Sodium nitroprusside-induced, but not desflurane-induced, hypotension decreases myocardial tissue oxygenation in dogs anesthetized with 8% desflurane

Abstract

To compare sodium nitroprusside (SNP)-induced hypotension with desflurane-induced hypotension for the effects on myocardial blood flow and tissue oxygenation in dogs.
Prospective, randomized, crossover, nonblinded.
University teaching hospital.
Male nonpurpose-bred hounds (n = 8).
Dogs were anesthetized with 8% desflurane. Catheters were inserted into the femoral artery and coronary sinus. A flow probe was placed in the left anterior descending (LAD) branch of the coronary artery. A sensor that measured myocardial oxygen pressure (PmO(2)) was inserted into the myocardium of the left ventricle. Myocardial oxygen consumption (MVO(2)) was calculated as LAD flow x arterial - coronary sinus oxygen content.
Measurements were made at baseline blood pressure levels of 99 mmHg (measure 1), during hypotension to 62 to 66 mmHg using intravenous SNP or 14% desflurane (measure 2), and during SNP or 14% desflurane with blood pressure support using phenylephrine (measure 3). Each dog randomly received both hypotensive treatments, separated by 1 hour. Baseline measures were PmO(2) = 46 +/- 9 mmHg, LAD flow = 43 +/- 11 mL/min, and MVO(2) = 2.47 +/- 0.73 mL O(2)/min. During hypotension induced with SNP, PmO(2) decreased 30% (p < 0.05), LAD flow increased 40% (p < 0.05), and MVO(2) did not change. During hypotension induced with 14% desflurane, PmO(2) did not change, and LAD flow and MVO(2) decreased 25% and 40% (p < 0.05). Blood pressure support with phenylephrine increased LAD flow and MVO(2) but did not change PmO(2) during SNP or 14% desflurane treatment.
SNP-induced hypotension produced myocardial vasodilation, but tissue oxygenation was impaired. PmO(2) was maintained during desflurane-induced hypotension.

Full text

Sodium Nitroprusside–Induced, but Not Desflurane-Induced, Hypotension
Decreases Myocardial Tissue Oxygenation in Dogs Anesthetized
With 8% Desflurane
William E. Hoffman, PhD, Ronald F. Albrecht II, MD, and Zivojin S. Jonjev, MD
Objective: To compare sodium nitroprusside (SNP)–in-
duced hypotension with desflurane-induced hypotension for
the effects on myocardial blood flow and tissue oxygenation
in dogs.
Design: Prospective, randomized, crossover, nonblinded.
Setting: University teaching hospital.
Participants: Male nonpurpose-bred hounds (n ⴝ8).
Interventions: Dogs were anesthetized with 8% desflu-
rane. Catheters were inserted into the femoral artery and
coronary sinus. A flow probe was placed in the left anterior
descending (LAD) branch of the coronary artery. A sensor
that measured myocardial oxygen pressure (PmO2) was in-
serted into the myocardium of the left ventricle. Myocardial
oxygen consumption (MV
˙O2) was calculated as LAD flow ⴛ
arterial ⴚcoronary sinus oxygen content.
Measurements and Main Results: Measurements were
made at baseline blood pressure levels of 99 mmHg (mea-
sure 1), during hypotension to 62 to 66 mmHg using intra-
venous SNP or 14% desflurane (measure 2), and during SNP
or 14% desflurane with blood pressure support using phen-
ylephrine (measure 3). Each dog randomly received both
hypotensive treatments, separated by 1 hour. Baseline mea-
sures were PmO2ⴝ46 ⴞ9 mmHg, LAD flow ⴝ43 ⴞ11
mL/min, and MV
˙O2ⴝ2.47 ⴞ0.73 mL O2/min. During hypo-
tension induced with SNP, PmO2decreased 30% (p<0.05),
LAD flow increased 40% (p<0.05), and MV
˙O2did not
change. During hypotension induced with 14% desflurane,
PmO2did not change, and LAD flow and MV
˙O2decreased
25% and 40% (p<0.05). Blood pressure support with phen-
ylephrine increased LAD flow and MV
˙O2but did not change
PmO2during SNP or 14% desflurane treatment.
