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1 Research and Development, PCO2 in the lumen and
serosa of cecum and jejunum was measured in mice. The anesthetic used
was a fentanyl-fluanisone-midazolam mixture.
PCO2 was recorded in vivo and
postmortem. PCO2 was 409 ± 32 Torr (55 ± 4 kPa) in the cecal lumen and 199 ± 22 Torr (27 ± 3 kPa) on the serosa in normal mice. Irrigation of the cecum
resulted in serosal and luminal PCO2
levels of 65-75 Torr. Cecal PCO2
was significantly lower in germ-free mice (65 ± 5 Torr). Cecal
PCO2 increased significantly after
introduction of normal bacterial flora into germ-free mice. Introduction of bacterial monocultures into germ-free mice had no
effect. After the deaths of the mice, cecal
PCO2 increased rapidly in normal
mice. The intestinal bacteria produced the majority of the cecal
PCO2, and the use of tonometry in
intestinal segments with a high bacterial activity should be
interpreted with caution. We propose that serosal
PCO2 levels >150-190 Torr
(20-25 kPa) in the cecum of mice with a normal circulation may
represent a state of gas supersaturation in the cecal wall.
carbon dioxide; carbon dioxide pressure; serosa; germ free; gnotobiotic; inherent unsaturation
GASTROINTESTINAL TONOMETRY is a technique approved for
clinical use by the American Food and Drug Administration. It is used to measure the intestinal tissue PCO2
(PtiCO2) for
assessment of shock (8), prognosis in critical care patients (5-9)
and in resuscitation (10). Organ blood flow distribution
and tissue oxygenation are uneven during states of shock, even during
compensated shock and hemodynamic stability. Redistribution of the
cardiac output to more vital organs leads to a disproportionate
reduction of the splanchnic blood flow. The inadequate oxygen delivery
will result in oxygen debt, anaerobic metabolism, and tissue acidosis in the splanchnic organs, which again will lead to increased
PtiCO2 in the mucosa (7). Although the viability and integrity of the
intestinal mucosa in itself is an important concern in critical care
patients, mucosal
PtiCO2 can also
be used as a systemic index in the assessment of shock, because blood
is preferentially distributed to other organs (8). Mucosal
PtiCO2 is
measured in saline within a gas-permeable silicone balloon at the tip
of a modified gastroduodenal tube that is introduced into the stomach
or sigmoid colon (8). The construction of the current equipment
restricts the clinical use of tonometry to nonsterile hollow organs
(i.e., the lumen of the intestinal tract), and the equilibration time
is relatively long (60-90 min), although newer
devices containing gas instead of saline are considerably faster.
Introduction of PCO2 microelectrodes
has enabled rapid measurement in all organs, including PCO2 measurements on the mesenteric
surface, in animal studies (1, 15, 21).
In a number of experimental (1, 16) and clinical studies
(5-10), tissue pH (pHi) has
been calculated on the basis of PtiCO2 measured
in the lumen of the intestine and systemic arterial bicarbonate
levels. pHi levels below ~7.3 are
considered to indicate intestinal ischemia (17). However, this
approach has been criticized (15, 21), and
PtiCO2
[or rather
PtiCO2 We have chosen to use the mouse as our model species, because we
expected the bacterial fermentation in the cecum to be a good example
of an intestinal segment with a high baseline
PCO2. We hypothesized that the
majority of the CO2 in the cecum
and large intestine of mice originates from bacterial fermentation. If
so, this indicates that the CO2
originates from sources other than the intestinal wall, and
PCO2 cannot be used as a diagnostic
index of tissue ischemia in intestinal segments where the
bacteria have a high metabolic rate.
PCO2 measurements were carried out in
the lumen of different segments of the intestinal tract in mice to test
for gastrointestinal segments with a high baseline
PCO2. Further measurements were
carried out to show that bacterial fermentation was the cause of the
high PCO2 levels. The latter
measurements were carried out in the lumen and on the serosa of the
cecum and the jejunum in the following groups of mice: mice with normal bacterial flora (conventional), conventional mice in which the cecal
content had been removed by irrigation, mice without any bacterial
flora (germ-free mice), mice with bacterial monocultures (gnotobiotic
mice), and germ-free mice cohoused with conventional mice to regain
normal bacterial flora (conventionalized germ-free mice). To test the
importance of an adequate blood supply, the diffusion of
CO2 from the intestinal lumen to
the serosa was investigated during no-flow ischemia (after the
animal was killed).
