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1 Shriners Burn Institute; 2 Departments of Anesthesia and Critical Care, 3 Pediatrics-Pulmonary Division, 4 Pulmonary and Critical Care Medicine and 5 Radiology and 6 Center for Engineering in Medicine, Massachusetts General Hospital; and 7 Harvard Medical School, Boston, Massachusetts 02114
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Regional changes in ventilation and perfusion occurring in the early hours after smoke inhalation injury were evaluated through the use of positron emission tomography. Five lambs were imaged before and 1, 2, and 4 h after receiving 100 breaths of cotton smoke. Utilizing a recently developed model of 13N tracer kinetics (3), we evaluated changes in ventilation, perfusion, shunt, and regional gas content in nondependent, middle, and dependent lung zones. The data demonstrated a progressive development of regional shunt in dependent (dorsal) regions in which perfusion remained the highest throughout the study. These findings, together with decreasing regional ventilation and fractional gas content in the dependent regions, correlated with decreasing arterial PaO2 values over the course of the study. A negative correlation between regional shunt fraction and regional gas content in dependent and middle regions suggests that shunt was caused by progressive alveolar derecruitment or flooding.
positron emission tomography
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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DEATHS SECONDARY TO
SMOKE inhalation may occur acutely at the scene of the fire
or days later as acute respiratory distress syndrome with development
of complicating pneumonia (7, 8). Alterations in diffusion
capacity, ventilation (
A), and perfusion (
)
have been considered as explanations for the progressive hypoxemia seen
in the most seriously injured (12, 15). Studies of
extravascular lung water accumulation have suggested that increases in
interstitial fluid volume in the early hours postinjury may result from
dilutional hypoproteinemia after fluid resuscitation or later in the
clinical course as burn edema begins to mobilize (11, 14, 16,
20).
Studies to date have allowed only global estimates of alterations in
A and . Delayed clearance after intravascular
injection of 133Xe in the early postinjury period have been
shown to correlate with later development of more extensive parenchymal
disease (12, 15). Abnormalities in 133Xe
clearance are thought to be related to underperfusion of
well-ventilated space or from impairment of A to
well-perfused regions. Pulmonary function tests, revealing changes in
both large and small airway resistance to gas flow with maintenance of
relatively normal lung volumes, seem to support the latter explanation
(15). Analysis of A/ using
multiple inert gas elimination technique (MIGET) by Robinson et al.
(17) demonstrated that in the first 24 h after
smoke inhalation the development of shunt and low
A/ regions was negligible, but there was
increased A to poorly perfused (high
A/) regions. By 72 h postinjury
when hypoxemia was detected, there was a marked increase in blood flow
to low A/ regions, yet there was still
negligible true shunt detected. Shimazu et al. (19),
however, demonstrated that both severity-related and time-related
hypoxemia resulted from the development of low A/ regions and, less consistently, from
shunt. Thus the question of whether early A/
mismatch results from alterations in A or remains.
Positron emission tomography (PET) analysis of
A/ is different from MIGET in that it allows
for the determination of regional rather than global alterations in
lung function. By measuring the distribution of the positron-emitting
radioisotope nitrogen-13 (13NN) activity after bolus
injection during apnea, an estimation of regional lung
(R) as well as an assessment of local shunt fraction
(S/R) can be made (see
accompanying paper, Ref. 3). With the resumption of
A, the rate of radiolabeled tracer removal can be
corrected for regional shunt to estimate regional A. Additionally, changes in regional gas content can be assessed by
analyzing changes in regional lung density in PET transmission scans.
