From Yagi Hospital (T.O., K.K., H.N., H.Y.); Second Department of
Internal Medicine, Faculty of Medicine, Kyushu University (S.I., M.F.),
Fukuoka, Japan.
Correspondence to Tsuyoshi Omae, MD, Cerebrovascular Disease Clinic, National Kyushu Medical Center, Jigyo-hama 1–8-1, Chuo-ku, Fukuoka, Japan, 810. E-mail omae{at}qmed.hosp.go.jp
Methods—Middle cerebral arterial blood flow velocity
(MCV) was measured using transcranial Doppler (TCD)
technique in a multiplace hyperbaric chamber. The Doppler probe was
fixed on the temporal region by a head belt, and the transcutaneous gas
measurement apparatus (tcPO2 and
tcPCO2) was fixed on the chest wall. MCV and
transcutaneous gas were measured continuously in eight healthy
volunteers under four various conditions: 1 atmosphere absolute (ATA)
air, 1 ATA oxygen (O2), 2 ATA air, and 2 ATA
O2. On the next step, the effect of environmental pressure
was studied in another eight healthy volunteers, in whom the
tcPo2 was kept at almost the same level under conditions of
both 1 ATA and 4 ATA by inhaling oxygen at 1 ATA.
Results—MCV of 1 ATA O2, 2 ATA air, and 2 ATA
O2 decreased, and tcPO2 increased
significantly in comparison with that of 1 ATA air. A significant
difference in MCV was observed between the O2 group and the
air group under the same pressure circumstance. On the other hand,
there were no differences in MCV or tcPO2
between 4 ATA air and 1 ATA plus O2, and the influence for
the MCV of the environmental pressure was not observed.
Conclusions—We conclude that hyperoxemia caused by HBO reduces
the CBF, but the high atmospheric pressure per se does not influence
the CBF in humans.
A recent development of ultrasonic instruments has enabled us to
evaluate noninvasively the cerebral circulation in humans.7
There are some reports about the cerebral hemodynamic
changes using these techniques in healthy volunteers,8 9 in
stroke patients,10 in patients with
hemodialysis,11 or in patients with syncope.12
Therefore, we decided to use this technique to examine the relationship
between HBO and CBF in the present study.
The aim of our study was to clarify the effects of HBO in different
atmospheric pressures on CBF in healthy adults.
Right MCV was measured by TCD (TransScan, EME) in a multiplace
hyperbaric chamber (KHO-301, Kawasaki Engineering Co). With the use of
a 2-MHz pulse Doppler probe, the sampling position and measurement
depth (range, 52 to 56 mm) were determined on the temporal region
at which maximal value with minimal noise was obtained, and the
Doppler probe was fixed at the place with a head belt. Moreover,
tcPO2 and tcPCO2
(OKV-7301, Nihon Koden Co, Japan) were continuously recorded on the
chest wall of the examinees during the experimental periods. The
electrode temperature was kept at 44°C before the calibration at
least for 20 minutes and during the study to produce the optimum
arterialization. All data were recorded after the
tcPO2 and tcPCO2 became
stable and had remained stable for more than 5 minutes. Blood pressure
was measured by mercury sphygmomanometer.
In the first series, we examined the effect of HBO on CBF. The TCD
probe and the transcutaneous gas measurement apparatus were
fixed after the examinees were kept in supine position inside the
chamber. The MCV was measured under four various conditions: 1 ATA air,
1 ATA oxygen (O2), 2 ATA air, and 2 ATA O2,
after the examinees were stable under each condition. In both groups of
1 ATA O2 and 2 ATA O2, 20 L/min of oxygen was
given to the examinees with a facial mask.
In the second series, we investigated the effect of high ambient
atmospheric pressure on CBF. The MCV under 4 ATA air was compared with
that measured under 1 ATA, which showed almost the same
tcPO2 level as that under 4 ATA by inhaling
various volumes of oxygen with a facial mask at 1 ATA circumstance (1
ATA plus O2).
