Influence of Enteral Oxygen Administration on the Slow Electrical Activity of the Intestine and Stomach S. Gelman, MD; M. Paz, MSc; E.
Levy,
MD
Thirty-eight starved cats, anesthetized with pentobarbital (Nembutal) sodium, received enteral administration of oxygen and other gases; the effect on intestinal motility as expressed by electrical activity was measured. Oxygen caused a notable increase in amplitude and frequency of slow electrical waves, while carbon dioxide and nitrogen caused no visible altera\s=b\
tions. Phentolamine
hydrochloride and propranolol hydrochloride together with atropine sulfate decreased the amplitude and frequency of oscillations to near zero; subsequent administration of enteral oxygen caused a notable increase in electrical activity, while enteral carbon dioxide produced no alterations. On the basis of our previous observations that enteral oxygen enhances oxygen and blood delivery to the gut wall, we suggest that the rise in stomach and intestinal electrical activity during enteral oxygen administration in conditions of surgical stress may be associated with an increase in oxygen and blood delivery to the gut wall.
(Arch Surg 111:566-574, 1976)
well-known phenomenon that under certain condi¬ such as surgical trauma, parallel changes take in or intestinal blood flow and gut motility. There is an inhibition of intestinal motility'" and a decrease in splanchnic blood flow."1" These changes can be caused by an increase in adrenergic discharge and excitais
Itplacetions,portal a
Accepted
for publication Dec 26, 1975. From the Department of Anesthesiology, Beilinson Medical Center, Petah Tikva, and the departments of physiology and pharmacology, Sackler School of Medicine, Tel Aviv University, Israel. Dr Gelman is now with Cleveland Metropolitan General Hospital. Reprint requests to Department of Anesthesiology, Cleveland Metropolitan General Hospital, 3395 Scranton Rd, Cleveland, OH 44109 (Dr
Gelman).
tion of -adrenoreceptors located in the intestinal and vascular walls. It has been shown that the decrease in either portal or total hepatic blood flow or both associated with operative stress and anesthesia can be modified by enterai oxygen administration." '-' The present work investigates the possibility that intes¬ tinal motility can be stimulated by enterai oxygen admin¬ istration, which leads to increased portal (intestinal) blood flow. METHODS
experiments were performed on 38 starved cats ranging in weight from 2.5 to 4.5 kg. Tracheostomy, catheterization of femoral artery and vein, and laparotomy were carried out under pentobarbital (Nembutal) sodium narcosis (40 mg/kg body weight). A pair of small silver needle electrodes was inserted 0.7 cm apart into the muscle layer on the front surface of the stomach, 3 to 4 cm above the pylorus. A second pair was inserted, also 0.7 cm apart, into the muscle layer of the intestinal wall, 15 to 20 cm below the pylorus. A polyethylene catheter was placed in the intestinal lumen 30 to 35 cm below the pylorus. The peritoneal cavity was The
then closed. The electrical activity of the stomach and intestine was recorded continuously according to the method of Condrea et al," and the mean values of amplitude and frequency were evaluated during the various experimental procedures. Low level amplifiers were used with an extra capacitor of 32 microfarads at the input. Electrocardiogram lead 2 and blood pressure in the femoral artery (measured by a transducer) were recorded at the same time. The oxygen tension of arterial blood samples was periodically deter¬ mined. Each cat was allowed to rest for 30 minutes following closure of the abdominal wall before the experiments were begun; during this time, the electrical activity of the stomach and intestine was recorded.
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During the experiments, oxygen, nitrogen, and carbon dioxide injected into the intestinal lumen by a syringe attached to the polyethylene catheter; 20 ml of gas was injected two to three were
times at 5- to 6-minute intervals at a flow rate of 5 to 7 ml/min to prevent distention of the intestinal wall. The 38 cats were divided into the following six groups. Group 1 (ten animals) received 20 ml of oxygen, two to three times, at 5- to 6-minute intervals. Group 2 (six animals) received carbon dioxide in the same manner as group 1. Group 3 (six animals) received nitrogen in the same manner as group 1.