Thus PET allows for a quantitative assessment of the distribution and
extent of injury and the corresponding alterations in physiology resulting from smoke inhalation. This study used PET to characterize the contribution of alterations in A,
R, and S/R to
the development of hypoxemia in the early hours after smoke inhalation.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Animal Preparation
The study was approved by the Massachusetts General Hospital Subcommittee on Research Animal Care. Five Hampshire lambs weighing 11.5-14.8 kg (mean 13 ± 1.4 kg) were anesthetized with sodium pentothal (250-300 mg bolus) and orally intubated with a 7.5-mm ID endotracheal tube. They were mechanically ventilated with inspired oxygen fraction (FIO2) of 0.50, inhalation-to-exhalation ratio of 1:2, positive end-expiratory pressure of 5 cmH2O, rate of 10 breaths/min, and tidal volume of 18 ± 2 ml/kg adjusted to establish a baseline arterial PCO2 > 35 < 45 Torr (Harvard Apparatus, Millis, MA). A Swan-Ganz catheter was placed in the left femoral vein (Edwards Swan Ganz-CCO/SvO2 8.0 Fr; Baxter Healthcare, Irvine, CA) to provide continuous measurements of cardiac output and pulmonary artery pressure. The distal port of the catheter was used for delivery of intravenous fluid (0.9 NS) at a maintenance rate for the duration of the study. The right femoral artery was cannulated for pressure monitoring and collection of arterial blood gas samples. Hemoglobin profiles and blood-gas analysis were measured by using the IL482 co-oximeter system and the 1620 pH/blood gas analyzer (Instrumentation Laboratory, Lexington, MA). Anesthesia was maintained for the duration of the study by use of intravenous sodium pentothal (500 mg/h) via a right femoral vein catheter. Animals were paralyzed with pancuronium (4 mg) before the first PET scan was obtained. The right external jugular vein was cannulated for administration of the 13NN-labeled saline.Experimental Setup
The experimental apparatus included a single-ring PET camera, polymerase chain reaction 1, a mechanical ventilator, a rebreathing circuit, and an infusion system described in detail previously (2, 22). 13NN (half life of ~9 min) was dissolved in previously degassed saline (0.1-0.2 µCi/ml). A sample of the 13NN-labeled saline was collected to assess its specific activity before intravenous injection.Imaging Protocol
A rapid-transmission scan was performed, and animal position was adjusted so as to maximize the cross-sectional area of the lungs in the imaging plane. This resulted in a transverse image plane at the apex of the heart just above the diaphragm.After optimization of animal position in the camera, a high-quality
transmission scan was acquired to be used for correction of gamma ray
energy attenuation by body tissues and supporting structures as well as
to calculate regional gas content. Image acquisition during the
transmission scan was conducted for 15 min during breathing and was
gated by using an electrical signal from the mechanical ventilator
marking the start of inhalation. Physiological parameters measured
included heart rate, systemic and pulmonary arterial pressures, cardiac
output (T), and airway opening pressure.
Measurements of pH, gas tensions, hemoglobin, carboxyhemoglobin, and
oxygen saturation values were obtained from arterial blood samples.
These parameters were measured before each PET scan as described below.
A Emission Scan Series
A was interrupted at end exhalation, and a bolus of
13NN-labeled saline solution was infused immediately into
the superior vena cava. Bolus volume was selected on the basis of the
specific activity of the infusate to produce images with consistent
number of counts per voxel. Simultaneously with the start of
infusion, collection of six consecutive images was initiated, each
with a scanning time of 10 s. At the end of the sixth image,
mechanical A was resumed, and four additional
consecutive images, each with a scanning time of 30 s, were
collected as the tracer washed out from the lungs. Collection of these
emission scans was not gated by the ventilator. A sample of the
infusate was collected to assess its specific activity.
After collection of a A/ emission scan series
in control conditions, the sheep was exposed to inhalation of 100 breaths of cotton smoke generated by using a modified bee smoker (Bee Keeper, Woburn MA). The smoke was delivered at the same VT
and frequency (10 breaths/min) as previously determined for eucapnea by
using a modified anesthesia breathing circuit and ventilator (Fig.
1). Immediately after the smoke exposure,
arterial blood gas and carboxyhemoglobin levels were measured.
Collection of PET images and physiological parameters was then
conducted 1, 2, and 4 h after the smoke inhalation exposure. At
the conclusion of the study, the animal was euthanized with an
intravenous injection of saturated potassium chloride.
