Different mechanisms of hydrogen in stomach and duodenum
ion removal
JOHN W. HARMON, MONTY WOODS, AND NELSON J. GURLL Department of Surgical Gastroenterology, Division of Surgery, Walter Reed Army Institute of Research, Washington, DC. 20012, and Uniformed Services University of Health Sciences, Bethesda, Maryland 20014
HARMON,JOHN W., MONTY Wools, ANDNELSON J. GURLL. Different mechanisms of hydrogen ion removal in stomach and duodenum. Am. J. Physiol. 235(6): E692-E698, 1978 or Am. J. Physiol.: Endocrinol. Metab. Gastrointest. Physiol. 4(6): E692-E698, 1978. -The acid-removing capability of the duodenal mucosa itself, without the secretions of Brunner’s glands, the pancreas, or liver, has recently become recognized. Whether this acid loss occurs by backdiffusion of hydrogen ion, bicarbonate neutralization, a combination of the above two processes, or some other mechanism, remains unclear. Experiments were carried out in dogs with chronic distal duodenal pouches or with gastric fundal pouches. Acid loss and CO, levels were measured simultaneously in situ. The hypothesis was that, if bicarbonate neutralization of acid was going on, CO, would appear in the pouches as a result of the reaction H+ + HCO, + H,O + CO,. In the duodenal pouches, Pcoa did rise as acid was lost. For 22 experimental observations, the net acid loss from the pouches (JH+> correlated directly and significantly with pouch Pco2 generation according to the equation JH+ = 7.6 A PcoZ + 75 (r = 0.79, P < 0.001). By contrast PcoZ levels were not increased in dogs with gastric pouches when the “barrier” was broken and acid loss occurred. When the system was run with a plastic cannula replacing the duodenal mucosal pouches and bicarbonate was infused to simulate the rates of acid loss seen in the duodenum, Pco2 levels in the plastic cannulas were similar to those seen in vivo. We, therefore, conclude that bicarbonate neutralization is responsible, at least in part, for acid loss in isolated canine duodenal loops. pH stat; Heidenhain bicarbonate
pouch;
gastric
mucosal
barrier;
dog;
ACID passes into the duodenum where the acid disappears and neutrality is restored. Until recently the restoration of neutrality in the duodenum was attributed solely to the neutralizing bicarbonate-rich secretions of Brunner’s glands and the pancreas and liver. More recently, various investigators have demonstrated that the duodenal mucosa itself has an independent mechanism for acid removal (1, 4, 5, 6, -13) The mechanism by which the duodenal mucosa removes acid to which it is exposed remains a subject of controversy. Proposed mechanisms include backdiffusion of acid, neutralization of acid, and a combination of these two processes. The objective of this study was to determine the role of bicarbonate in the acid loss that occurs in distal GASTRIC
l
duodenal pouches. A further aim was to compare the mechanism of acid disappearance from duodenal pouches with the acid disappearance that occurs from gastric fundic pouches with the gastric mucosal barrier broken. Our experimental approach was to measure acid loss from mucosal pouches in vivo while simultaneously measuring PcoZ within the pouches. Our hypothesis was that, if acid were neutralized by the reaction of NaHCO, + HCl + NaCl + HZ0 + COZ, we would observe si.multaneous acid disappearance and CO, appearance within the pouches. On the other hand, if H+ were backdiffusing in exchange for Na we would expect to see acid loss without an increase in Pcog .
