arrest (13 levels of the variable). If a significant interaction was present (O2 × time), then pairwise comparisons were performed by examining the simple effects. The effect of O2 on peak flow (and minimum resistance) was determined by using a paired t-test.In experiment 2, the various interventions were compared by using repeated-measures analysis of variance testing for two main effects: the specific interventions (RA vs. RA+LBNP vs. RA+LBNP+VC vs. O2+LBNP+VC; 4 levels) and the flow (or resistance) during the 3 min of measurement (13 levels). Comparisons of the four interventions at a given time point were performed by examining the simple effects. A one-way analysis of variance was used to compare peak responses, and, when a significant F-value was observed, Tukey's test was used to determine differences between mean values. All data are expressed as means ± SE. A P < 0.05 was considered statistically significant.
RESULTS
Experiment 1
Effects of O2 on resting values. The effects of O2 on MAP, heart rate, resting forearm flow, and FVR are shown in Table 1. O2 (100%) increased MAP and vascular resistance, whereas resting heart rate fell and resting forearm flow was unchanged.
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1 · 100 ml1, and resistance is
expressed as
mmHg · ml1 · min · 100 ml. * P < 0.05.
If resting flow were subtracted from postischemic values, we would have still observed an O2 effect (main effect P < 0.004; interaction P < 0.001; simple effects showing statistical differences at each time point). The heart rate and blood pressure data for this experiment are shown in Table 2.
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Experiment 2
Compared with RA alone, RA+LBNP and RA+ LBNP+VC did not alter the minimal vascular resistance. However, the minimum FVR response during O2+LBNP+VC was different from that seen during RA alone (Fig. 3). The peak flow was not different during the four interventions.
1 · min · 100 ml) under 4 study conditions in experiment
2 (n = 7). RA, room
air; LBNP, lower body negative pressure; VC, venous congestion.
* P < 0.05, Tukey's test.
When data were analyzed over the entire 3 min of collection, an
intervention simple effect was noted at most time points (Fig. 4, A and
B). Analysis of the curves (Fig. 4)
suggests that the various interventions had a graded effect on flow and
resistance. If conductance values were analyzed, we would have noted
similar effects (intervention main effect
P < 0.001; interaction
P < 0.001). The heart rate and blood
pressure data for experiment 2 are
shown in Table 3. It is interesting to note
that an intervention main effect was present for both heart rate and
MAP. Analysis of this mean data suggests that
O2 raised MAP and lowered heart
rate even in the presence of LBNP and VC.
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Comparison of Experiments 1 and 2
In an effort to examine the influence of limb congestion and heightened sympathetic tone on the vascular effects of O2 effect, we compared the O2 trial during experiment 1 to O2+LBNP+VC in experiment 2. LBNP+VC did not lower peak flow or raise minimal vascular resistance. However, LBNP+VC did reduce flow and raise resistance during later stages of the 3-min postischemic data collection periods (Fig. 5).
DISCUSSION
A prior study demonstrated that supplemental O2 lowers cardiac output and raises left ventricular filling pressures in nonhypoxic congestive heart failure patients (7). In this prior report, we were unable to determine whether O2 had a direct effect on peripheral blood vessel dilator capacity.
In the present study, O2 caused a rise in MAP, a fall in heart rate, and an increase in FVR. We would surmise that O2 had a direct effect on vascular resistance, thereby raising MAP and evoking a baroreflex-mediated fall in heart rate. These observations are consistent with prior reports demonstrating that O2 evokes a direct peripheral vasoconstrictor effect (1). Bredle et al. (1) used a perfused hindlimb technique in a canine model to examine the effects of O2 on the peripheral circulation. Hyperoxia caused a rise in limb vascular resistance and a fall in limb O2 consumption, suggesting that O2 vasoconstricts and redistributes blood flow within the canine hindlimb.
