Adenosine deaminasc activity was studied in the gastric mucosa of patients with peptic ulcer in retation to utter iacafisation and treztmcnt with ranitidine or sucralfate. Enzyme activities observed in the corpus mucosa were higher at a distance of over 2 cm from the ulcer margin than that recorded close to the ulcer. A significant decrease in adenosine deaminase activity &as found after treatment with ranitidine but not with sucralfate. In the antral mucosa. enzyme activity was canstant in all the groups observed. The evaluation of adenosinc dcaminase activity in gastric mucosd can be usefd for studies of pathologic changes in the stomach.
Adenosinc deaminase: Gastric ulcer: Ranitidine: Swralfate
1. Introduction
2. Materials and methods
Adenosine can affect the gastric mucosa by improvement of blood flow (Gerber and Guth, 19891, modulation of the acid secretion in response to histamine and acetylcholine (Gerber et a!.. 1984) and inhibition of both basal and stimulated gastrin release (Harty and Franklin, 1984). It has been also suggested that adenosine participates in gastric functional and morphologic changes, e.g. acid hypersecretion (Mozsik ei a!., 1976) or peptic ulcer genesis (Mozsik et a!.. 1980). Adenosine deaminase !_4DA). the main enzyme of adenosine degradation. has proved to be a useful too! for studies of adenosine-mediated functions. For example, a positive correlation was found between ADA activity in the fundic mucosa and basal or maxima! acid outputs (Namiot et a!., 1990). The present study was undertaken to determine the activity of ADA in the gastric mucosa of patients with peptic ulcer in relation to ulcer localisation and treatment with ranitidine or sucralfate.
Correspondence !hiadrckrs Bialystok.
to: Z. Namiot.
Regional Poland.
Hospita!.
Department
of Gastroenterology.
Skiodowska
Sweet
3.
J.
15-950
Fifty-one subjects (37 men. 14 women). non-smokers. with mean age of 48 (range 26-78). were included in the study. They were divided into three groups. The 1st group consisted of $6 patients with gastric ulcer confirmed endoscopicaliy. None had received any drugs for at least two weeks before the examination (control group). The 2nd group included 19 patients with gastric ulcer treated for two weeks with ranitidine (Ranigast. Polfa). 150 mg twice daily. The 3rd group comprised 16 patients with gastric ulcer treated for two weeks with sucralfate (Venter. KREW. 1 g, four times daily. Each group was divided into two subgroups according to ulcer localisation in the antntm or corpus. Prepyloric ulcers were excluded from the study. All patients had a previous ulcer history. Table 1 gives details of the patients. An overnight fast was followed by gastric endoscopy performed with a gastrofiberoscope (G!F KlO. Oiympus). The last antiulcer tablets were given 12 h before the endoscopic examination. Six biopsy samples of antra! or corpus mucosa. each weighing 4-8 mg. were taken up to 2 cm and over 2 cm from the ulcer margin. The activity of ADA in the mucosa! homogenates was measured by determination of the ammonia liberated from the substrate according to the method of Chancy and ??Zarbach (1962). Protein was assayed by the method
No signs of malignancy were observed in the mucosal samples taken for histologic evaluation.
Mo2sik et al. (19801 found an elevated adenosine ~o~ce~trat~o~ in the gastric mucosa close to a peptic ulcer. Our resutts demonstrated that ADA activity in the junta-ulcer mucosa was low. esthetically, the Iow ADA activity in the ulcer region may be responsible for the elevated concentration of adenosine. However, both a high adenosine concentration and increased ADA activity in the gastric mucosa of the patients with acid h~e~e~retion were observed Wozsik et al., 1980; ~amiot et al.. 19 It should be stressed that mucosal ADA activity was significantly higher at the distance of over 2 cm from the ulcer margin out only in the corpus region, e.g. in the gastric area secreting bydr~hIoric acid. This finding co~~~~s a relationship between ADA activity and the secretory function of the stomach Wamiot et al., 19901. The significant decrease of ADA activity in the corpus mucosa was observed after treatment with ranitidine. It could be explained by the effect of the Hz-receptor blocking agent either on gastric secretion or on mucosal blood flow (Dijbrilnte et al., 1987; Namiot et al., 1990). The lack of change in ADA
%~~WWX bra
deammase
actit?:
in the gastric mucosa of patients with peptic ulcer in relation
to ulcer localisation
GX inker margm. The control grmtp had not been treated with any drug for at least two weeks:
BW artb
aad sucdbte
1 g faur times ADA
ranitidine
(corpus, antrum)
daily for two weeks. The re$ults are expressed as the meanskS.D.