Conclusion: SNP-induced hypotension produced myocar-
dial vasodilation, but tissue oxygenation was impaired.
PmO2was maintained during desflurane-induced hypo-
tension.
Copyright 2002, Elsevier Science (USA). All rights reserved.
KEY WORDS: myocardial, oxygen, anesthesia, inhalation,
desflurane, controlled hypotension, sodium nitroprusside
(SNP)
SODIUM NITROPRUSSIDE (SNP) may be used to treat
hypertension and to decrease afterload in patients with
cardiac disease.1,2 Although SNP produces myocardial vasodi-
lation, the hypotensive drug may promote coronary steal and
worsen myocardial ischemia.3,4 This possibility is consistent
with reports that SNP increases pulmonary shunting and de-
creases capillary perfusion and tissue oxygenation in skeletal
muscle and brain.5-8 Little is known of the effect of SNP-
induced hypotension on myocardial tissue oxygenation.
In addition to SNP, desflurane and isoflurane produce myo-
cardial vasodilation.9-11 The cardiodepressant effect of these
anesthetics is associated with decreased myocardial oxygen
consumption (MV
˙O2). Early studies suggested that isoflurane
may produce steal and increase the risk of myocardial hypoxia
and ischemia.12 Subsequent patient or animal studies indicated,
however, that neither desflurane nor isoflurane produces
steal.13-15 Although SNP and inhalation anesthetics produce
vasodilation, the effect of each treatment on myocardial tissue
oxygenation may be different.8The purpose of this study was
to compare the hypotensive effects of SNP and 14% desflurane
on left anterior descending (LAD) artery flow, MV
˙O2and
myocardial oxygen pressure (PmO2) in dogs anesthetized with
8% desflurane.
MATERIAL AND METHODS
This study was approved by the Institutional Animal Care Commit-
tee, and experiments were performed at the West Side Veterans Ad-
ministration Animal Research Facilities in Chicago. Eight nonpurpose-
bred male hounds (23 to 28 kg) were fasted overnight. On the day of
the study, the dog was anesthetized with 5 mg/kg of propofol, intu-
bated, and ventilated with 8% desflurane (1.1 minimum alveolar con-
centration in the dog) and inspired oxygen concentration of 30% in
nitrogen. Catheters were inserted into the femoral artery for blood
pressure recording and blood gas sampling and into the femoral vein
for fluid and drug administration. Sterile saline was infused intrave-
nously (4 mL/kg/h) for fluid maintenance.
An incision was made at the left fifth intercostal space, and the left
heart ventricle was exposed. The LAD segment of the coronary artery
was dissected above the first diagonal branch, and a 2-mm Transonics
flow probe (Transonics Inc, Ithaca, NY) was placed on the artery. A
catheter was inserted into the coronary sinus through the great coronary
vein for blood sampling. A Paratrend tissue probe (Codman Inc,
Newark, NJ), which is a clinical instrument that has been validated to
measure tissue gases, was inserted. The probe measures PO2and
temperature and was calibrated on the day of the study using precision
gases. The probe is 0.5 mm in diameter and was inserted into the
middle myocardium in the region of the LAD parallel to the surface at
a depth of 6 mm using a 20G angiocatheter. Arterial PCO2was adjusted
to 40 ⫾2 mmHg, and myocardial temperature was maintained at 38°C
using a warming pad.
After a 45-minute equilibration period, arterial and coronary sinus
blood samples were taken, and LAD flow and PmO2were measured as
baseline. Hypotension was induced randomly by intravenous infusion
of SNP (2.4 to 4.0
␮
g/kg/min) or by increasing end-tidal desflurane to
14 ⫾1% to produce a target mean arterial pressure (MAP) of 65 ⫾5
mmHg. After a 10-minute equilibration at the hypotensive level, a
second measurement was made of LAD flow, PmO2, and blood gases.
The hypotensive drug treatment was continued, and intravenous phen-
ylephrine was infused to return blood pressure to baseline levels for 10
minutes before the third measurement. All treatments were then termi-
nated, and control conditions with 8% desflurane were reestablished.