Group 4 (ten animals) received an a-adrenal-blocking drug (phentolamine hydrochloride, 1 mg/kg body weight, intravenous¬ ly), a /¡-adrenal-blocking drug (propranolol hydrochloride, 1 mg/ kg, intravenously), a choline-blocking drug (atropine sulfate, 0.4 mg/kg, intravenously), and then enterai oxygen in the same group 1. 5 (six animals) received the same pharmacologie treat¬ ment as group 4, followed by enterai carbon dioxide. Group 6 (six animals, three cats from group 4 and three cats from group 5) received oxygen inhalation for 15 minutes before the pharmacologie and enterai gas treatments. Four additional cats underwent tracheostomy and the femoral artery and vein were catheterized; laparotomy and catheterization of portal vein via a branch of mesenteric vein were performed. In these cats, slow electrical activity of the gut was not recorded, but Po, and oxygen saturation in the arterial, venous, and portal blood were measured before and during oxygen inhalation. The purpose of blocking the digestive tract receptors with the drugs was to determine the effectiveness of enterai oxygen administration under conditions of full pharmacologie denervation of the muscle wall of the gut. The oxygen inhalation allowed us to study the influence of increased arterial blood oxygen tension on the stomach and intestinal motility. The amplitude and frequency of the electrical slow waves' oscillations recorded from the stomach and intestinal walls were compared before and during the inhala¬ manner as
Group
tion procedure. Wilcoxon nonparametric statistical test was applied to compare the results obtained during the two successive phases of the
experiment."
RESULTS
During the first 30 minutes following surgical prepara¬ tion of the animal, the slow wave electrical activity of the stomach and intestinal muscles was recorded. Group 1.—Within a few minutes after enterai oxygen administration, eight of the ten animals showed an increase in amplitude and frequency of slow electrical waves (Fig 1). In the two remaining animals, no visible alterations were noticed. Enterai oxygen administration had a greater effect in animals with lower baseline elec¬ trical activity. For all ten cats in this group, the average amplitude increase was 82% and 86% for stomach and intestinal electrical activity, respectively; the average frequency increase was 47% and 20% for stomach and intestinal activity, respectively (Table). Groups 2 and 3.—Neither the enterai carbon dioxide nor nitrogen administration were accompanied by any visible alterations in the stomach and intestinal activity (Fig 2 and 3, Table). Group 4.—Phentolamine and propranolol together with
atropine decreased the amplitude and frequency of motility oscillations to near zero. Administration of enterai oxygen after the pharmacologie treatment caused an increase in the amplitude and frequency of slow electrical waves in all experimental animals (Fig 4); the amplitude more than doubled both in stomach and intestinal activity (Table). Group 5.—Once the motility oscillations were reduced to near zero by the pharmacologie agents, carbon dioxide administration did not
cause
alterations in the electrical
activity (Fig 5).
Group 6.—This group included an additional four cats. via the tracheostomic cannula led to notable increase in the arterial blood oxygen tension (from 92 ± 6 to 510 ± 15 mm Hg) and in oxygen saturation (from 96% ± 10.1% to 99% ± 9.7%). It did not, however, cause any alterations in stomach and intestinal activity (Fig 6), and did not cause alterations in oxygen tension and oxygen saturation in portal blood; Po2 in portal blood before oxygen inhalation was 68 ± 8.2 and during oxygen inhala¬ tion it was 66 ± 8.7 mm Hg. The difference was not
Oxygen inhalation
statistically significant.