METHODS
Initially experiments were carried out using the following system. Surgical preparation Three mongrel dogs weighing 20-30 kg were prepared with IO-cm-long duodenal pouches drained at -each end by a modified Gregory cannula. The proximal end of the pouch was 5 cm distal to the aancreatic ducts, and the distal end was at the ligameit of Treitz. The proximal ends of the pouches were free of Brunner’s glands by histologic examination. Bowel continuity was restored by duodenojejunostomy. A Thomas cannula was placed in the stomach to insure by inspection that the stomach was empty during experiments. Three weeks were allowed for recovery from the operation before starting tests. Tests were never run on consecutive days and never more than twice a week on each dog. Food but not water was withheld for 18 h before testing, and the dogs were studied awake and minimally restrained in Pavlov slings. Another group of three mongrel dogs weighing 20-30 kg was prepared with gastric Heidenhain pouches similar in size and shape to the duodenal pouches. Biopsy confirmed that the distal ends of these pouches did not extend into the antrum so that the pouches were indeed fundic. The two ends of these pouches were drained with Gregory cannulas to permit perfusion by the same system as used with the duodenal pouches. These pouches of denervated gastric mucosa permitted comparison of the acid handling mechanisms of gastric mucosa with that of duodenal mucosa. l
Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
DUODENAL
AND
GASTRIC
ACID
E693
FLUXES
pH stat system (Fig. 1) , Acid loss from the duodenal pouches was measured continuously using a recirculating system incorporating a variable-speed peristaltic pump (Harvard Apparatus Co., Millis, MA) and a reservoir. The fluid level in the reservoir was adjusted to a point 5 cm above the pouch level. The duodenal pouch volume was 20-30 cc with 70 ml total volume in the reservoir pouch system. The reservoir prevented a buildup of pressure within the system any greater than 10 cm of water. The temperature within the system was kept at 37°C as confirmed by a thermometer, immersed in the reservoir using a thermostat regulated heat exchanger (Haake, Berlin, Germany) perfusing a water chamber around the reservoir. The electrodes of a pH stat titration system (Radiometer TT2b, Copenhagen, Denmark) were immersed in the reservoir to permit continuous pH monitoring. Titration to a fixed pH value with 0.4 N HCl was accomplished with an autoburette (Radiometer, ABU 12, Copenhagen, Denmark). The amount of acid added to keep pH constant thus equaled the acid lost. The system was calibrated every day prior to use. The pH meter was calibrated with known HCl solutions with hydrogen ion concentration equal to that to be measured on the given experimental day, and at 37OC (10). The autoburette’s ability to measure acid loss was calibrated by neutralizing known amounts of NaOH or NaHCO, with the perfusion system in operation. When the system was tested with 0.24 ml of 200 peq/ml NaOH (48 peq), the mean -+ standard deviation for 10 measurements were as follows: 47 t 1.6 peq at pH 7, 48 t 2.2 at pH 2, and 48 t 8.1 at pH 1. Acid test solutions (ATS) were prepared with HCl or NaOH to achieve pH levels from 9 to 1.3 on previously calibrated electrodes (10). These solutions were then adjusted to 310 t 5 mosmol with NaCl. DlJODENAL
MUCOSAL
POUCH