Compression and decompression speeds in the chamber were 0.1
kg/cm2 per minute or less, and decompression time was
slightly longer than compression time. These evaluations were monitored
using a diving computer (ProAladin), and we followed its instructions
during decompression. MCV of the examinees was measured after air
breathing followed by O2 inhalation under the same pressure
circumstance. The MCV was recorded after the examinees' condition
became stable for at least 15 minutes.
Data presented in the text and tables are expressed as
mean±SD, and comparative studies among the groups were statistically
evaluated by ANOVA and Fisher's protected least significant difference
test. Results were considered significantly different at values of
P<.05.
On the other hand, the tcPO2 increased
significantly under conditions of 1 ATA O2, 2 ATA air, and
2 ATA O2 in comparison with that in the control group, and
those in the groups with O2 inhalation were significantly
higher than those breathing air at the same pressure. On the contrary,
although the values of tcPCO2 were not
different among conditions of 1 ATA air (38±4 mm Hg), 1 ATA
O2 (37±4 mm Hg), and 2 ATA air (37±4 mm Hg),
tcPCO2 under 2 ATA O2 (33±5
mm Hg) decreased significantly (P<.05). Blood pressure and
pulse rate showed no change during the experimental periods in all
groups (Table 1
As the next step, we compared the pressure effect of 4 ATA with that of
1 ATA (control). As the environmental pressure rose from 1 ATA to 4
ATA, tcPO2 increased, from 75.8±12.0 to
418.9±46.6 mm Hg. In order to get the same
tcPO2 level in 1 ATA as in 4 ATA air, the
examinees inhaled various volumes of oxygen with a facial mask at 1
ATA. As a result, tcPO2 of the examinees
increased from 75.8±12.0 to 416.4±46.2 mm Hg at 1 ATA with
oxygen (1 ATA plus O2). The tcPCO2
values were not different among 1 ATA air (38±3 mm Hg), 4 ATA
air (37±4 mm Hg), and 1 ATA plus O2 (37±5
mm Hg). We compared the MCV of 4 ATA air with that of 1 ATA plus
O2 (Table 2
So far, there are several reports that have measured CBF under the HBO
circumstance. However, almost all of those reports are on animal
experiments,1 2 3 4 and human studies are few.5 6
The results of the animal experiments have shown that HBO decreases
CBF. Conditions such as hyperoxemia5 14 and
hypocapnia due to hyperventilation2 6 have been
considered as reasons for such a phenomenon, but a clear view is not
yet estimated. Nowadays, it has been considered that the increase of
arterial oxygen tension causes constriction of the
superficial cortical arterioles,15 16 17 18 which leads to the
decrease in the CBF.
The development of an ultrasonic technique has enabled us to measure
CBF changes noninvasively without any hazard in humans.7
The TCD expresses the flow velocity of the middle cerebral artery,
although it does not show real quantitative cerebral blood flow
velocity.19 However, it has been reported that the changes
in MCV obtained by TCD have an excellent correlation with the changes
in CBF as measured withother techniques.10 20 21 Therefore,
we accepted the TCD technique for evaluating cerebral
hemodynamics under the HBO circumstance in humans.
In the present human study, CBF of 1 ATA O2, 2 ATA air,
and 2 ATA O2 decreased significantly in comparison with
that of 1 ATA air. The decrease of CBF was remarkable, especially under
conditions of 1 ATA O2 and 2 ATA O2, although
no significant difference was observed between the groups. Our results
coincided with the results by Lambertsen et al6 who found a
25% reduction of CBF at 3.5 ATA in humans using the nitrous oxide
method. Kanai et al22 reported the effect of HBO on blood
flows in the common, internal, and external carotid arteries and the
vertebral artery in humans by transcutaneous ultrasonic blood
rheography. They demonstrated the reduction of blood flow by HBO in the
arteries except the vertebral artery.