COMMENT
The results of this study demonstrate that enterai oxygen administration can effectively stimulate the stomach and intestinal motility (Fig 1 and 4, Table). While the exact mechanism by which this takes place is beyond the scope of this work, several conclusions can be drawn. It is well known that increase in pressure within a segment of intestine may cause that segment to contract." Thus, it is possible that the increase in stomach and intestinal motility observed in our experiments may have been caused, not by the enterai oxygen itself, but rather by dilation of the intestine and distention of the wall. In order to prevent this mechanical influence, the intraluminal oxygen injection was carried out at low flow (5 to 7 ml/ min). In addition, we found that enterai nitrogen and carbon dioxide administered in the same manner did not produce any changes in the stomach and intestinal motility (Fig 2, 3, and 5, Table). Thus, the mechanical factor of enterai oxygen administration as a basis for the increased motility can be eliminated, and the role of the oxygen itself as the stimulating agent can be considered. One could postulate that a change in pH may have caused the increased stomach and intestinal motility. As our results show, enterai carbon dioxide administration, which led to a pH decrease in the intestinal content, produced no changes in the stomach and intestinal motility (Fig 2 and 5, Table). Thus, it can be assumed that the increase in stomach and intestinal electrical activity during enterai oxygen administration was not directly related to altera¬ tions in the pH of the stomach and intestinal content. The possibility that the motility stimulation during enterai oxygen administration is a reflex phenomenon was also considered. However, sympathetic and parasympathetic nervous motor control of the gut was eliminated by our experiments, demonstrating the stimulating effect of enterai oxygen on stomach and intestinal motility, in spite
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Before Enterai Oxygen Administration Stomach
Intestine
After Enterai
Oxygen Administration Stomach
I
1
1
= Intestine
Fig 1.—Influence of enterai oxygen administration of
pharmacologie
on
stomach and intestinal electrical
denervation of the gut muscle wall
receptors (group 4 [Fig 4, Table]).
Laparotomy is known to cause splanchnic vasoconstric¬ tion and a resultant decrease in intestinal blood flow on the one hand,""1 and a decrease in gut motility on the other.1"516" The exact relationship between this decreased
activity.
blood (and therefore oxygen) supply to the gut wall and the decreased gut motility during surgical trauma is also unclear, but it must not be ignored. It has been shown that under these conditions of surgical stress, enterai oxygen administration leads to a rise in oxygen content in the portal blood'-lvl" and an increase in the splanchnic blood
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Before Enterai Carbon Dioxide Administration
Stomach
Intestine
After Enterai Carbon Dioxide Administration
Stomach
Intestine
Fig
2.—Influence of enterai carbon dioxide administration
on
stomach and intestinal electrical
flow." It appears that there is a relationship between this improvement in blood and oxygen delivery to the wall of the gut and the increase in gut motility observed in our '-
experiments.
The greater effectiveness of enterai oxygen administra¬ tion seen in our animals with low baseline motility may be
activity.
related to their
more extreme physiologic reaction to surgical trauma, whereby they show much greater increase in stomach and intestinal motility following improvement
in blood and oxygen supply to the gut. An increase in oxygen tension in arterial blood during oxygen inhalation via tracheostomic cannula did not
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Before Enterai Nitrogen Administration Stomach
Intestine
After Enterai
Nitrogen Administration Stomach
Intestine
L Fig
F=F=R 3.—Influence of enterai
-1=1
nitrogen
administration
on
3
I
stomach and intestinal electrical activity.
Fig
4—Influence of enterai oxygen administration on stomach and intestinal activity after pharmacologie denervation of gut.
electrical
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Before Atropine, Phentolamine, and Stomach
Propranolol Injection
Intestine
After
Atropine, Phentolamine,
and
Propranolol Injection Before Enterai Oxygen Administration Stomach
m
m
—«
m
f*Üf-1
ir»
i
j
il...-."
!
«
I
-
»
-
.
ii-
fffff
.
zi
Intestine
mi r~
_j
"" -"1-:,
I
After
Atropine, Phentolamine,
and
ÜB . ^»
T"~ ':"~"rr~
:-:-l>7''
,:
Propranolol Injection and
Enterai
Stomach
Intestine
Downloaded From: http://archsurg.jamanetwork.com/ by a New York University User on 06/21/2015
Oxygen
·,-·!
Administration
1
Before Atropine, Phentolamine, and Propranolol Stomach
Injection
Intestine
After
Atropine, Phentolamine, and Propranolol Injection
Before Enterai Carbox Dioxide Administration
Stomach
Intestine
After Atropine, Phentolamine, and Propranolol Injection and Enterai Carbon Dioxide Administration Stomach
Intestine
Downloaded From: http://archsurg.jamanetwork.com/ by a New York University User on 06/21/2015
Fig
5.—Influence of enterai carbon dioxide administration on stomach and activity after pharmacologie denervation of gut.
intestinal electrical
Fig 6.—Influence
of oxygen inhalation
on
stomach and intestinal electrical
Before
activity.