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Data Analysis
Image processing. PET data were corrected for camera sensitivity and for tissue attenuation. The gating scheme yielded two images corresponding to the first and second half of the breathing cycle. Given that inspiratory time of the ventilator was set at 30% of the breathing cycle, the first gated image captured all inspiration and the initial rapid phase of exhalation, and the second gated image captured the slower last phase of exhalation in which lung volume is close to functional residual capacity. This second gated transmission scan was used for attenuation correction of the emission scans collected during apnea, whereas the sum of the two gated transmission scans was used for attenuation correction of the images collected ungated during breathing in the washout. Image reconstruction was then performed with a convolution back-projection algorithm by using a Hanning filter to yield an effective spatial resolution of 10 mm determined from the width at one-half height of a point source image. Resulting images consisted of an interpolated matrix of 159 × 159 voxels of dimension 2 × 2 × 10 mm.
Lung field masks were defined from the transmission scans taken in control conditions and 1 h after exposure to smoke. The masks were divided into three regions of interest (ROI) [nondependent (ND), middle (M), and dependent (D)] each of approximately equal number of voxels. The average volume of imaged lung corresponded to 104 ml or ~12% of a lung volume for a sheep of this size. Tracer kinetics data was obtained for each ROI from the respective average regional activity per voxel for each of the sequential PET images (Fig. 2).
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A was reinstituted. Because
13NN did not have a preferential solubility in nonaerated
alveoli, a peak activity was reached soon after injection but then
diminished during apnea, reflecting intrapulmonary shunt.
A nonlinear model described in detail in the accompanying paper
(3) was used to analyze the tracer kinetics data of each ROI. Briefly, the model assumed that each ROI was made of a nonaerated compartment (in which blood flow was pure shunt) and an aerated and
ventilated compartment. The model was implemented in the SIMULINK software package (The MathWorks, Natick, MA) and fitted to the regional
tracer kinetics data by use of a nonlinear identification toolkit
(Cambridge Control, Cambridge, UK) modified to include the time
averaging inherent to PET imaging. This analysis yielded estimates of
regional fraction relative to cardiac output
(R/T), regional shunt fraction
(S/R), and regional specific
A (sA) of the aerated compartment
for each ROI (Fig. 2). In all animals studied, activity in ND regions
stayed constant or slightly increased during breath hold. Shunt in
these ND regions was thus presumed to be negligible. In several
animals, a semilog plot of regional activity vs. time clearly
demonstrated departure from a single exponential washout model. For
those cases, the model was modified to include two independent
subcompartments with different specific A rates,
sA1 for the "fast" subcompartment
and sA2 for the "slow"
subcompartment. An effective regional index of sA in those regions was calculated as a -weighted average of the two subcompartment sA
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A1,
sA2, 1, and
2 are the regional sA and
of the two intraregional subcompartments.
Regional gas content fraction (Fgas) for each
condition was estimated from the regional value of the corresponding
transmission scan that was proportional to regional tissue density
(
lung). By delineating a region of interest over the
heart with assumed density heart = 1, Fgas was calculated for each voxel as
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Calculations.
Average regional per voxel relative to total of the
imaged lung slice per voxel, R/imT, was
calculated from the regional R/T
parameter identified by the model as
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S/imT, was calculated as
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S/R is the regional
shunt fraction of each ROI and
R/T is the fraction of regional
blood flow relative to cardiac output.
Regional A of aerated compartments relative
to the total A of the imaged lung,
A, for each ROI was
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A- ratio,
A/R, for each ROI was calculated
as
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Statistical analysis. Data were analyzed by using repeated-measures ANOVA techniques. Dunnett's multiple-comparison procedure was used to compare the difference between the three time points after smoke inhalation and the baseline control if there was significant overall difference among the four time points. Mixed-effects regression models were used to study the relationship between model parameters and arterial PO2 (PaO2). All statistical analyses were performed by using SAS (Cary, NC) with significance set at the 0.05 level.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Table 1 shows a summary of
physiological variables measured during the study. Mean
carboxyhemoglobin (COHgb) was 81% immediately after exposure to smoke.
Because inspired gas had FIO2 of
0.50 during the remainder of the study, COHgb levels consistently
declined, reaching near-normal levels by 4 h. Mean
PaO2 was 63 Torr after smoke exposure. Despite a
relative improvement after 1 h, PaO2 significantly decreased at 2 and 4 h compared with preexposure. Mean heart rate declined during the study, reaching significance at
4 h. Systolic and diastolic systemic pressures had significant declines at 1, 2, and 4 h. T remained stable
throughout the study. Mean pulmonary artery pressure increased
(reaching significance after 4 h), whereas pulmonary
vascular resistance steadily increased and at 4 h reached levels
significantly higher than preexposure levels. Airway opening pressure
progressively increased throughout the study.