PCOz measurement. In vivo measurement of Pcoz in the pouches was accomplished during exposure to the various acid test solutions using an indwelling Silastic membrane cannula attached to a mass spectrometer (Medspect, Baltimore, MD). The Midspect was calibrated daily to known standards that were also measured by conventional means on a Corning pH/blood gas 161-analyzer (Corning Scientific Instruments, Medfield, MA). A venous blood sample from the foreleg was taken during each 10-min period of observation and Pm2 was measured on the Corning pH/blood gas 161analyzer. The peak Pcoz in the pouch was measured at each pH by stopping perfusion and clamping the catheters to and from the pouch to prevent escape of CO, via leaks from the reservoir and to limit the volume into which the COz would equilibrate. Levels of Pm2 rose to peak values within 20 min of observation, and these levels were higher than those seen with the perfusate circulating. The CO, generated within the pouch was expressed as the amount by which the peak pouch Pm2 exceeded simultaneous systemic venous blood Pm2 and this value we call APco,. Using this method, acid loss and Pco2 in the pouch were not measured simultaneously. Initially they were measured simultaneously with the solution circulating, but CO, was lost from the reservoir and the Pcoz never rose above 60 mmHg. We found that by measuring acid loss at a certain pH with the pump circulating for 10 min and then stopping the pump and clamping the catheters to and from the pouch, PCQ rose over lo-20 min to a peak value as high as 134 mmHg. We therefore adopted this method of measuring Pcoz. Experimental design. 1) To determine whether or not CO, was generated within the duodenal pouches as acid was removed from them, a series of three experiments were carried out in which 22 observations of duodenal PREPARATION
STAT
FIG. 1. The pH stat system. Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
E694 acid loss and pouch PcoZ were made at pH levels ranging from 9 to 1.3. The rate of acid loss was analyzed as a function of the excess of duodenal pouch PcoZ over simultaneous venous blood PcoZ (APcQ using regression analysis. By using APco, instead of just pouch Pco~, we obtained a measurement of the CO2 being produced in the pouch above that which might appear in the pouch by diffusion from the venous blood. 2) The possibility was raised that levels of Pcoz would also rise in gastric mucosal pouches in which acid was “backdiffusing.” In that case the mechanism of acid loss in the duodenum could not be differentiated from the mechanism of acid loss in the stomach. Accordingly a series of experiments were carried out in dogs with gastric fundal pouches, Acid backdiffusion was initiated with either 5 mM Na salicylate or 10 mM Na taurocholate. Three gastric fundal pouch experiments were compared with three duodenal pouch experiments in which the rates of acid loss from the duodenal and gastric pouches were the same. With the rate of acid loss being the same, the PO* excess should be the same if the mechanisms of acid loss were the same. If the PCQ excess were greater in the duodenal pouches than in the gastric pouches, this would be consistent with the hypothesis that bicarbonate neutralization of acid was generating CO, within the duodenal pouches, whereas acid backdiffusion in exchange for the Na was not generating CO, within the gastric pouches. The differences in the means were evaluated with Student t test for unpaired numbers. 3) To determine whether or not the levels of Pco2 observed in the duodenal pouches were consistent with bicarbonate neutralization of the acid being lost from the pouches, a series of experiments were performed in which the pH stat system was run with a large-bore plastic cannula replacing the duodenal pouch. ATS containing HCl at pH2 with NaCl added to achieve 310 + 5 mosM was circulated through the system. By the addition of NaHCO,, rates of acid loss of 200, 400, and 800 peq/lO min were achieved in the system. The Pm2 in the plastic cannula was measured at these rates of bicarbonate neutralization. The levels of PcoZ were compared with the levels of PcoZ seen in the duodenal pouches at similar rates of acid loss. If bicarbonate neutralization of acid were occurring in the duodenal pouches, one would expect the Pco2 values seen in the plastic pouches during bicarbonate neutralization to be similar to these seen in the duodenum.