Oxygen Inhalation Stomach
Intestine
T=v=f
]
^* ^^^ ^ After
Oxygen Inhalation Stomach
Intestine
Downloaded From: http://archsurg.jamanetwork.com/ by a New York University User on 06/21/2015
The Influence of Enterai Gas Administration Stomach
Group
Gas Administered
1
CO, N,
4t
*
Activity (Mean
Baseline Values
±
Stomach and Intestinal Electrical
on
Intestinal Activity
SE)*
Experimental Values
Baseline Values
(Mean
±
SE)*
Experimental Values Amplitude 0.65 ± 0.11f
Frequency 27.3±3.8f
Frequency
Amplitude
Frequency
0.40 ± 0.08 0.48 ±0.12
29.8 ± 7.2t 15.7 ±3.6 14.1 ±3.8
0.35 ± 0.06 0.32 ±0.08 0.29 ± 0.07
23.1 3.7 17.4 ±3.9 17.1 ±4.1
0.30 ±0.10 0.32 ± 0.09
17.8 ±4.1 16.9 ±4.3
16.3 ±2.1
0.95±0.14|
21.8 ±
0.21 ± 0.06
14.8 ±3.7
0.43 ± 0.10t
18.2 ±
14.3±2.9 13.8 ±3.4
Near zero 0.48 ±0.13
Nearzero 13.7 ±3.9
0.40±0.11 0.44 ±0.10
16.1 ±3.2 14.8 ±3.1
Near zero 0.42 ± 0.14
Near zero 14.6 ±3.8
Amplitude
Frequency
0.46 ±0.07 0.38 ±0.06 0.51 ±0.07
20.2 ±4.9 14.1 ±3.1 13.4 ±3.3
0.40 ±0.09
0.44±0.10 0.47 ±0.12
Amplitude 0.84±0.11t
Activity
02 after
atropine, phentolamine, propranolol
5Í
C02
6
Q2 inhalation
2.9f
3.9f
after
atropine, phentolamine, propranolol
Values of amplitude of
waves are
given in
mv, of
frequency in oscillations
per minute.
t A significant difference (P
Levy,
MD
Thirty-eight starved cats, anesthetized with pentobarbital (Nembutal) sodium, received enteral administration of oxygen and other gases; the effect on intestinal motility as expressed by electrical activity was measured. Oxygen caused a notable increase in amplitude and frequency of slow electrical waves, while carbon dioxide and nitrogen caused no visible altera\s=b\
tions. Phentolamine
hydrochloride and propranolol hydrochloride together with atropine sulfate decreased the amplitude and frequency of oscillations to near zero; subsequent administration of enteral oxygen caused a notable increase in electrical activity, while enteral carbon dioxide produced no alterations. On the basis of our previous observations that enteral oxygen enhances oxygen and blood delivery to the gut wall, we suggest that the rise in stomach and intestinal electrical activity during enteral oxygen administration in conditions of surgical stress may be associated with an increase in oxygen and blood delivery to the gut wall.
(Arch Surg 111:566-574, 1976)
well-known phenomenon that under certain condi¬ such as surgical trauma, parallel changes take in or intestinal blood flow and gut motility. There is an inhibition of intestinal motility'" and a decrease in splanchnic blood flow."1" These changes can be caused by an increase in adrenergic discharge and excitais
Itplacetions,portal a
Accepted
for publication Dec 26, 1975. From the Department of Anesthesiology, Beilinson Medical Center, Petah Tikva, and the departments of physiology and pharmacology, Sackler School of Medicine, Tel Aviv University, Israel. Dr Gelman is now with Cleveland Metropolitan General Hospital. Reprint requests to Department of Anesthesiology, Cleveland Metropolitan General Hospital, 3395 Scranton Rd, Cleveland, OH 44109 (Dr
Gelman).