After a 1-hour recovery period, a second baseline measurement was
From the Departments of Anesthesiology and Physiology, University
of Illinois at Chicago, Chicago, IL.
Supported by a grant from Baxter Healthcare Company.
Address reprint requests to William E. Hoffman, PhD, Department of
Anesthesiology, M/C 515, University of Illinois at Chicago, 1740 West
Taylor Street, Chicago, IL 60612. E-mail: whoffman@uic.edu
Copyright 2002, Elsevier Science (USA). All rights reserved.
1053-0770/02/1603-0004$35.00/0
doi:10.1053/jcan.2002.124134
286 Journal of Cardiothoracic and Vascular Anesthesia, Vol 16, No 3 (June), 2002: pp 286-289

made with an end-tidal desflurane concentration of 8%, followed by the
second of the 2 hypotensive drug treatments and phenylephrine infu-
sion. Each dog received both hypotensive drug treatments.
Arterial and coronary sinus blood gases and pH were measured using
an Instrumentation Laboratories 1670 Blood Gas Analyzer (Lexington,
MA). Blood hemoglobin and oxygen content were measured using an
Instrumentation Laboratories 482 co-oximeter, and total oxygen con-
tent was calculated by adding the oxygen dissolved in plasma. MV
˙O2
was calculated as follows: MV
˙O2⫽LAD flow ⫻(arterial blood
oxygen content ⫺coronary sinus blood oxygen content). Myocardial
vascular resistance was calculated as MAP ⫼LAD flow.
Data are reported as mean ⫾SD. Physiologic variables were com-
pared between baseline, hypotensive, and phenylephrine treatments
within each group using a repeated measures analysis of variance with
Tukey tests for post hoc comparisons. Comparisons between groups
were made by analysis of variance with Tukey tests for post hoc
comparison. A pvalue ⬍0.05 was considered significant.
RESULTS
MAP, heart rate, arterial gases, and pH are shown in Table 1.
MAP decreased 30% with SNP infusion and 14% with desflu-
rane without a significant change in heart rate. Arterial blood
gases and pH remained at baseline levels during all treatments.
Immediately after insertion of the tissue probe into the myo-
cardium, PmO2decreased to 10 to 20 mmHg and pH to 7.15 to
7.20. Within 30 minutes, PmO2increased to ⬎40 mmHg, and
pH increased to ⬎7.30; both measures were stable during the
remaining equilibration and baseline periods. During SNP-
induced hypotension, PmO2decreased 25% and remained
lower during blood pressure support with phenylephrine (Fig
1). Tissue pH decreased from 7.33 ⫾0.11 to 7.28 ⫾0.12
during SNP treatment (p⬍0.05). During 14% desflurane-
induced hypotension and phenylephrine treatment, neither
PmO2nor tissue pH (7.32 ⫾11) changed from baseline.
LAD flow increased during SNP-induced hypotension with-
out a change in MV
˙O2(Fig 1). With phenylephrine infusion,
LAD flow and MV
˙O2increased. During 14% desflurane infu-
sion, LAD flow decreased 30%, and MV
˙O2decreased 40%.
During 14% desflurane and phenylephrine infusion, LAD flow
and MV
˙O2increased to baseline levels. Myocardial vascular
resistance decreased during SNP infusion from 2.43 ⫾0.63
mmHg/mL/min at baseline to 1.09 ⫾0.23 mmHg/mL/min (p⬍
0.05) and remained at 1.08 ⫾0.31 mmHg/mL/min during
phenylephrine infusion. Vascular resistance did not change
during 14% desflurane infusion from 2.75 ⫾0.85 mmHg/mL/
min at baseline to 2.71 ⫾0.65 mmHg/mL/min and 2.38 ⫾0.80
mmHg/mL/min during phenylephrine infusion.
DISCUSSION
In dogs anesthetized with 8% desflurane, during SNP-in-
duced hypotension to 62 mmHg, LAD flow increased 40% and
PmO2decreased 30%. This finding agrees with reports that
SNP-induced hypotension impaired capillary perfusion and tis-
sue oxygenation even while it produced vasodilation.5-8 In
contrast to SNP, desflurane-induced hypotension decreased
LAD flow and MV
˙O2and did not change PmO2; this may be
partially due to the cardiodepressant effects of large-dose des-
flurane.9,10 These data confirm that the myocardial effects of
SNP and desflurane are different and suggest that SNP may
decrease tissue oxygenation.
