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Comparison of dexamethasone and nedocromil sodium on neurogenic oedema formation
288 TISSUE AND PLASMA GASTRIN MOLECULAR TREATED WITH OMEPRAZOLE
FORMS
IN PATIENTS
I. NEMETH, J. NAFRADF, I. LONOVICS*, A. VARRO, G.J. DOCKRAY, Physiological Laboratory, Univ. Liverpool, Liverpool, U.K. "lst Dept. Medicine, Szeged, Hungary Active, amidated gastrins (G34, G17) are generated from inactive progastrin by steps involving endopeptidase cleavage and amidation. We have cxamlned how inhibition of acid secretion by omeprazole influences progastrin-derived peptides in patients with duodenal ulcer disease (N=13). Blood, antr~l and duodenal biopsies were taken at initial endoscopy, after 6 weeks omeprazole, and after a further 6 weeks treatment-free period. Proga~in, Gly-extended gastrin, G17 and total amidated gastrin were determined by ILIA. Omeprazole treatment significantly increased fasting plasma concentrations of both amidated gastrin (18.2±3.8 to 33.7 +6.1 pmol/1, p <0.05) and G17 (6.3 :!:0.9 to 13.6± 1.6 pmol/l, p <0.001). Six weeks after stopping omeprazole, plasma gastrin had returned to pretreatment levels. Antral mucosal progastrin was significantly increased following omeprazole treatment (1.08±0.18 to 2.26±0.42 nmol/g tissue, p <0.05) and decreased to pretreatment levels in the treatment-free period. No significant differences were seen in the levels of antral amidated or Gly-extended gastrin, or in the duodenal immunoreactive gastrins, with treatment. Conclusion. 1, Omeprazole reversibly increases plasma G17 and amkLa.t~ gastrin, and antral progastrin, but not duodenal gastrins. 2, Acute achlorhydria-indueed changes in gastrin processing occur in antrum, but not duodenum.
COMPARISON OF DEXAMETHASONE AND NEDOCROMIL SODIUM ON NEUROGENIC OEDEMA FORMATION. P.NEWBOLD AND S.D.BRAIN, PharmacologyGroup and VascularBiologyResearch Center, King's College, Manresa Rd., London SW3 6LX. Anti-i,~AmmAtory steroids (dexamethau~) and the cromgglymte-like corn.lxz.~i ~ (NS) ~ v e been ~
to act at ~
nerve ~
investigated the e e k ~ ~ dexametlmone (DEX) and NS oa ~
.
so~'um
w e have
to moe~tte ~
oedem fm~mim indeced by canaan tu ramt dor~ ~ aaa by ~ ~ n ~e~e mtlemN mr~e ~ :ruem ~ . Oedemafonmtiea i a d ~ by test at~ts (0.~mti.~) in the skin ~ ~ ~ v,m memrea ~ a~um~ation of t ~ I . . ~ , ~ , (i.v.) f m skin sims. l~l~ts ~-m ~ with ~ ~ i.v: ~ ) ,
(eK lnm~)kaw o~lma ~r 3s.7~.4, lZ~0.~and 3LS~3~ (n~_)~ significantly ~ 0 . 0 1 , n=6)inlu'bited ~
U .n~t ~
~X
to HA- and BK.-induced 6edems.but badno e~ect on
o...,
.
.
.
.
.
O~kma in th~ paw~~mts was m ~ d b y ~ ~' z , I - ~ (i.v.) into t ~ s~anto q .c~m~ stimulat/on ~f the imlated ~tenous nerveln the le~htad l~W (10V, 2]Rz, lms_&~a~n tbr 5 min)~. Net ocde~mwas cxprmed m oedma in 1~ paw mimmh a l oakmu in r i ~ t pew. l ~ s Winepmmm~d with
DEX (lmll/kg-s.c.), NS (10mlP'klliv.) ~r ~ v~dcle. ~ ~ gave net obdem of 13.0,3.4pPl0emg m the rat paw.(n-6). DEX ~ to 4.3~-0.4, (n.,6). NS had no-e~]~eeto~ oetllelemm ~ In conclusionDEX appmemto inhibit oedmm ~
e~_the . ~ (P<0.01) ~
i~'l~e eedema
nerve s a m ~ o ~ electrical"sfinmlmt~.~sm~ory n out not that induced by cbem~t:alstimulation and lqS had no effect on neumgenic oedem,s. The n.~t.misms for
these differencesare unclear. 1. P.Newbold& S.D.Brain (1993) Br. £ Pharmacoi. 108, 705-710. 2. K.LEseoR& S.D. Brain (1993) Br. d. Pharmacol. 110, 772-776. P.N. is a SERC traded Phi). student. We thank Fisons for support.