tion of -adrenoreceptors located in the intestinal and vascular walls. It has been shown that the decrease in either portal or total hepatic blood flow or both associated with operative stress and anesthesia can be modified by enterai oxygen administration." '-' The present work investigates the possibility that intes¬ tinal motility can be stimulated by enterai oxygen admin¬ istration, which leads to increased portal (intestinal) blood flow. METHODS
experiments were performed on 38 starved cats ranging in weight from 2.5 to 4.5 kg. Tracheostomy, catheterization of femoral artery and vein, and laparotomy were carried out under pentobarbital (Nembutal) sodium narcosis (40 mg/kg body weight). A pair of small silver needle electrodes was inserted 0.7 cm apart into the muscle layer on the front surface of the stomach, 3 to 4 cm above the pylorus. A second pair was inserted, also 0.7 cm apart, into the muscle layer of the intestinal wall, 15 to 20 cm below the pylorus. A polyethylene catheter was placed in the intestinal lumen 30 to 35 cm below the pylorus. The peritoneal cavity was The
then closed. The electrical activity of the stomach and intestine was recorded continuously according to the method of Condrea et al," and the mean values of amplitude and frequency were evaluated during the various experimental procedures. Low level amplifiers were used with an extra capacitor of 32 microfarads at the input. Electrocardiogram lead 2 and blood pressure in the femoral artery (measured by a transducer) were recorded at the same time. The oxygen tension of arterial blood samples was periodically deter¬ mined. Each cat was allowed to rest for 30 minutes following closure of the abdominal wall before the experiments were begun; during this time, the electrical activity of the stomach and intestine was recorded.
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During the experiments, oxygen, nitrogen, and carbon dioxide injected into the intestinal lumen by a syringe attached to the polyethylene catheter; 20 ml of gas was injected two to three were
times at 5- to 6-minute intervals at a flow rate of 5 to 7 ml/min to prevent distention of the intestinal wall. The 38 cats were divided into the following six groups. Group 1 (ten animals) received 20 ml of oxygen, two to three times, at 5- to 6-minute intervals. Group 2 (six animals) received carbon dioxide in the same manner as group 1. Group 3 (six animals) received nitrogen in the same manner as group 1.
Group 4 (ten animals) received an a-adrenal-blocking drug (phentolamine hydrochloride, 1 mg/kg body weight, intravenous¬ ly), a /¡-adrenal-blocking drug (propranolol hydrochloride, 1 mg/ kg, intravenously), a choline-blocking drug (atropine sulfate, 0.4 mg/kg, intravenously), and then enterai oxygen in the same group 1. 5 (six animals) received the same pharmacologie treat¬ ment as group 4, followed by enterai carbon dioxide. Group 6 (six animals, three cats from group 4 and three cats from group 5) received oxygen inhalation for 15 minutes before the pharmacologie and enterai gas treatments. Four additional cats underwent tracheostomy and the femoral artery and vein were catheterized; laparotomy and catheterization of portal vein via a branch of mesenteric vein were performed. In these cats, slow electrical activity of the gut was not recorded, but Po, and oxygen saturation in the arterial, venous, and portal blood were measured before and during oxygen inhalation. The purpose of blocking the digestive tract receptors with the drugs was to determine the effectiveness of enterai oxygen administration under conditions of full pharmacologie denervation of the muscle wall of the gut. The oxygen inhalation allowed us to study the influence of increased arterial blood oxygen tension on the stomach and intestinal motility. The amplitude and frequency of the electrical slow waves' oscillations recorded from the stomach and intestinal walls were compared before and during the inhala¬ manner as
Group
tion procedure. Wilcoxon nonparametric statistical test was applied to compare the results obtained during the two successive phases of the
experiment."
RESULTS
During the first 30 minutes following surgical prepara¬ tion of the animal, the slow wave electrical activity of the stomach and intestinal muscles was recorded. Group 1.—Within a few minutes after enterai oxygen administration, eight of the ten animals showed an increase in amplitude and frequency of slow electrical waves (Fig 1). In the two remaining animals, no visible alterations were noticed. Enterai oxygen administration had a greater effect in animals with lower baseline elec¬ trical activity. For all ten cats in this group, the average amplitude increase was 82% and 86% for stomach and intestinal electrical activity, respectively; the average frequency increase was 47% and 20% for stomach and intestinal activity, respectively (Table). Groups 2 and 3.—Neither the enterai carbon dioxide nor nitrogen administration were accompanied by any visible alterations in the stomach and intestinal activity (Fig 2 and 3, Table). Group 4.—Phentolamine and propranolol together with
atropine decreased the amplitude and frequency of motility oscillations to near zero. Administration of enterai oxygen after the pharmacologie treatment caused an increase in the amplitude and frequency of slow electrical waves in all experimental animals (Fig 4); the amplitude more than doubled both in stomach and intestinal activity (Table). Group 5.—Once the motility oscillations were reduced to near zero by the pharmacologie agents, carbon dioxide administration did not
cause
alterations in the electrical
activity (Fig 5).