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Average results of regional PET-derived parameters are presented
in Fig. 3 and Table
2. There was a vertical gradient in R/imT favoring the D regions at all time points in
the study. After smoke inhalation, R/imT of
the ND region was relatively unchanged. In D regions,
R/imT slightly declined in the hours after injury,
whereas R/imT gradually increased in the M region. These changes did not reach significance by ANOVA. Thus there was only
a minor redistribution of from D regions to M regions over
the course of the study.
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A of D regions decreased throughout the study,
reaching statistically significant levels after 2 h.
A/R gradually increased in ND
regions, whereas it steadily decreased in D regions reaching significance after 4 h.
Shunt, represented by a gradual drop in regional activity during the
breath-hold period, was not detected in ND regions throughout the
study. S/R progressively
increased in D regions after smoke exposure and reached statistical
significance by 2 h (P < 0.05) and 4 h
(P < 0.005). Because of the large
R/imT of the D regions and the progressive
increase in S/R of those
regions, the fraction of shunting imaged blood flow,
S/imT, increased after each time interval reaching
significance by 4 h.
There was also a vertical dependence of Fgas favoring ND
regions and decreasing toward D regions. Such a gradient increased with
time after smoke exposure as Fgas significantly decreased in D regions from 0.45 in control to 0.26 after 4 h of exposure to
smoke. A plot between regional shunt fraction and Fgas,
including all animals at all data points in the study for M and D
regions (Fig. 4), showed a negative
correlation (R = 
0.86) between these PET-derived
parameters.
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A negative correlation was detected between
PaO2 and
A/R for ND regions and a positive
correlation between the same parameters for D regions (Table
3). In D regions, changes in
A, R/imT, S/R, and Fgas
correlated most strongly with the decline in PaO2 seen
in the hours after inhalation exposure (Table 3). A substantial
negative correlation was found between PaO2 and
S/R in D regions and overall
shunt fraction S/imT.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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More than two million Americans suffer from thermal injury each
year. Of the nearly 8,000 associated fatalities, more than 80% are
attributed to smoke inhalation (25). It is presently believed that there are three mechanisms through which injury is
induced: thermal injury to the airways, asphyxiation secondary to the
gaseous products of pyrolysis, and injury induced by the inhalation of
particulate matter in the smoke (1, 5a, 9, 18, 21, 23, 25). In our study, intubation of the animal and cooling of the
smoke in an anesthesia bellows before delivery to the animal (Fig. 1)
minimized local thermal injury to the airway as a factor leading to
pulmonary dysfunction. Alterations in the gaseous environment during a
fire predispose the victim to asphyxiation secondary to the low ambient
oxygen tension and high concentrations of noxious gases created through
the process of pyrolysis. Carbon monoxide exerts its detrimental
effects by shifting the oxygen hemoglobin saturation curve to the left.
Thus there is interference with oxygen binding to hemoglobin;
therefore, delivery of oxygen to the tissues and cellular respiration
is hampered. In an effort to assure an adequate level of smoke exposure
in our study, all animals received 100 breaths of cotton smoke, which
resulted in mean COHgb levels of 81% immediately postexposure. By all
standards, this level of COHgb indicates a very severe level of
exposure. In an effort to minimize generalized and particularly cardiac ischemia and/or dysfunction due to the leftward shift
of the oxygen hemoglobin saturation curve and thus the resultant
hypoxemia, animals were placed on FIO2 of
0.50 immediately after induction of injury. As indicated in Table 1,
this resulted in relatively rapid reduction of COHbg levels to nearly
normal after 4 h. There was a significant decrease in
PaO2 values seen within the first hour after induction
of the injury. However, no significant changes in relative
A, , and shunt were seen at that time
(Table 2). It is likely that the changes in PaO2 at
this early time interval are due to carbon monoxide replacement of
oxygen bound to the hemoglobin, but we cannot rule out early changes in
A/ distributions occurring at length scales
smaller than the size of the ROIs analyzed in this study. As the hours
after injury progressed, carbon monoxide levels gradually decline and
hemoglobin molecules are more available to bind with oxygen. The
progressive declines in PaO2 at 2 and 4 h are
more likely to be attributable to changes in lung function (6,
13) than those seen at 1 h.