Animal model.
Conventional mice with a normal intestinal flora and mice with a highly
specialized and defined bacterial flora were included in the
experiments in a protocol approved by the Nycomed Institutional Animal
Care and Use Committee (Table 1). The mice
with a normal bacterial flora were male HsdHan:NMRI and Hsd:ICR mice
(Harlan, UK) and male Bk:NMRI mice (B&K Universal,
Sweden). The mice with a well-defined bacterial flora were
male and female KI:NMRI mice with either no bacterial flora (germ-free
mice), bacterial monoculture (gnotobiotic), or germ-free mice cohoused
with conventional mice to regain normal bacterial flora
(conventionalized germ-free mice). The KI:NMRI mice were supplied by
Tore Midtvedt, Laboratory of Medical Microbial Ecology, Karolinska
Institute, Stockholm, Sweden. The animals were housed, four to six
animals per cage (polycarbonate size III, B&K Universal, Norway), with
autoclaved aspen tree bedding (B&K Universal, Norway) in a controlled
environment (21 ± 2°C, 15 ± 10% relative humidity, 12-h light
cycle in daylight phase, and 15 air changes/h) for an acclimatization
period of at least 7 days. The germ-free, gnotobiotic, and
conventionalized germ-free KI:NMRI mice were housed in special
isolators and maintained on autoclaved R36 diet (Lactamin, Sweden),
while the conventional mice received RM1(E)SQC diet (Special Diets
Services, UK). The gnotobiotic KI:NMRI mice were monoassociated with
Lactobacillus acidophilus (LA5),
Clostridium difficile (ATCC-9689), or
Escherichia coli (X7), 10-11 days
before measurement of
PCO2. Bacterial strains
were supplied by Tore Midtvedt. Colonizations were achieved by smearing
the fur of germ-free KI:NMRI mice with the bacterial monocultures as
the animals were introduced into their respective sterile isolators.
Conventionalization of germ-free KI:NMRI mice was achieved by cohousing
germ-free KI:NMRI animals with HsdHan:NMRI mice for 15 days before
measurement of PCO2. Bacterial monoassociation and conventionalization of germ-free KI:NMRI mice were
confirmed by aerobic and anaerobic microbiological examination of
intestinal samples from colon and cecum obtained at the time of
PCO2 measurements. Total aerobic
count, Enterobacteriaceae and
Lactobacillus/Enterococcus numbers
were carried out after smearing of diluted intestinal samples on blood
agar plates incubated for 18-24 h at 37°C in an atmosphere of
air-5% CO2. Total anaerobic count
and Clostridium perfringens/difficile
numbers were carried out after smearing of diluted intestinal samples
on blood agar plates incubated for 18-24 h at 37°C in an
anaerobic atmosphere.
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
arterial PCO2 (PaCO2)] has been
proposed to be the best measure of ischemia (17). Normal
values for
PtiCO2 (or
PtiCO2 PaCO2) have not been established in the
clinical population, because most studies refer to calculated
pHi. On the basis of experiments
in pigs, mucosal
PtiCO2 levels
of 78 ± 16 Torr are considered normal, whereas mucosal
PtiCO2 levels
of 128 ± 34 Torr are considered critical (15). However, it has not
been studied whether the baseline PtiCO2 varies
in different parts of the gastrointestinal tract, and, when diagnosing
intestinal ischemia, we rely on the assumption that the
baseline PtiCO2
values are equal. Most tonometry studies have been carried
out in jejunum/small intestine, which, compared with the large
intestine, is largely devoid of microflora; therefore, it is important
to determine whether our assumptions regarding PtiCO2 baseline
values also apply to the large intestine. It is assumed in tonometry
that the PCO2 measured under normal circumstances originates from the oxidative metabolism of the intestinal wall, whereas the CO2
is produced by protons buffered by
HCO
3 under ischemic conditions (20).