Group 6.—This group included an additional four cats. via the tracheostomic cannula led to notable increase in the arterial blood oxygen tension (from 92 ± 6 to 510 ± 15 mm Hg) and in oxygen saturation (from 96% ± 10.1% to 99% ± 9.7%). It did not, however, cause any alterations in stomach and intestinal activity (Fig 6), and did not cause alterations in oxygen tension and oxygen saturation in portal blood; Po2 in portal blood before oxygen inhalation was 68 ± 8.2 and during oxygen inhala¬ tion it was 66 ± 8.7 mm Hg. The difference was not
Oxygen inhalation
statistically significant.
COMMENT
The results of this study demonstrate that enterai oxygen administration can effectively stimulate the stomach and intestinal motility (Fig 1 and 4, Table). While the exact mechanism by which this takes place is beyond the scope of this work, several conclusions can be drawn. It is well known that increase in pressure within a segment of intestine may cause that segment to contract." Thus, it is possible that the increase in stomach and intestinal motility observed in our experiments may have been caused, not by the enterai oxygen itself, but rather by dilation of the intestine and distention of the wall. In order to prevent this mechanical influence, the intraluminal oxygen injection was carried out at low flow (5 to 7 ml/ min). In addition, we found that enterai nitrogen and carbon dioxide administered in the same manner did not produce any changes in the stomach and intestinal motility (Fig 2, 3, and 5, Table). Thus, the mechanical factor of enterai oxygen administration as a basis for the increased motility can be eliminated, and the role of the oxygen itself as the stimulating agent can be considered. One could postulate that a change in pH may have caused the increased stomach and intestinal motility. As our results show, enterai carbon dioxide administration, which led to a pH decrease in the intestinal content, produced no changes in the stomach and intestinal motility (Fig 2 and 5, Table). Thus, it can be assumed that the increase in stomach and intestinal electrical activity during enterai oxygen administration was not directly related to altera¬ tions in the pH of the stomach and intestinal content. The possibility that the motility stimulation during enterai oxygen administration is a reflex phenomenon was also considered. However, sympathetic and parasympathetic nervous motor control of the gut was eliminated by our experiments, demonstrating the stimulating effect of enterai oxygen on stomach and intestinal motility, in spite
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Before Enterai Oxygen Administration Stomach
Intestine
After Enterai
Oxygen Administration Stomach
I
1
1
= Intestine
Fig 1.—Influence of enterai oxygen administration of
pharmacologie
on
stomach and intestinal electrical
denervation of the gut muscle wall
receptors (group 4 [Fig 4, Table]).
Laparotomy is known to cause splanchnic vasoconstric¬ tion and a resultant decrease in intestinal blood flow on the one hand,""1 and a decrease in gut motility on the other.1"516" The exact relationship between this decreased
activity.
blood (and therefore oxygen) supply to the gut wall and the decreased gut motility during surgical trauma is also unclear, but it must not be ignored. It has been shown that under these conditions of surgical stress, enterai oxygen administration leads to a rise in oxygen content in the portal blood'-lvl" and an increase in the splanchnic blood
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Before Enterai Carbon Dioxide Administration
Stomach
Intestine
After Enterai Carbon Dioxide Administration
Stomach
Intestine
Fig
2.—Influence of enterai carbon dioxide administration
on
stomach and intestinal electrical
flow." It appears that there is a relationship between this improvement in blood and oxygen delivery to the wall of the gut and the increase in gut motility observed in our '-
experiments.