activity. nM NH,
/mg of protein
per min
COrpUS
Antrum
Up to 2 cm r
QverZem *
UptoZcm
53.68f I3.s4 a
lOQ.19f30.01 50.34 2 14.00 d
45.84 f 15.84 41.17+ 15.00
dO.01f 10.17 h
*
and distance
was given l50 mg twice daily for
OverZcm * 42.01~ 15.00 44.5 1+ 14.39
in the gastric mucosa can be useful for studies of various pathologic states of the stomach, especially those states connected with secretory changes.
Gerber, J.G. and P.H. Guth, 1989. Ru4e 04 aderruske in tk btood flow response to pentagastrin in the rat. J. ~~~~~.
gattic hp.
Ther. 25t.55U. and PA. Franklin. IW4. Effect3 of e~~~~~~ a endogenous adenosine a’n gastrin release from rat a’nzrrtlmuco~. Gastroentero~ogy Xh. 1I07. Lusty. 0.H NJ. Rose&rough. A.L. Farr and RJ. RandAP. 1951. Protek measurement with the F&in pkno! reaynz. 1. B&.
Warty. RF.
Acknowledgement This work was supported by the Polish Programme for Basic Research 06-02.
References Chaney. A.L. and E.P. Marbach, 1%2, Modified reagents for determination of urea and ammonia, Clin. Chem. 8. 130. Diibriinte, Z., Z. KahBn. J. I.&g and V. Varr6, 1987. Mucosal blood
Chem. 193. 265. Mozsik, G., F. Vizi and J. Kutas.
1976. A ce~lul,ar-b~~~~~~~ evaluation of gastrk bcxiy mucosa an”d muscular fayer i&npatients with different basal acidoutput. Stand. J. Gastroenterot. 11.205. Mozsik, 6.. J. Kutas. L. Nagy and F. Tarnok. 19x0. Biocbemisa~ of antraf ulcer in patknts. Acta Med. Aca’d. Sci. Hung. 37. 39. Namiot. Z.. J. Rutkiewicz. 3. Stasiewicz and J. G&ski. 19W Aderxosinr deaminase activity in tbr human gastrkc mucosa tn relatmn to acid secretion. Digestion 45. 172.
Adenosinc deaminase: Gastric ulcer: Ranitidine: Swralfate
1. Introduction
2. Materials and methods
Adenosine can affect the gastric mucosa by improvement of blood flow (Gerber and Guth, 19891, modulation of the acid secretion in response to histamine and acetylcholine (Gerber et a!.. 1984) and inhibition of both basal and stimulated gastrin release (Harty and Franklin, 1984). It has been also suggested that adenosine participates in gastric functional and morphologic changes, e.g. acid hypersecretion (Mozsik ei a!., 1976) or peptic ulcer genesis (Mozsik et a!.. 1980). Adenosine deaminase !_4DA). the main enzyme of adenosine degradation. has proved to be a useful too! for studies of adenosine-mediated functions. For example, a positive correlation was found between ADA activity in the fundic mucosa and basal or maxima! acid outputs (Namiot et a!., 1990). The present study was undertaken to determine the activity of ADA in the gastric mucosa of patients with peptic ulcer in relation to ulcer localisation and treatment with ranitidine or sucralfate.
Correspondence !hiadrckrs Bialystok.
to: Z. Namiot.
Regional Poland.
Hospita!.
Department
of Gastroenterology.
Skiodowska
Sweet
3.
J.