HARMON,
WOODS,
AND
GURLL
the 22 experimental observations, the net acid loss from the pouches (JH+) correlated directly and significantly with the pouch CO, excess (APco,) according to the equation JH + = 7.6APcoz + 75 (r = 0.79, P < ,001) (Fig. 2). Is CO, generated within a gastric pouch as acid is lost by backdiffusion.. 2 When acid backdiffusion was induced in the gastric fundal pouches by either 5 mM Na salicylate or 10 mM Na taurocholate, CO, levels did not build up within the pouches. In the gastric fundal pouch taurocholate experiments, whereas acid loss was 228 t 16 peq/lO min, pouch Pco2 was 15 -t 1 mmHg less than venous blood PcoZ so that a pouch Pco2 deficit was present relative to venous blood. The duodenal pouches meanwhile generated a pouch PcuZ excess of 39 + 10 mmHg when acid loss was at the similar rate of 240 * 3peq/lO min (Fig. 3). In the gastric fundal pouch Na salicylate experiments, whereas acid loss was 95 t 26 peq/lO min, pouch PcoZ was 11 t 2 mmHg less than venous blood, so again a pouch PcoZ deficit was present. The matched duodenal pouches meanwhile generated a pouch PcoZ excess of 13 -t- 5 mmHg (Fig. 4). Does bicarbonate neutralization of acid in vitro, at rates seen in vivo, generate similar PCU~ levels to those
RESULTS
Is CO, generated within duodenal pouches as acid is lost? The PcoZ in the pouches was equal to or less than systemic venous blood Pco2 when the pH of the pouches was 7 or 9, and acid was not being removed from the pouches. When the acidity in the pouch perfusates was higher, acid loss occurred and CO, levels increased. The highest value of PcoZ within a pouch was observed at pH 1.3 when the rate of acid loss was 740 peq/lO min, and the pouch PcoZ was 134 mmHg. At that time, systemic venous blood PcoZ was 39 mmHg so that the duodenal pouch CO* excess (APco,) was 95 mmHg. For
1
T
40
0
I
80
A GO2 2. This graph shows the results of 22 measurements of duodenal pouch acid loss in peq/lO min and simultaneous pouch PCO, generation expressed as amount by which pouch Pcoz exceeded venous blood Pco2 (APco&. Duodenal pouch PCQ generation (Afco,) correlated positively and significantly with net rate of acid loss, JH+. FIG.
Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
DUODENAL
AND
GASTRIC
ACID
E695
FLUXES
FIG. 3. These bar graphs demonstrate a difference in mechanism of acid loss between duodenal pouches and gastric pouches with “acid backdiffusion” induced by 10 mM Na taurocholate. Rates of acid loss are similar at 240 and 228 peq/lO min, respectively, but CO, is being generated in duodenal pouches with pouch PcoB 39 mmHg greater than simultaneous venous blood Pco2. In contrast, PCQ in gastric mucosal pouches was 11 mmHg less than venos blood Pco2 during backdiffusion showing that CO, was not being generated in gastric pouches.
*
p
ion removal
JOHN W. HARMON, MONTY WOODS, AND NELSON J. GURLL Department of Surgical Gastroenterology, Division of Surgery, Walter Reed Army Institute of Research, Washington, DC. 20012, and Uniformed Services University of Health Sciences, Bethesda, Maryland 20014
HARMON,JOHN W., MONTY Wools, ANDNELSON J. GURLL. Different mechanisms of hydrogen ion removal in stomach and duodenum. Am. J. Physiol. 235(6): E692-E698, 1978 or Am. J. Physiol.: Endocrinol. Metab. Gastrointest. Physiol. 4(6): E692-E698, 1978. -The acid-removing capability of the duodenal mucosa itself, without the secretions of Brunner’s glands, the pancreas, or liver, has recently become recognized. Whether this acid loss occurs by backdiffusion of hydrogen ion, bicarbonate neutralization, a combination of the above two processes, or some other mechanism, remains unclear. Experiments were carried out in dogs with chronic distal duodenal pouches or with gastric fundal pouches. Acid loss and CO, levels were measured simultaneously in situ. The hypothesis was that, if bicarbonate neutralization of acid was going on, CO, would appear in the pouches as a result of the reaction H+ + HCO, + H,O + CO,. In the duodenal pouches, Pcoa did rise as acid was lost. For 22 experimental observations, the net acid loss from the pouches (JH+> correlated directly and significantly with pouch Pco2 generation according to the equation JH+ = 7.6 A PcoZ + 75 (r = 0.79, P < 0.001). By contrast PcoZ levels were not increased in dogs with gastric pouches when the “barrier” was broken and acid loss occurred. When the system was run with a plastic cannula replacing the duodenal mucosal pouches and bicarbonate was infused to simulate the rates of acid loss seen in the duodenum, Pco2 levels in the plastic cannulas were similar to those seen in vivo. We, therefore, conclude that bicarbonate neutralization is responsible, at least in part, for acid loss in isolated canine duodenal loops. pH stat; Heidenhain bicarbonate