The influence of SNP on myocardial blood flow has been
evaluated in previous studies. Crystal et al11 reported that SNP
is a potent coronary vasodilator that increased myocardial
blood flow in dogs anesthetized with fentanyl and midazolam.
A direct myocardial vasodilating effect of SNP was suggested
by the fact that coronary blood flow increased more than in
other vascular beds during SNP infusion.16 Myocardial blood
flow increased during SNP-induced hypotension even though
cardiac work decreased.17 Other studies found that SNP did not
change MV
˙O2.18 This finding is consistent with the present
results that LAD flow increased with no significant change in
MV
˙O2.
A major finding of this study is that PmO2decreased even
though MV
˙O2was constant during SNP infusion. The uncou-
pling of MV
˙O2and PmO2suggests that within limits, myocar-
dial oxygen uptake is not dependent on PmO2. The baseline
PmO2under anesthetized conditions represented an oxygen-
ation state mediated by capillary perfusion that allowed normal
myocardial function. When SNP infusion decreased PmO2,
baseline levels of myocardial oxygen uptake were maintained,
but the risk of ischemic acidosis increased. The lower PmO2
during SNP infusion did not change during phenylephrine
treatment even though MV
˙O2increased. This finding suggests
that PmO2is related to the effect of SNP on capillary perfusion
and is not dependent on myocardial perfusion pressure or
oxygen uptake. Dogs have an extensive coronary collateral
circulation similar to patients with long-standing atheroscle-
rotic disease.19,20 These dogs did not have vascular disease,
however, that may limit vasodilation produced by SNP. It is
hypothesized that the attenuation of myocardial oxygenation by
SNP could worsen ischemia in humans if the vasodilatory
effect of the drug were limited by regional vascular disease.
Table 1. Mean Arterial Pressure Heart Rate and Arterial Blood Gases
n Treatment
MAP
(mmHg)
HR
(beats/min)
PaO2
(mmHg)
PaCO2
(mmHg) pH
SNP 8 Baseline 99 ⫾11 138 ⫾9 147 ⫾22 40 ⫾2 7.33 ⫾0.05
8 Hypotension 62 ⫾5* 139 ⫾14 136 ⫾29 38 ⫾3 7.31 ⫾0.04
8 BP support 94 ⫾12 143 ⫾23 137 ⫾439⫾4 7.31 ⫾0.09
14% Desflurane 8 Baseline 99 ⫾10 132 ⫾13 145 ⫾17 38 ⫾2 7.32 ⫾0.09
8 Hypotension 66 ⫾5* 130 ⫾24 135 ⫾29 38 ⫾2 7.31 ⫾0.11
8 BP support 100 ⫾5 133 ⫾21 133 ⫾22 40 ⫾4 7.29 ⫾0.12
NOTE. Mean ⫹SD. Blood pressure (BP) support during hypotensive drug treatment was produced by phenylephrine infusion.
Abbreviations: MAP, mean arterial pressure; HR, heart rate.
*p⬍0.05 compared with baseline.
287MYOCARDIAL TISSUE OXYGEN PRESSURE

The effects of SNP on LAD flow and PmO2are consistent
with other studies showing that SNP increases arteriovenous
shunting and decreases capillary perfusion and tissue oxygen-
ation in other organs.5-8 This finding may be related to the
vasodilating effect of nitric oxide on coronary collateral ves-
sels.21 In patients, SNP-induced hypotension increased in-
trapulmonary shunting and worsened pulmonary gas exchange
compared with nitroglycerin-induced hypotension.5,22 In skel-
etal muscle, SNP-induced hypotension produced vasodilation
but decreased capillary blood flow 50% and tissue oxygenation
21%.6A similar hypotensive treatment with adenosine pro-
duced no change in capillary flow or tissue oxygenation. A
micropuncture study in hamsters confirmed that SNP-induced
hypotension decreased functional capillary density and pro-
duced hypoxia in skeletal muscle, changes not seen during
hypotension with nitroglycerin.7In dog brain tissue, SNP-
induced hypotension increased brain blood flow but decreased
capillary perfusion and tissue oxygenation.8These studies sug-
gest that SNP may decrease PmO2by attenuating myocardial
capillary perfusion, even though myocardial blood flow in-
creased.