In this series, although the tcPO2 in 2 ATA
O2 was significantly higher than that in 1 ATA
O2, the values of MCV were not different between 1 ATA
O2 and 2 ATA O2. Ohta5 demonstrated
a tendency toward an increase in CBF at the level of 2.5 ATA
O2, following gradual decreases in CBF to the level of 2
ATA O2. These results suggested that the relation between
tcPO2 and CBF is not linear. Further
examination is need to clarify the relation. Although low
PCO2 conditions were sometimes encountered
under the condition of HBO, our results suggested the reason for the
MCV decrease under HBO conditions was mainly due to hyperoxemia.
Although the tcPCO2 level may influence the MCV
at 2 ATA O2 in the first series, the decrease of
tcPCO2 level seems unlikely to be the only
cause of the decrease in MCV because of the CO2 vasomotor
reactivity level.14 23 24
Although hyperoxemia due to inhalation of high doses of O2
reduced MCV under 1 ATA and 2 ATA in the first series, it remained
unclear about the effect of the atmospheric pressure on CBF.
In our second series, we compared MCV of 4 ATA air with that of 1 ATA
plus O2 and also found that ambient atmospheric pressure
did not produce any influences on CBF in humans. In the animal study,
Hordnes and Tyssebotn4 examined the relationship between
partial arterial oxygen tension and CBF in rats, and
reported that the ambient atmospheric pressure did not show any changes
in CBF.
Although these results suggest that the changes in
PO2 affect the CBF, the effect is much smaller
than that in PCO2. The changes in
PO2 may not influence the assessment of
PCO2 reactivity in hyperventilation or
CO2 inhalation tests except the O2 inhalation
test.
In summary, oxygen inhalation reduced MCV under 1 ATA and 2 ATA, and
there was no MCV difference between 4 ATA and 1 ATA when
tcPO2 was kept at the same level by inhaling
O2 at 1 ATA. We conclude that the hyperoxemia causes CBF
reduction under HBO conditions and that the ambient atmospheric
pressure does not influence the CBF.
Received September 2, 1997;
revision received October 20, 1997;
accepted October 20, 1997.
© 1998 American Heart Association, Inc.
Original Contributions
Effects of High Atmospheric Pressure and Oxygen on Middle Cerebral Blood Flow Velocity in Humans Measured by Transcranial Doppler
Abstract
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Background and Purpose—There are
several reports that have studied the effects of hyperbaric oxygen
(HBO) on cerebral blood flow (CBF). However, most of the reports have
been of animal experiments, and human studies are few so far. The aim
of this study is to clarify the relationship between HBO and CBF
in humans.
Key Words: cerebral blood flow • hyperbaric oxygenation • oxygen • ultrasonics
Introduction
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
There are only a few
papers reported on CBF under HBO circumstances.1 2 3 4
However, most of the reports are of animal experiments, and human
studies are few,5 6 because it is quite difficult to
measure CBF in humans under such a special condition.
Subjects and Methods
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Our study consisted of two series. In the first series, the
effect of HBO on CBF was observed in eight healthy volunteers; and in
the second series, the influence of high atmospheric pressure on CBF
was examined in another eight young normal volunteer subjects. All of
them received an explanation of this study, and informed consent was
taken; the study was approved by the hospital ethics committee. The sex
breakdown of each group was almost the same, and age was 28.1±4.7
(mean±SD) years in the former series and 26.6±5.5 years in the
latter.
Results
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
The mean MCV values under the conditions of 1 ATA air, 1 ATA
O2, 2 ATA air, and 2 ATA O2 were 65±15,
52±16, 61±13, and 50±13 cm/s, respectively. The mean MCVs of 1 ATA
O2, 2 ATA air, and 2 ATA O2 decreased
significantly in comparison with that of 1 ATA air (the control group),
and at the same time, a significant difference was observed between the
O2 group and the air group under the same pressure
circumstance. The mean MCV values of 1 ATA O2 and 2 ATA
O2 were essentially the same (Table 1
, Fig 1).