pouch;
gastric
mucosal
barrier;
dog;
ACID passes into the duodenum where the acid disappears and neutrality is restored. Until recently the restoration of neutrality in the duodenum was attributed solely to the neutralizing bicarbonate-rich secretions of Brunner’s glands and the pancreas and liver. More recently, various investigators have demonstrated that the duodenal mucosa itself has an independent mechanism for acid removal (1, 4, 5, 6, -13) The mechanism by which the duodenal mucosa removes acid to which it is exposed remains a subject of controversy. Proposed mechanisms include backdiffusion of acid, neutralization of acid, and a combination of these two processes. The objective of this study was to determine the role of bicarbonate in the acid loss that occurs in distal GASTRIC
l
duodenal pouches. A further aim was to compare the mechanism of acid disappearance from duodenal pouches with the acid disappearance that occurs from gastric fundic pouches with the gastric mucosal barrier broken. Our experimental approach was to measure acid loss from mucosal pouches in vivo while simultaneously measuring PcoZ within the pouches. Our hypothesis was that, if acid were neutralized by the reaction of NaHCO, + HCl + NaCl + HZ0 + COZ, we would observe si.multaneous acid disappearance and CO, appearance within the pouches. On the other hand, if H+ were backdiffusing in exchange for Na we would expect to see acid loss without an increase in Pcog .
METHODS
Initially experiments were carried out using the following system. Surgical preparation Three mongrel dogs weighing 20-30 kg were prepared with IO-cm-long duodenal pouches drained at -each end by a modified Gregory cannula. The proximal end of the pouch was 5 cm distal to the aancreatic ducts, and the distal end was at the ligameit of Treitz. The proximal ends of the pouches were free of Brunner’s glands by histologic examination. Bowel continuity was restored by duodenojejunostomy. A Thomas cannula was placed in the stomach to insure by inspection that the stomach was empty during experiments. Three weeks were allowed for recovery from the operation before starting tests. Tests were never run on consecutive days and never more than twice a week on each dog. Food but not water was withheld for 18 h before testing, and the dogs were studied awake and minimally restrained in Pavlov slings. Another group of three mongrel dogs weighing 20-30 kg was prepared with gastric Heidenhain pouches similar in size and shape to the duodenal pouches. Biopsy confirmed that the distal ends of these pouches did not extend into the antrum so that the pouches were indeed fundic. The two ends of these pouches were drained with Gregory cannulas to permit perfusion by the same system as used with the duodenal pouches. These pouches of denervated gastric mucosa permitted comparison of the acid handling mechanisms of gastric mucosa with that of duodenal mucosa. l
Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
DUODENAL
AND
GASTRIC
ACID
E693
FLUXES
pH stat system (Fig. 1) , Acid loss from the duodenal pouches was measured continuously using a recirculating system incorporating a variable-speed peristaltic pump (Harvard Apparatus Co., Millis, MA) and a reservoir. The fluid level in the reservoir was adjusted to a point 5 cm above the pouch level. The duodenal pouch volume was 20-30 cc with 70 ml total volume in the reservoir pouch system. The reservoir prevented a buildup of pressure within the system any greater than 10 cm of water. The temperature within the system was kept at 37°C as confirmed by a thermometer, immersed in the reservoir using a thermostat regulated heat exchanger (Haake, Berlin, Germany) perfusing a water chamber around the reservoir. The electrodes of a pH stat titration system (Radiometer TT2b, Copenhagen, Denmark) were immersed in the reservoir to permit continuous pH monitoring. Titration to a fixed pH value with 0.4 N HCl was accomplished with an autoburette (Radiometer, ABU 12, Copenhagen, Denmark). The amount of acid added to keep pH constant thus equaled the acid lost. The system was calibrated every day prior to use. The pH meter was calibrated with known HCl solutions with hydrogen ion concentration equal to that to be measured on the given experimental day, and at 37OC (10). The autoburette’s ability to measure acid loss was calibrated by neutralizing known amounts of NaOH or NaHCO, with the perfusion system in operation. When the system was tested with 0.24 ml of 200 peq/ml NaOH (48 peq), the mean -+ standard deviation for 10 measurements were as follows: 47 t 1.6 peq at pH 7, 48 t 2.2 at pH 2, and 48 t 8.1 at pH 1. Acid test solutions (ATS) were prepared with HCl or NaOH to achieve pH levels from 9 to 1.3 on previously calibrated electrodes (10). These solutions were then adjusted to 310 t 5 mosmol with NaCl. DlJODENAL