FORMS
IN PATIENTS
I. NEMETH, J. NAFRADF, I. LONOVICS*, A. VARRO, G.J. DOCKRAY, Physiological Laboratory, Univ. Liverpool, Liverpool, U.K. "lst Dept. Medicine, Szeged, Hungary Active, amidated gastrins (G34, G17) are generated from inactive progastrin by steps involving endopeptidase cleavage and amidation. We have cxamlned how inhibition of acid secretion by omeprazole influences progastrin-derived peptides in patients with duodenal ulcer disease (N=13). Blood, antr~l and duodenal biopsies were taken at initial endoscopy, after 6 weeks omeprazole, and after a further 6 weeks treatment-free period. Proga~in, Gly-extended gastrin, G17 and total amidated gastrin were determined by ILIA. Omeprazole treatment significantly increased fasting plasma concentrations of both amidated gastrin (18.2±3.8 to 33.7 +6.1 pmol/1, p <0.05) and G17 (6.3 :!:0.9 to 13.6± 1.6 pmol/l, p <0.001). Six weeks after stopping omeprazole, plasma gastrin had returned to pretreatment levels. Antral mucosal progastrin was significantly increased following omeprazole treatment (1.08±0.18 to 2.26±0.42 nmol/g tissue, p <0.05) and decreased to pretreatment levels in the treatment-free period. No significant differences were seen in the levels of antral amidated or Gly-extended gastrin, or in the duodenal immunoreactive gastrins, with treatment. Conclusion. 1, Omeprazole reversibly increases plasma G17 and amkLa.t~ gastrin, and antral progastrin, but not duodenal gastrins. 2, Acute achlorhydria-indueed changes in gastrin processing occur in antrum, but not duodenum.
COMPARISON OF DEXAMETHASONE AND NEDOCROMIL SODIUM ON NEUROGENIC OEDEMA FORMATION. P.NEWBOLD AND S.D.BRAIN, PharmacologyGroup and VascularBiologyResearch Center, King's College, Manresa Rd., London SW3 6LX. Anti-i,~AmmAtory steroids (dexamethau~) and the cromgglymte-like corn.lxz.~i ~ (NS) ~ v e been ~
to act at ~
nerve ~
investigated the e e k ~ ~ dexametlmone (DEX) and NS oa ~
.
so~'um
w e have
to moe~tte ~
oedem fm~mim indeced by canaan tu ramt dor~ ~ aaa by ~ ~ n ~e~e mtlemN mr~e ~ :ruem ~ . Oedemafonmtiea i a d ~ by test at~ts (0.~mti.~) in the skin ~ ~ ~ v,m memrea ~ a~um~ation of t ~ I . . ~ , ~ , (i.v.) f m skin sims. l~l~ts ~-m ~ with ~ ~ i.v: ~ ) ,
(eK lnm~)kaw o~lma ~r 3s.7~.4, lZ~0.~and 3LS~3~ (n~_)~ significantly ~ 0 . 0 1 , n=6)inlu'bited ~
U .n~t ~
~X
to HA- and BK.-induced 6edems.but badno e~ect on
o...,
.
.
.
.
.
O~kma in th~ paw~~mts was m ~ d b y ~ ~' z , I - ~ (i.v.) into t ~ s~anto q .c~m~ stimulat/on ~f the imlated ~tenous nerveln the le~htad l~W (10V, 2]Rz, lms_&~a~n tbr 5 min)~. Net ocde~mwas cxprmed m oedma in 1~ paw mimmh a l oakmu in r i ~ t pew. l ~ s Winepmmm~d with
DEX (lmll/kg-s.c.), NS (10mlP'klliv.) ~r ~ v~dcle. ~ ~ gave net obdem of 13.0,3.4pPl0emg m the rat paw.(n-6). DEX ~ to 4.3~-0.4, (n.,6). NS had no-e~]~eeto~ oetllelemm ~ In conclusionDEX appmemto inhibit oedmm ~
e~_the . ~ (P<0.01) ~
i~'l~e eedema
nerve s a m ~ o ~ electrical"sfinmlmt~.~sm~ory n out not that induced by cbem~t:alstimulation and lqS had no effect on neumgenic oedem,s. The n.~t.misms for
these differencesare unclear. 1. P.Newbold& S.D.Brain (1993) Br. £ Pharmacoi. 108, 705-710. 2. K.LEseoR& S.D. Brain (1993) Br. d. Pharmacol. 110, 772-776. P.N. is a SERC traded Phi). student. We thank Fisons for support.