By analyzing the tracer kinetics data derived from the PET scans with
the methodology described in the accompanying paper (3),
we were able to quantify regional alterations in A, R, and S/R
during smoke inhalation injury for the first time. Before we discuss
the imaging results, it is important to acknowledge the technical
limitations of our technique. First, because we used a single-slice PET
camera, the data obtained come only from a 1-cm slice of the lung.
Although we positioned the animal in the camera so as to maximize the
imaging area of the lung, the 1-cm-thick slice only included a small
fraction (~12%) of the lung. This technical limitation may not be an
issue for modern multislice PET cameras capable of measuring large
regions of the lung, but in our study the data are limited in terms of detecting changes that may or may not have occurred in other portions of the lung. Also because of this limitation, parameters such as
A or R were normalized by the
average A or flow per voxel within the imaged lung
and the parameters R/imT and
S/imT are normalized by the total blood flow to the
imaged lung slice. The parameters
S/R and Fgas do
reflect absolute regional values within the ROI. A second limitation of
our technique relates to the spatial resolution of the PET images and
the large size of the ROIs used. As discussed in detail elsewhere
(10, 22), our reconstruction algorithm yields images with
a spatial resolution of 1 cm limiting information about tracer location
to volumetric elements of 1 ml. In this study, we averaged the imaging
data into three large ROIs each of approximately the same volume. This averaging had two main advantages: 1) it reduced the amount
of computation time required by the nonlinear parameter identification algorithm to a manageable time, and 2) it greatly reduced
the magnitude of imaging noise in the data yielding model predictions with excellent fit to the experimental data (3). The
disadvantage of averaging the data is the loss of detailed spatial
information. Thus the identified parameters A,
R/imT, and Fgas need to be taken as
average values within the ROIs, and it is impossible to determine the
precise location of shunting units within a resolution element or the
ROI. Fortunately, assessment of regional shunt does not depend on
spatial resolution but rather on the fraction of the tracer reabsorbed
during the apneic period. Thus the parameter S/R should still accurately
reflect the fraction of shunting blood flow within the given ROI, and
it does not require individual identification of shunting units.
The ND regions showed no evidence of local shunt. In cases showing
large intrapulmonary shunt in the D and M regions, a small increase in
regional activity was evident in the ND regions toward the end of the
apneic period, suggesting the effect of 13NN tracer
recirculation. Maintenance of local R/imT along with steadily increasing A in ND regions caused the
progressive increase in A/R
during the 4 h of the study. Both R/imT and
A to M regions displayed minor increases resulting
in little change in their average
A/R over the 4 h. There was
also little change in S/R with
time in M regions. In D regions, however, A markedly declined over the course of the study, whereas
R/imT showed a small decrease, resulting in a
monotonic drop in A/R.
R/imT was highest in the D regions at all points of
the study. In the control conditions, this distribution would be
expected in a normal supine sheep on the basis of previous studies of
sheep and dogs in the supine position (5) and consistent
with the West et al. model of pulmonary (24). As
injury progressed, regional A and fractional gas
content in D regions progressively decreased. In an effort to preserve
oxygenation and A/ matching, one would have
expected a significant shift of away from D regions. This
occurred but not to the extent that would have matched the change in
A. As a result,
A/R progressively decreased in D
regions in the hours after smoke inhalation injury. The result of a
limited redistribution of R away from D regions is
different from results in the model of acute lung injury by
intravenously injected oleic acid, which shows a major redistribution
of blood flow away from dependent regions and a preservation of
oxygenation (4). Instead, our results are similar to those
obtained by the same group of investigators when oleic acid was
injected together with endotoxin. This suggests that smoke inhalation
injury may be accompanied by a local disturbance in hypoxic
vasoconstriction possibly caused by increased endogenous nitric oxide production.
We found blood flow to shunting regions to be the single most
predictive factor for the decline in PaO2.