MUCOSAL
POUCH
PCOz measurement. In vivo measurement of Pcoz in the pouches was accomplished during exposure to the various acid test solutions using an indwelling Silastic membrane cannula attached to a mass spectrometer (Medspect, Baltimore, MD). The Midspect was calibrated daily to known standards that were also measured by conventional means on a Corning pH/blood gas 161-analyzer (Corning Scientific Instruments, Medfield, MA). A venous blood sample from the foreleg was taken during each 10-min period of observation and Pm2 was measured on the Corning pH/blood gas 161analyzer. The peak Pcoz in the pouch was measured at each pH by stopping perfusion and clamping the catheters to and from the pouch to prevent escape of CO, via leaks from the reservoir and to limit the volume into which the COz would equilibrate. Levels of Pm2 rose to peak values within 20 min of observation, and these levels were higher than those seen with the perfusate circulating. The CO, generated within the pouch was expressed as the amount by which the peak pouch Pm2 exceeded simultaneous systemic venous blood Pm2 and this value we call APco,. Using this method, acid loss and Pco2 in the pouch were not measured simultaneously. Initially they were measured simultaneously with the solution circulating, but CO, was lost from the reservoir and the Pcoz never rose above 60 mmHg. We found that by measuring acid loss at a certain pH with the pump circulating for 10 min and then stopping the pump and clamping the catheters to and from the pouch, PCQ rose over lo-20 min to a peak value as high as 134 mmHg. We therefore adopted this method of measuring Pcoz. Experimental design. 1) To determine whether or not CO, was generated within the duodenal pouches as acid was removed from them, a series of three experiments were carried out in which 22 observations of duodenal PREPARATION
STAT
FIG. 1. The pH stat system. Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
E694 acid loss and pouch PcoZ were made at pH levels ranging from 9 to 1.3. The rate of acid loss was analyzed as a function of the excess of duodenal pouch PcoZ over simultaneous venous blood PcoZ (APcQ using regression analysis. By using APco, instead of just pouch Pco~, we obtained a measurement of the CO2 being produced in the pouch above that which might appear in the pouch by diffusion from the venous blood. 2) The possibility was raised that levels of Pcoz would also rise in gastric mucosal pouches in which acid was “backdiffusing.” In that case the mechanism of acid loss in the duodenum could not be differentiated from the mechanism of acid loss in the stomach. Accordingly a series of experiments were carried out in dogs with gastric fundal pouches, Acid backdiffusion was initiated with either 5 mM Na salicylate or 10 mM Na taurocholate. Three gastric fundal pouch experiments were compared with three duodenal pouch experiments in which the rates of acid loss from the duodenal and gastric pouches were the same. With the rate of acid loss being the same, the PO* excess should be the same if the mechanisms of acid loss were the same. If the PCQ excess were greater in the duodenal pouches than in the gastric pouches, this would be consistent with the hypothesis that bicarbonate neutralization of acid was generating CO, within the duodenal pouches, whereas acid backdiffusion in exchange for the Na was not generating CO, within the gastric pouches. The differences in the means were evaluated with Student t test for unpaired numbers. 3) To determine whether or not the levels of Pco2 observed in the duodenal pouches were consistent with bicarbonate neutralization of the acid being lost from the pouches, a series of experiments were performed in which the pH stat system was run with a large-bore plastic cannula replacing the duodenal pouch. ATS containing HCl at pH2 with NaCl added to achieve 310 + 5 mosM was circulated through the system. By the addition of NaHCO,, rates of acid loss of 200, 400, and 800 peq/lO min were achieved in the system. The Pm2 in the plastic cannula was measured at these rates of bicarbonate neutralization. The levels of PcoZ were compared with the levels of PcoZ seen in the duodenal pouches at similar rates of acid loss. If bicarbonate neutralization of acid were occurring in the duodenal pouches, one would expect the Pco2 values seen in the plastic pouches during bicarbonate neutralization to be similar to these seen in the duodenum.