Other sources of CO2 may be
relevant, and we hypothesized that bacterial fermentation in certain
parts of the gastrointestinal tract may contribute a large proportion
of the CO2. The contribution
of bacterial fermentation to intestinal
PCO2 has not been very
thoroughly assessed in humans, and the number of relevant references is
limited (3, 4, 12). The PCO2 in flatus was measured in these references; therefore, it is impossible to
predict local intestinal
PtiCO2 levels
or local bacterial CO2 production.
In rats, intracolonic PCO2 tensions
were clearly related to the bacterial metabolism of the intestinal flora, compared with germ-free rats (2).
MATERIALS AND METHODS
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
Table 1.
In vivo PCO2 levels at t = 0
Anesthesia and calibration of PCO2 probes. The mice were anesthetized with 0.1 ml/10 g of a 1:1:2 mixture of Hypnorm (fentanyl citrate; 0.315 mg/ml), Fluanisone (10 mg/ml; Janssen-Cilag), and Dormicum (Midazolam, 5 mg/ml; Roche) and sterile water given subcutaneously. Anesthesia was supplemented as needed according to clinical signs. The animals were placed in dorsal recumbency on a heating pad (39°C) to maintain normal body temperature. The four PCO2 microelectrodes (type MI 720; Microelectrodes, Londonderry, NH) were consistently used for the same intestinal segment and not interchanged. Immediately before the experiment, the PCO2 microelectrodes were calibrated with a three-point calibration in CO2 solutions ranging from 25.5 to 182.3 Torr. The microelectrodes were tested against the known PCO2 of saline solutions measured in a blood-gas machine (AVL 995, Biomedical Instruments, Austria, and Radiometer ABL 3, Radiometer, Denmark). According to the manufacturer, the PCO2 microelectrodes are linear and valid for PCO2 measurements up to 630 Torr (90 kPa) at 37°C. Measurements of PCO2 were carried out between 1100 and 2300. PCO2 levels in the germ-free and gnotobiotic KI:NMRI mice were measured within 4 h after they were removed from their isolators. All saline used for irrigation and for keeping the intestines moist during measurements was at 39°C.
Measurement of luminal PCO2 in different segments of the bowel. After midline laparotomy, the PCO2 microelectrodes were introduced into the stomach, jejunum, basis cecum, and the cranial and transverse colon via antimesenteric incisions in the duodenum, jejunum, apex cecum, and cranial colon, respectively. This screening of different bowel segments was carried out in conventional HsdHan:NMRI mice.
Measurement of luminal and serosal PCO2 in the cecum and jejunum. To further describe the PCO2 levels of the cecum and jejunum, conventional HsdHan:NMRI, Hsd:ICR, and Bk:NMRI mice and germ-free, gnotobiotic, and conventionalized germ-free KI:NMRI mice were used. The apex and corpus cecum and a jejunal loop were exteriorized after bilateral paramedian suprapubic incisions. Two PCO2 microelectrodes were positioned in the lumen of the basis cecum and 2-3 cm into the jejunal lumen, through incisions in the apex cecum and the antimesenteric jejunum, respectively. The tip of the intraluminal microelectrodes was positioned in the center of the intestinal content, and direct contact with the mucosa was avoided. Both intestinal segments were repositioned into the abdomen with the microelectrodes maintained in position. Another two PCO2 microelectrodes were positioned perpendicular to the serosal surface of the basis and corpus cecum and a jejunal loop for measurements of serosal PCO2. These microelectrodes were manually positioned for the duration of the experiment, avoiding pressure on the intestinal wall. To show how the cecal content contributed to the PCO2, the cecum was emptied of its intestinal contents before the probe was positioned in a separate group of HsdHan:NMRI mice (irrigated HsdHan:NMRI mice). The exteriorized apex cecum was opened, and the cecum was irrigated, with a minimum of 10 ml isotonic saline by rectal lavage until the effusate consisted of saline only. The cecum was closed and repositioned, 1-2 ml of saline were infused to obtain normal cecal filling, and the animal was allowed to stabilize for 10 min before the PCO2 microelectrodes were positioned as described above.