Desflurane, in end-tidal concentrations of 8% to 12.2%,
decreased arterial pressure and systemic vascular resistance
without a change in cardiac output in dogs.10 In dog hearts,
3.6% to 14.4% desflurane decreased MV
˙O2and increased
myocardial blood flow when myocardial perfusion pressure
was supported.9The authors found that 14% desflurane de-
creased arterial pressure, MV
˙O2, and LAD flow. These data
suggest the decrease in myocardial blood flow during 14%
desflurane infusion was an autoregulatory change related to a
decrease in oxygen demand. This suggestion is supported by
the fact that PmO2did not change during 14% desflurane
treatment. LAD flow and MV
˙O2increased when blood pressure
was supported with phenylephrine, but PmO2did not change.
This fact agrees with the suggestion that there is an optimal
PmO2for normal myocardial function. PmO2was maintained
during 14% desflurane infusion whether MV
˙O2decreased or
increased. One question is how the results seen here with
desflurane may relate to other inhalation anesthetics. The au-
thors have performed hypotensive studies in dogs using isoflu-
rane and observed a similar effect on LAD flow, MV
˙O2, and
PmO2(unpublished results). It is unlikely that these studies
could be performed in humans because of the invasive nature of
the probe measurement of myocardial tissue gases.
PmO2measures have been previously reported. Before car-
dioplegic arrest in dogs, PmO2was 36 ⫾8 mmHg.23 During
cardiopulmonary bypass in dogs, PmO2averaged 44 ⫾7
mmHg.24 In pigs, PmO2was 13 ⫾2 mmHg in the subendo-
cardium at baseline and decreased to 5 ⫾1 mmHg during LAD
occlusion.25 PmO2during normocapnia before coronary steno-
sis was 52 ⫾7 mmHg in epicardium (2 mm deep) and 37 ⫾2
mmHg in endocardium (8 mm deep) in dogs and decreased
50% during coronary artery stenosis in both regions.26 These
results suggest there is a PO2gradient from the epicardium to
the subendocardium. The baseline PmO2measurements in mid-
dle myocardium (6 mm deep) are consistent with these reports.
It was assumed in this study that LAD flow would change in
a similar manner to total myocardial blood flow. Changes in
coronary venous blood oxygen content were also assumed to be
consistent with the local oxygenation changes in the LAD
region. Because SNP and phenylephrine were given intrave-
nously and desflurane was inhaled, it is likely that the myocar-
dial effects of these treatments were global and that the as-
sumptions are valid. There would be advantages, however, to
Fig 1. Tissue oxygen pressure (top), LAD artery flow (middle), and
myocardial oxygen consumption (bottom) during baseline anesthe-
sia with 8% desflurane (treatment 1), hypotension with SNP or 14%
desflurane (treatment 2), and continued hypotensive treatment com-
bined with blood pressure support using phenylephrine (treatment
3). Mean ⴞSD. Asterisks indicate difference from baseline (p<0.05).
288 HOFFMAN ET AL

measuring regional myocardial blood with other techniques,
such as radioactive microspheres, that would better describe
blood flow in epicardial and endocardial regions.
It is possible that phenylephrine treatment directly affected
myocardial vascular resistance. Investigators reported, how-
ever, that phenylephrine has little direct effect on myocardial
vascular resistance.27 In this study, phenylephrine did not in-
crease vascular resistance during either SNP or 14% desflurane
treatment. This result supports the conclusion that phenyleph-
rine had no direct effect on myocardial vascular resistance.
In conclusion, these results show that SNP-induced hypoten-
sion decreased PmO2. In comparison, desflurane-induced hy-
potension did not change PmO2. These results are consistent
with previous findings that SNP decreased capillary perfusion
and tissue oxygenation even though it produced vasodilation.
ACKNOWLEDGMENT
The authors thank Rick Ripper, CVT, for his surgical support in this
study.
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