View this table:
[in a new window]
Table 1. Physiological Variables and
Middle Cerebral Arterial Blood Flow Velocities
View larger version (27K):
[in a new window]
Figure 1. Bar graphs show MCV under the conditions of 1 ATA
air, 1 ATA O2, 2 ATA air, and 2 ATA O2. Left,
systolic blood flow velocity; center, diastolic
blood flow velocity; and right, mean blood flow velocity. All values
are mean±SD. *P<.05. 
). ). MCVs of 4 ATA
air and the 1 ATA plus O2 group were 64±14 and 62±13
cm/s, respectively, and there was no significant difference between the
two groups (Table 2, Fig 2).
View this table:
[in a new window]
Table 2. Physiological Variables and
Middle Cerebral Arterial Blood Flow Velocities
View larger version (20K):
[in a new window]
Figure 2. Bar graphs show MCV under the conditions of 1 ATA
air, 4 ATA air, and 1 ATA+O2. Left, systolic blood
flow velocity; center, diastolic blood flow velocity; and
right, mean blood flow velocity. All values are mean±SD.
**P<.01.
Discussion
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
Kety and Schmidt13 first described a method to measure
CBF in humans using nitrous oxide in a low concentration, although it
was an invasive technique. As the next methods to measure CBF,
techniques using radioisotopes, eg, 133Xe,
125I, 99mTc, or computed tomography with cold
Xe, have been devised. These methods are noninvasive, but at the same
time inadequate for detection of the CBF under a high pressure
circumstance.
Selected Abbreviations and Acronyms
ATA
=
atmosphere absolute
CBF
=
cerebral blood flow
HBO
=
hyperbaric oxygen
MCV
=
middle cerebral arterial blood flow velocity
TCD
=
transcranial Doppler
tcPCO2
=
transcutaneous carbon dioxide tension
tcPO2
=
transcutaneous oxygen tension
Acknowledgments
The authors thank Riko Co Ltd for valuable technical support. We
are also grateful to Michiya Yoshizato, Tomomi Takamura, Mami Saito,
Shinji Hiraki, and Yuki Okamoto for technical assistance throughout
this study and to volunteers and colleagues of Yagi hospital.
References
Top
Abstract
Introduction
Subjects and Methods
Results
Discussion
References
This article has been cited by other articles:
 |
|
 |
|
  S. Iscoe and J. A. Fisher Hyperoxia-Induced Hypocapnia: An Underappreciated Risk Chest, July 1, 2005; 128(1): 430 - 433. [Full Text] [PDF]
|
|
|
|
 |
|
 B. Clavo, L. Catala, J. L. Perez, V. Rodriguez, and F. Robaina Ozone Therapy on Cerebral Blood Flow: A Preliminary Report Evid. Based Complement. Altern. Med., December 1, 2004; 1(3): 315 - 319. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Johnston, L. A. Steiner, A. K. Gupta, and D. K. Menon Cerebral oxygen vasoreactivity and cerebral tissue oxygen reactivity{dagger} Br. J. Anaesth., June 1, 2003; 90(6): 774 - 786. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. B. Singhal, R. M. Dijkhuizen, B. R. Rosen, and E. H. Lo Normobaric hyperoxia reduces MRI diffusion abnormalities and infarct size in experimental stroke Neurology, March 26, 2002; 58(6): 945 - 952. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. T. Demchenko, A. E. Boso, T. J. O'Neill, P. B. Bennett, and C. A. Piantadosi Nitric oxide and cerebral blood flow responses to hyperbaric oxygen J Appl Physiol, April 1, 2000; 88(4): 1381 - 1389. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. J. Girling, G. Cavill, and R. P. Mahajan The Effects of Nitrous Oxide and Oxygen on Transient Hyperemic Response in Human Volunteers Anesth. Analg., July 1, 1999; 89(1): 175 - 175. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||