When stable PCO2 levels of all four microelectrodes had been recorded (t = 0), the animals were killed by an intracardiac injection of 0.2 ml pentobarbital sodium (50 mg/ml), and the PCO2 values during the resulting no-flow ischemia were recorded. PCO2 values were recorded at 30, 60, 90, and 120 s and at 3, 4, and 5 min postmortem. Stability of the in vivo PCO2 values was indicated as a standard feature of the PCO2 microelectrodes when the dPCO2/dt decreased below a fixed value. Stable PCO2 values were usually obtained ~3-10 min after introduction of the microelectrodes.Statistics.
All references to results in the text, figures, and tables are means ± SE. Unless otherwise stated, all reference to results in the text
are in vivo PCO2 levels at
t = 0. Parametric and nonparametric
Kruskal-Wallis ANOVA has been applied on the results of the lumen and
serosa at t = 0, followed by a
pairwise Mann-Whitney rank sum test on relevant groups. Jandel
Sigmastat version 2.0 was used for the statistical analyses, and the
chosen levels of significance (P < 0.05 and P < 0.01) were
corrected (Bonferroni) for multiple comparisons
(n = 7) to
P 
0.007 and P 0.001. Linear regression analysis
and Pearson's product-moment-correlation analysis of the
PCO2 levels and time of recording
were carried out to determine how
PCO2 levels in the cecal lumen of
conventional mice varied with the time of recording.
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RESULTS |
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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Measurement of luminal PCO2
in different segments of the bowel.
The luminal PCO2 in different
gastrointestinal segments of conventional HsdHan:NMRI mice with a
normal bacterial flora is shown in Fig 1.
The PCO2 in the stomach, jejunum, and
colon was in the range of 135-175 Torr (18-23 kPa) and
considerably less than the 390 Torr (52 kPa) in the cecum.
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Measurement of luminal and serosal
PCO2 in the cecum and jejunum.
We hypothesized that the source of the very high
PCO2 in the cecal lumen was bacterial
fermentation. To test this hypothesis, we included in these experiments
mice with a normal bacterial flora (conventional mice), conventional
mice from which the cecal content had been removed by irrigation, mice
without any bacterial flora (germ-free mice), mice with bacterial
monocultures (gnotobiotic mice), and germ-free mice cohoused with
conventional mice to regain a normal bacterial flora (conventionalized
germ-free mice). All in vivo PCO2
data (t = 0) are included in Table 1,
and the postmortem PCO2 data from 0 to 5 min after death are illustrated in Figs.
2-4. The statistical differences in in vivo
PCO2 between the different groups of
mice are included in Table 2.
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INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
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Our experiments strongly indicate that the very high PCO2 levels in the lumen of the cecum (400-570 Torr) are caused by the presence of bacteria. In addition, the serosal PCO2 of the cecum in conventional mice was unexpectedly high. The PCO2 levels in the cecal serosa of germ-free KI:NMRI and irrigated HsdHan:NMRI mice were close to normal tissue PCO2 (60-75 Torr), as expected for aerobic metabolism, while mean values up to 200 Torr were measured on the cecal serosa of conventional animals. Theoretically, this could be due to ischemia or bacterial metabolism in the intestinal lumen. However, normal tissue PCO2 levels were recorded on the serosa of germ-free and gnotobiotic KI:NMRI and irrigated HsdHan:NMRI mice; because probe placement in these mice was carried out as in conventional mice, it seems unlikely that the placement of PCO2 microelectrodes caused local ischemia in the intestinal wall. In addition, the modest increase in PCO2 that occurred after death in the jejunum of all mouse groups and in the cecum of irrigated HsdHan:NMRI mice and germ-free mice, indicates that the PCO2 microelectrodes detect tissue ischemia in intestinal segments even where there is little or no bacterial activity. The anesthesia protocol (Hypnorm-Dormicum) used in this model has been shown to have no effect on the arterial blood gases (both PaCO2 and arterial PO2) and arterial pH of rats during 2 h of anesthesia, and the same is likely to be true in mice (18). Thus ischemia resulting from the anesthetic and surgical regime is unlikely to explain the PCO2 differences between the different groups of mice. In conclusion, PCO2 levels exceeding 60-75 Torr in the cecal serosa and lumen of conventional mice are unlikely to be caused by ischemia in the living mouse, and the data from irrigated HsdHan:NMRI mice and germ-free mice strongly indicate that the very high PCO2 levels in conventional mice are caused by bacterial CO2 production in the lumen. These results indicate that the PCO2 baseline varies considerably in different parts of the gastrointestinal tract in mice and particularly in intestinal segments with a high bacterial activity. The content of bacteria in the colon of humans is high, and it is likely that this will influence the baseline values for PCO2. Although the small intestine is nearly sterile in normal humans, large numbers of bacteria can be found in these segments during critical care conditions.