15-950
Fifty-one subjects (37 men. 14 women). non-smokers. with mean age of 48 (range 26-78). were included in the study. They were divided into three groups. The 1st group consisted of $6 patients with gastric ulcer confirmed endoscopicaliy. None had received any drugs for at least two weeks before the examination (control group). The 2nd group included 19 patients with gastric ulcer treated for two weeks with ranitidine (Ranigast. Polfa). 150 mg twice daily. The 3rd group comprised 16 patients with gastric ulcer treated for two weeks with sucralfate (Venter. KREW. 1 g, four times daily. Each group was divided into two subgroups according to ulcer localisation in the antntm or corpus. Prepyloric ulcers were excluded from the study. All patients had a previous ulcer history. Table 1 gives details of the patients. An overnight fast was followed by gastric endoscopy performed with a gastrofiberoscope (G!F KlO. Oiympus). The last antiulcer tablets were given 12 h before the endoscopic examination. Six biopsy samples of antra! or corpus mucosa. each weighing 4-8 mg. were taken up to 2 cm and over 2 cm from the ulcer margin. The activity of ADA in the mucosa! homogenates was measured by determination of the ammonia liberated from the substrate according to the method of Chancy and ??Zarbach (1962). Protein was assayed by the method
No signs of malignancy were observed in the mucosal samples taken for histologic evaluation.
Mo2sik et al. (19801 found an elevated adenosine ~o~ce~trat~o~ in the gastric mucosa close to a peptic ulcer. Our resutts demonstrated that ADA activity in the junta-ulcer mucosa was low. esthetically, the Iow ADA activity in the ulcer region may be responsible for the elevated concentration of adenosine. However, both a high adenosine concentration and increased ADA activity in the gastric mucosa of the patients with acid h~e~e~retion were observed Wozsik et al., 1980; ~amiot et al.. 19 It should be stressed that mucosal ADA activity was significantly higher at the distance of over 2 cm from the ulcer margin out only in the corpus region, e.g. in the gastric area secreting bydr~hIoric acid. This finding co~~~~s a relationship between ADA activity and the secretory function of the stomach Wamiot et al., 19901. The significant decrease of ADA activity in the corpus mucosa was observed after treatment with ranitidine. It could be explained by the effect of the Hz-receptor blocking agent either on gastric secretion or on mucosal blood flow (Dijbrilnte et al., 1987; Namiot et al., 1990). The lack of change in ADA
%~~WWX bra
deammase
actit?:
in the gastric mucosa of patients with peptic ulcer in relation
to ulcer localisation
GX inker margm. The control grmtp had not been treated with any drug for at least two weeks:
BW artb
aad sucdbte
1 g faur times ADA
ranitidine
(corpus, antrum)
daily for two weeks. The re$ults are expressed as the meanskS.D.
activity. nM NH,
/mg of protein
per min
COrpUS
Antrum
Up to 2 cm r
QverZem *
UptoZcm
53.68f I3.s4 a
lOQ.19f30.01 50.34 2 14.00 d
45.84 f 15.84 41.17+ 15.00
dO.01f 10.17 h
*
and distance
was given l50 mg twice daily for
OverZcm * 42.01~ 15.00 44.5 1+ 14.39
in the gastric mucosa can be useful for studies of various pathologic states of the stomach, especially those states connected with secretory changes.
Gerber, J.G. and P.H. Guth, 1989. Ru4e 04 aderruske in tk btood flow response to pentagastrin in the rat. J. ~~~~~.
gattic hp.
Ther. 25t.55U. and PA. Franklin. IW4. Effect3 of e~~~~~~ a endogenous adenosine a’n gastrin release from rat a’nzrrtlmuco~. Gastroentero~ogy Xh. 1I07. Lusty. 0.H NJ. Rose&rough. A.L. Farr and RJ. RandAP. 1951. Protek measurement with the F&in pkno! reaynz. 1. B&.
Warty. RF.
Acknowledgement This work was supported by the Polish Programme for Basic Research 06-02.
References Chaney. A.L. and E.P. Marbach, 1%2, Modified reagents for determination of urea and ammonia, Clin. Chem. 8. 130. Diibriinte, Z., Z. KahBn. J. I.&g and V. Varr6, 1987. Mucosal blood
Chem. 193. 265. Mozsik, G., F. Vizi and J. Kutas.
1976. A ce~lul,ar-b~~~~~~~ evaluation of gastrk bcxiy mucosa an”d muscular fayer i&npatients with different basal acidoutput. Stand. J. Gastroenterot. 11.205. Mozsik, 6.. J. Kutas. L. Nagy and F. Tarnok. 19x0. Biocbemisa~ of antraf ulcer in patknts. Acta Med. Aca’d. Sci. Hung. 37. 39. Namiot. Z.. J. Rutkiewicz. 3. Stasiewicz and J. G&ski. 19W Aderxosinr deaminase activity in tbr human gastrkc mucosa tn relatmn to acid secretion. Digestion 45. 172.