HARMON,
WOODS,
AND
GURLL
the 22 experimental observations, the net acid loss from the pouches (JH+) correlated directly and significantly with the pouch CO, excess (APco,) according to the equation JH + = 7.6APcoz + 75 (r = 0.79, P < ,001) (Fig. 2). Is CO, generated within a gastric pouch as acid is lost by backdiffusion.. 2 When acid backdiffusion was induced in the gastric fundal pouches by either 5 mM Na salicylate or 10 mM Na taurocholate, CO, levels did not build up within the pouches. In the gastric fundal pouch taurocholate experiments, whereas acid loss was 228 t 16 peq/lO min, pouch Pco2 was 15 -t 1 mmHg less than venous blood PcoZ so that a pouch Pco2 deficit was present relative to venous blood. The duodenal pouches meanwhile generated a pouch PcuZ excess of 39 + 10 mmHg when acid loss was at the similar rate of 240 * 3peq/lO min (Fig. 3). In the gastric fundal pouch Na salicylate experiments, whereas acid loss was 95 t 26 peq/lO min, pouch PcoZ was 11 t 2 mmHg less than venous blood, so again a pouch PcoZ deficit was present. The matched duodenal pouches meanwhile generated a pouch PcoZ excess of 13 -t- 5 mmHg (Fig. 4). Does bicarbonate neutralization of acid in vitro, at rates seen in vivo, generate similar PCU~ levels to those
RESULTS
Is CO, generated within duodenal pouches as acid is lost? The PcoZ in the pouches was equal to or less than systemic venous blood Pco2 when the pH of the pouches was 7 or 9, and acid was not being removed from the pouches. When the acidity in the pouch perfusates was higher, acid loss occurred and CO, levels increased. The highest value of PcoZ within a pouch was observed at pH 1.3 when the rate of acid loss was 740 peq/lO min, and the pouch PcoZ was 134 mmHg. At that time, systemic venous blood PcoZ was 39 mmHg so that the duodenal pouch CO* excess (APco,) was 95 mmHg. For
1
T
40
0
I
80
A GO2 2. This graph shows the results of 22 measurements of duodenal pouch acid loss in peq/lO min and simultaneous pouch PCO, generation expressed as amount by which pouch Pcoz exceeded venous blood Pco2 (APco&. Duodenal pouch PCQ generation (Afco,) correlated positively and significantly with net rate of acid loss, JH+. FIG.
Downloaded from www.physiology.org/journal/ajpendo by ${individualUser.givenNames} ${individualUser.surname} (130.070.008.131) on October 6, 2018. Copyright © 1978 American Physiological Society. All rights reserved.
DUODENAL
AND
GASTRIC
ACID
E695
FLUXES
FIG. 3. These bar graphs demonstrate a difference in mechanism of acid loss between duodenal pouches and gastric pouches with “acid backdiffusion” induced by 10 mM Na taurocholate. Rates of acid loss are similar at 240 and 228 peq/lO min, respectively, but CO, is being generated in duodenal pouches with pouch PcoB 39 mmHg greater than simultaneous venous blood Pco2. In contrast, PCQ in gastric mucosal pouches was 11 mmHg less than venos blood Pco2 during backdiffusion showing that CO, was not being generated in gastric pouches.
*
p