The CO2 generated in the intestine is removed by the mucosal blood supply and transported to the lungs for exhalation or is passed as flatus. The vascular absorption and pulmonary excretion account for >95% of the clearance after administration of CO2 into the lumen of the stomach in humans and jejunum and ileum of the dog (3, 4, 12, 13). Accordingly, diffusion of CO2 from the lumen and into the cecal wall and the importance of the circulation in the CO2 removal are demonstrated by the steep gradient of CO2 observed from lumen to serosa in vivo. The importance of the circulation and of the characteristics of the cecal wall as a barrier to CO2 diffusion is further demonstrated by the rapid decline of the CO2 gradient (i.e., increase in serosal PCO2) that occurs immediately after the death of the animals, when cecal wall tissue PCO2 rapidly approaches luminal PCO2 levels of 400-570 Torr (Figs. 2 and 3). Although not statistically different, the lower in vivo serosal PCO2 and the slower postmortem increase in serosal PCO2 in Hsd:ICR mice may suggest differences in the characteristics of the cecal wall as a barrier to CO2 diffusion.
The screening of various segments of the gastrointestinal tract,
including the cecum and colon, showed that the cecum is the only region
with intraluminal PCO2 levels as high
as 390 Torr, despite comparable bacterial counts in cecum and colon (~108-109
colony-forming units/ml feces) (14). This suggests a higher metabolic
activity of the bacteria in the cecum compared with colon, in
accordance with the normal physiological function of the cecum in mice
and other rodents. As shown by Poulsen et al. (14), analysis of
bacterial ribosomal RNA activity and of bacterial generation time in
the cecum and colon also suggests that the metabolic activity occurs
mainly in the cecum. The metabolic activity of the cecal bacteria is
also suggested by the PCO2 levels in
relation to our time of measurement. During the time of measurement (1100-2300), the PCO2 showed a
positive correlation with time (
= 17.4 ± 5.3 Torr/h,
P = 0.03, r2 = 0.28). This
reflects the nocturnal feeding habits of mice and suggests a circadian
rhythm of diet fermentation. Because the PCO2 measurements were distributed
evenly throughout the day, we consider this correlation to be without
effect when comparing the mean PCO2
levels of different mouse groups. The luminal
PCO2 of the colon in mice (164 ± 12 Torr) was twice as high as the values reported in rats (83 ± 12 Torr) (2), probably a result of the measurements in rats being carried out in the lower and caudal colon, whereas our measurements in mice
were made closer to the cecum in the cranial and transverse colon. As
demonstrated by comparable PCO2
levels in the lumen of cecum and jejunum in irrigated HsdHan:NMRI mice,
the metabolism of the cecal wall per se contributes the same low amount of CO2 as does the jejunum, both
in vivo and during postmortem ischemia. In the cecum of
conventional mice, both luminal and serosal
PCO2 are largely a reflection of
bacterial metabolism, and the use of tonometry to detect cecal wall
ischemia and to assess viability is not possible.