In the present study, we found that supplemental O2 reduced vasodilator responses after 10 min of forearm ischemia. In experiment 2, LBNP and limb congestion had no effect on peak flow or minimal resistance. When supplemental O2 was added, minimal resistance rose and the rate of return of O2 toward baseline was increased. Comparison of the data from experiments 1 and 2 suggests that limb congestion and LBNP accelerate the rate of return of peak flow toward baseline. These results suggest that supplemental O2 has a very potent effect on the peripheral circulation that is capable of partially opposing powerful dilator influences within the ischemic forearm that are independent of any potential central cardiac effects. These effects of O2 are not obscured in the presence of heightened sympathetic tone and limb congestion.
Potential Mechanisms For Our Findings
It is unlikely that 100% O2 increased sympathetic tone and reduced peak forearm flow. Prior data suggest that if supplemental O2 has any effect on sympathetic discharge, it acts to reduce it (8, 20). Nitric oxide, a free radical generated in endothelium from L-arginine by nitric oxide synthase, is an important vasorelaxant (15). This substance has been found to be important in mediating vasodilatory responses seen during exercise (5, 17). However, its role in mediating postischemic flow is less clear. Recent work by Tagawa et al. (25) suggests that it has a modest effect on total flow and no effect on peak flow. It is interesting to note that nitric oxide is destroyed by O2, hemoglobin, and other free radicals. Studies by Obara et al. (16) suggest that prolonged exposures of rabbits to 100% O2 reduced both endothelial-dependent and -independent pulmonary arterial dilator responses. Of note, these effects were prevented by pretreatment with superoxide dismutase, a free radical scavenger.Recently it has been suggested that nitric oxide is delivered to the tissues via oxygenated hemoglobin. It is intriguing to speculate that hyperoxygenated blood decreases O2 extraction by the tissue (1) and in the process diminishes nitric oxide delivery, thereby reducing tissue vasodilation (10). Clearly, more work will be necessary to test this intriguing hypothesis.
Prior work using a neonatal umbilical arterial model demonstrated that O2 reduced prostacyclin formation by 30% (24), and prostacyclin is an important vasodilating prostaglandin (24). These prior findings are relevant to the present report because vasodilating prostaglandins, as opposed to nitric oxide, are thought to play an important role in determining the magnitude of both the peak and total reactive hyperemic responses to forearm ischemia (2, 3, 12).
Results of experiment 2, and comparison of experiments 1 and 2, suggest that heightened sympathetic tone and limb congestion do not act in concert with 100% O2 to reduce peak flow or to increase minimal resistance. However, these factors do appear to accentuate the effect of O2 on the total postischemic flow response. Mechanistic interpretation of these data will require further study. Parenthetically, the lack of effect of limb congestion and LBNP on peak flow and minimal resistance is consistent with prior observations (21, 22).
Limitations
First, our findings do not in themselves provide evidence that this peripheral vascular effect of O2 is physiologically detrimental to normal subjects or individuals with heart failure. Future studies examining exercise will be necessary to address this. It should be emphasized that prior work in canine models suggests that hyperoxia not only lowers limb flow but may also cause a maldistribution of blood flow and a concomitant paradoxical reduction in O2 extraction (1). In experiment 2, we used acute alterations in limb volume and sympathetic tone to mimic chronic peripheral responses seen in heart failure. It will be important to examine the effects of O2 on forearm flow responses directly in subjects with decompensated congestive heart failure.In conclusion, this study demonstrates that O2 decreases the magnitude of the limb vasodilator response to forearm ischemia. These effects of O2 are still noted when sympathetic nervous system activity and forearm interstitial volume are acutely increased.
ACKNOWLEDGEMENTS
We appreciate the technical support of Kristen Gray and Michael Herr and also the expert typing of Jennifer Stoner.
FOOTNOTES
Address for reprint requests: L. I. Sinoway, Division of Cardiology, The Milton S. Hershey Medical Center, PO Box 850, Hershey, PA 17033.
Received 23 August 1996; accepted in final form 24 January 1997.
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