The greater effectiveness of enterai oxygen administra¬ tion seen in our animals with low baseline motility may be
activity.
related to their
more extreme physiologic reaction to surgical trauma, whereby they show much greater increase in stomach and intestinal motility following improvement
in blood and oxygen supply to the gut. An increase in oxygen tension in arterial blood during oxygen inhalation via tracheostomic cannula did not
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Before Enterai Nitrogen Administration Stomach
Intestine
After Enterai
Nitrogen Administration Stomach
Intestine
L Fig
F=F=R 3.—Influence of enterai
-1=1
nitrogen
administration
on
3
I
stomach and intestinal electrical activity.
Fig
4—Influence of enterai oxygen administration on stomach and intestinal activity after pharmacologie denervation of gut.
electrical
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Before Atropine, Phentolamine, and Stomach
Propranolol Injection
Intestine
After
Atropine, Phentolamine,
and
Propranolol Injection Before Enterai Oxygen Administration Stomach
m
m
—«
m
f*Üf-1
ir»
i
j
il...-."
!
«
I
-
»
-
.
ii-
fffff
.
zi
Intestine
mi r~
_j
"" -"1-:,
I
After
Atropine, Phentolamine,
and
ÜB . ^»
T"~ ':"~"rr~
:-:-l>7''
,:
Propranolol Injection and
Enterai
Stomach
Intestine
Downloaded From: http://archsurg.jamanetwork.com/ by a New York University User on 06/21/2015
Oxygen
·,-·!
Administration
1
Before Atropine, Phentolamine, and Propranolol Stomach
Injection
Intestine
After
Atropine, Phentolamine, and Propranolol Injection
Before Enterai Carbox Dioxide Administration
Stomach
Intestine
After Atropine, Phentolamine, and Propranolol Injection and Enterai Carbon Dioxide Administration Stomach
Intestine
Downloaded From: http://archsurg.jamanetwork.com/ by a New York University User on 06/21/2015
Fig
5.—Influence of enterai carbon dioxide administration on stomach and activity after pharmacologie denervation of gut.
intestinal electrical
Fig 6.—Influence
of oxygen inhalation
on
stomach and intestinal electrical
Before
activity.
Oxygen Inhalation Stomach
Intestine
T=v=f
]
^* ^^^ ^ After
Oxygen Inhalation Stomach
Intestine
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The Influence of Enterai Gas Administration Stomach
Group
Gas Administered
1
CO, N,
4t
*
Activity (Mean
Baseline Values
±
Stomach and Intestinal Electrical
on
Intestinal Activity
SE)*
Experimental Values
Baseline Values
(Mean
±
SE)*
Experimental Values Amplitude 0.65 ± 0.11f
Frequency 27.3±3.8f
Frequency
Amplitude
Frequency
0.40 ± 0.08 0.48 ±0.12
29.8 ± 7.2t 15.7 ±3.6 14.1 ±3.8
0.35 ± 0.06 0.32 ±0.08 0.29 ± 0.07
23.1 3.7 17.4 ±3.9 17.1 ±4.1
0.30 ±0.10 0.32 ± 0.09
17.8 ±4.1 16.9 ±4.3
16.3 ±2.1
0.95±0.14|
21.8 ±
0.21 ± 0.06
14.8 ±3.7
0.43 ± 0.10t
18.2 ±
14.3±2.9 13.8 ±3.4
Near zero 0.48 ±0.13
Nearzero 13.7 ±3.9
0.40±0.11 0.44 ±0.10
16.1 ±3.2 14.8 ±3.1
Near zero 0.42 ± 0.14
Near zero 14.6 ±3.8
Amplitude
Frequency
0.46 ±0.07 0.38 ±0.06 0.51 ±0.07
20.2 ±4.9 14.1 ±3.1 13.4 ±3.3
0.40 ±0.09
0.44±0.10 0.47 ±0.12
Amplitude 0.84±0.11t
Activity
02 after
atropine, phentolamine, propranolol
5Í
C02
6
Q2 inhalation
2.9f
3.9f
after
atropine, phentolamine, propranolol
Values of amplitude of
waves are
given in
mv, of
frequency in oscillations
per minute.
t A significant difference (P