The microbiology of the cecum and colon shows that, although bacterial monoassociation of germ-free KI:NMRI mice occurred as expected, intestinal monocultures of L. acidophilus, C. difficile, and E. coli did not result in any increased production of CO2. This finding is to be expected, most likely due to the lack of substrate needed for CO2 production in monocultures (2). Despite comparable aerobic and anaerobic bacterial counts, the higher numbers of Enterobacteriaceae in conventionalized germ-free KI:NMRI mice compared with the HsdHan:NMRI mice may indicate that the transfection during cohousing was incomplete at the time of sampling, as has also been observed by others (19). This may be reflected in the cecal PCO2 levels of conventionalized germ-free KI:NMRI mice that were higher than those of germ-free KI:NMRI mice but lower than those of HsdHan:NMRI mice.
Do PCO2 levels >190 Torr in the cecal wall represent a state of gas supersaturation? A tissue PCO2 level of 60-75 Torr was expected on the serosal surface of the intestines, including the cecum, but PCO2 levels >190 Torr were measured in conventional animals in our study. To our knowledge, such high tissue PCO2 under normal conditions has never been described before.
During tissue metabolism, O2 is utilized and CO2 is produced. The total gas tension decreases, because the effective solubility of CO2 in the body is greater than the effective solubility of O2. The result is a decreased total gas tension of the tissues, also known as the "inherent unsaturation" or "O2 window" (22). The sum of the alveolar partial pressures is 760 Torr (101.3 kPa) at normal atmospheric pressure, and PO2 and PCO2 exert a pressure of 103 and 41 Torr, respectively. Water vapor and nitrogen make up the remaining 616 Torr in the alveoli as well as in arterial and venous blood (22). In the tissue cells, PO2 and PCO2 have been reported to be 10 and 49 Torr, respectively, resulting in a sum of partial pressures of 675 Torr and an inherent unsaturation of 85 Torr during normal aerobic metabolism (11). Others have reported a normal tissue PCO2 of 60-90 Torr (20), resulting in a maximum inherent unsaturation of 50-85 Torr during aerobic metabolism at normal atmospheric pressure. If additional CO2 (from the cecal lumen) constantly diffuses into tissues with an otherwise normal perfusion (cecal wall), it may increase the total tissue PCO2 level from the normal 60-90 to >150-190 Torr, despite constant and rapid tissue dissociation of CO2. This additional CO2 may be sufficient to exceed the normal inherent unsaturation, i.e., the total gas tension in the tissue exceeds the atmospheric pressure. If this occurs in areas with a low hydrostatic blood pressure (such as the capillary system, postcapillary venules, veins, and surrounding interstitium), the total gas tension will exceed the total hydrostatic pressure (atmospheric pressure and blood pressure,) and gas supersaturation will ensue. Because the in vivo PCO2 levels of 196-199 Torr measured on the cecal serosa of HsdHan:NMRI and Bk:NMRI mice reflect the lowest level on the mural PCO2 gradient, it is obvious that subserosal and deeper blood vessels are exposed to even higher PCO2 levels. Experiments with normal mice, to verify the above theory, confirm that gas supersaturation does occur in the cecal wall of this species (H. Rasmussen, unpublished observations). In conclusion, baseline PtiCO2 levels in different intestinal segments vary markedly in mice. This precludes the use of mucosal tonometry to detect ischemia and to assess viability in intestinal segments where the bacterial metabolism is high. The bacterial activity around the tip of the tonometry balloon should be considered when tonometry is used in humans, particularly if small intestinal overgrowth is suspected or if tonometry is applied in colonic segments cranial to the sigmoid colon. In addition, we propose that bacterial fermentation in the cecal lumen and the normal, but insufficient, vascular clearance of CO2 may create a state of supersaturation in the cecal wall of conventional mice.| |
ACKNOWLEDGEMENTS |
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We thank Arshad Mohammed, Bente Spilling, Eva Østerlund, and Johannes Bergstedt for skillful technical assistance. We also thank Merete Hofshagen for the microbiological examination of intestinal samples.
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FOOTNOTES |
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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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: H. Rasmussen, Research and Development, Nycomed Imaging AS, PO Box 4220, Torshov, N-0401 Oslo, Norway (E-mail: hras{at}nycomed.com).
Received 25 February 1998; accepted in final form 23 November 1998.
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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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, Serosa; 
, lumen. Values
at t = 0 are stable values before
killing. Values from 0 to 5 min are postmortem values. When error bars
are not shown, they are smaller than symbols of graph.