Because of the small change in R/imT and the
regional increase in S/R to D
zones, the total fraction of shunting blood flow progressively
increased over the experiment from 8 to 27%. The etiology of the
increase in shunt may be found in the analysis of Fgas that
steadily declined in D regions and the inverse relationship between
Fgas and S/R (Fig.
4). The finding that regional shunt fraction increased as Fgas became <0.5 suggests that progressive alveolar
derecruitment and/or alveolar flooding by edema and endothelial leak
could have been the causes of the increase in
S/R after smoke inhalation.
Previously, the most extensive studies of A/
changes by smoke inhalation were carried out by using MIGET. Robinson
et al. (17) proposed that in the first 24 h after
smoke inhalation exposure, alterations in A/
matching were caused by shifting A away from poorly
perfused areas causing regions of low A/. Shunt development was found to be minimal (17). However,
close analysis of their data reveals consistently higher predicted vs. actual PaO2 values in the first 72 h after
smoke inhalation. The differences between predicted and actual values
were greatest 24 h after exposure. This suggests the presence of
shunt that may have not been adequately estimated by their
calculations. In fact, Shimazu et al. (19) demonstrated
that in moderate and severe inhalation injury both shunt and low
A/ regions developed in the first 24 h.
Our study clearly indicates that, within the first hours after smoke
inhalation, A/ mismatch and hypoxemia result
from the development of shunt and low A/
predominantly in the dependent portions of the lung. Blood flow
and shunt in nondependent and middle regions are maintained at nearly
preinjury levels. MIGET relies on the injection of six inert
gases dissolved in saline and then simultaneous sampling of pulmonary
gas and systemic blood and determination of the corresponding gas
concentrations by chromatography. Such a method yields a global index
of A/ heterogeneity but does not allow
assessment of the independent contributions of A and
to such heterogeneity. Analysis of tracer kinetics data from
PET assumes each lung region to be composed of two compartments: one of
pure shunt and another aerated and ventilated compartment. Because of
the low solubility of 13NN in blood and tissues compared
with air, tracer delivered to aerated compartments, in proportion to
regional , remained constant during apnea. In contrast, tracer
delivered to nonaerated regions was carried away by pulmonary ,
providing the basis for estimating an index of regional shunt fraction.
Once R and A/R
were identified, regional A could be estimated by
fitting the model to the tracer kinetics data obtained during the
washout. Relative values of regional A/ and
S/R can therefore be obtained. It
is possible that our method of delivering the smoke may have caused a
more rapid progression of the injury, resulting in shunt and low
A/ regions that were visible in dependent
regions as early as 2 h.
In summary, a nonlinear model for analysis of regional 13NN
kinetics measured by PET yielded information about regional changes in
A, R, and
S/R after an exposure to smoke
inhalation. In contrast to prior studies, we found that in the early
hours immediately after smoke inhalation substantial shunt developed that was localized in dependent regions of the lung where was highest. The development of hypoxemia correlated with the development of decreasing Fgas in dependent regions and increased blood
flow to regions of shunt. This study has demonstrated that PET is a useful tool for evaluation of regional alterations in lung function in
response to injury. Analysis can be made of the relative contributions of altered airway function (A), pulmonary
and shunt, and parenchymal dysfunction (Fgas) to the
alteration in gas exchange. Radiation estimates for imaging
A and of a whole human lung with this
technique using a multiring PET camera yield a total radiation exposure
to the patient no greater than that from two high-resolution computed
tomography slices. We therefore conclude that this technique may have
clinical applicability.
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ACKNOWLEDGEMENTS |
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This study was funded by National Heart, Lung, and Blood Institute Grant HL-38267f and by Massachusetts General Hospital Center for Engineering in Medicine, The Shriners Burn Institute, and The Cystic Fibrosis Foundation.
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FOOTNOTES |
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Address for reprint requests and other correspondence: J. G. Venegas, Dept. of Anesthesia, Clinics 2, Massachusetts General Hospital, Fruit St., Boston, MA 02114 (E-mail: jvenegas{at}vqpet.mgh.harvard.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
March 29, 2002;10.1152/japplphysiol.00911.2001
Received 4 September 2001; accepted in final form 27 March 2002.
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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)
and M regions (
). Data include all animals and all time
points in the study.