Influence of acid and angiogenesis on kinetics of gastric ulcer healing in rats: interaction with indomethacin

1995 ◽  
Vol 268 (2) ◽  
pp. G276-G285 ◽  
Author(s):  
A. Schmassmann ◽  
A. Tarnawski ◽  
B. M. Peskar ◽  
L. Varga ◽  
B. Flogerzi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Granulation Tissue ◽  
Ulcer Healing ◽  
Healing Rate ◽  
Late Phase ◽  
Gastric Ulcers ◽  
Gastric Ulcer Healing ◽  
Ulcer Healing Rate ◽  
Kinetics Of ◽  
Stimulation Of

Indomethacin delays healing of experimental gastric ulcers. We investigated whether inhibition of gastric acid secretion by omeprazole or stimulation of angiogenesis by basic fibroblast growth factor (bFGF) may reverse this delay. Rats with gastric ulcers induced by cryoprobe were treated subcutaneously with either placebo, indomethacin (2 x 0.5 mg/kg), bFGF (2 x 100 micrograms/kg), omeprazole (1 x 40 mumol/kg), indomethacin plus omeprazole, or indomethacin plus bFGF given daily for 8, 10, 15, and 22 days. Ulcer size, epithelial cell proliferation, angiogenesis, and maturation of granulation tissue were sequentially quantified. Omeprazole significantly accelerated ulcer healing in an early phase (days 3-8). In contrast, bFGF accelerated healing in a late phase (days 10-15). Indomethacin significantly delayed ulcer healing in late phase and decreased prostaglandin generation, cell proliferation, angiogenesis, and maturation of granulation tissue. Despite stimulation of angiogenesis, bFGF did not reverse indomethacin-induced delay in ulcer healing. In contrast, omeprazole reversed indomethacin-induced effects on angiogenesis, cell proliferation, maturation of granulation tissue, and ulcer healing rate.

Annexin-1 modulates repair of gastric mucosal injury

2008 ◽  
Vol 294 (3) ◽  
pp. G764-G769 ◽  
Author(s):  
Gary R. Martin ◽  
Mauro Perretti ◽  
Roderick J. Flower ◽  
John L. Wallace
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Mucosal Injury ◽  
Formyl Peptide Receptor ◽  
Gastric Mucosal Damage ◽  
Gastric Ulcers ◽  
Wild Type ◽  
Gastric Ulcer Healing ◽  
Annexin 1 ◽  
Deficient Mice

Annexin-1 is a glucocorticoid-inducible protein that plays an important effector role in the resolution of inflammation and has recently been shown to contribute to the resistance of the stomach to injury. Using an integrated genetic and pharmacological approach, we have tested the hypothesis that annexin-1 contributes to the healing of mucosal injury, given that such injury is accompanied by an inflammatory response, which is often associated with an overexpression of annexin-1 expression. Gastric ulcers were induced in mice through serosal application of acetic acid. Annexin-1 expression during the healing of the ulcers was examined. The effects on gastric ulcer healing of treatment with an annexin-1 mimetic (Ac2-26), an antagonist of the annexin-1 receptor (Boc2), or a glucocorticoid (dexamethasone) were examined. Finally, susceptibility to and healing of indomethacin-induced gastric lesions were compared in wild-type and annexin-1-deficient mice. Expression of annexin-1 was significantly increased in the gastric ulcer margin throughout the healing process. Treatment with an annexin-1 mimetic (Ac2-26) significantly enhanced gastric ulcer healing. In contrast, both dexamethasone and an formyl peptide receptor-like-1 (FPRL-1) antagonist impaired the early phase of ulcer healing. Annexin-1-deficient mice exhibited the same susceptibility as wild-type mice to indomethacin-induced gastric damage, but the healing of that damage was impaired in the former. These data support the hypothesis that annexin-1 contributes significantly to the process of healing of gastric mucosal damage.

Endothelin-1, an ulcer inducer, promotes gastric ulcer healing via mobilizing gastric myofibroblasts and stimulates production of stroma-derived factors

2006 ◽  
Vol 290 (5) ◽  
pp. G1041-G1050 ◽  
Author(s):  
Tsutomu Nishida ◽  
Shingo Tsuji ◽  
Arata Kimura ◽  
Masahiko Tsujii ◽  
Syuji Ishii ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Angiogenic Factors ◽  
Gastric Epithelium ◽  
Gastric Ulcers ◽  
Ulcer Formation ◽  
Peptic Ulcers ◽  
Converting Enzyme ◽  
Potent Inducer ◽  
Gastric Ulcer Healing

Endothelin (ET)-1 is a potent inducer of peptic ulcers. The roles of ET-1 in ulcer healing, however, have remained unclear, and these were investigated in mice. Gastric ulcers were induced in mice by serosal application of acetic acid. Three days later, mice were given a neutralizing ET-1 antibody or nonimmunized serum. The ulcer size, amount of fibrosis and myofibroblasts, and localization of ET-1 and ETA/B receptors were analyzed. To elucidate the mechanisms underlying the effects of ET-1, we examined the proliferation, migration, and release of growth and angiogenic factors in gastric myofibroblasts with or without ET-1. The expression of prepro-ET-1 (an ET-1 precursor) and ET-converting enzyme-1 was examined in gastric myofibroblasts using RT-PCR. Immunoneutralization of ET-1 delayed gastric ulcer healing. The areas of fibrosis and myofibroblasts were smaller in the anti-ET-1 antibody group than in the control. ET-1 was expressed in the gastric epithelium, myofibroblasts, and other cell types. ETA receptors, but not ETB receptors, were present in myofibroblasts. ET-1 increased proliferation and migration of gastric myofibroblasts. ET-1 stimulated the release of hepatocyte growth factor, VEGF, PGE2, and IL-6 from gastric myofibroblasts. mRNA for prepro-ET-1 and ET-converting enzyme-1 was also expressed. ET-1 promotes the accumulation of gastric myofibroblasts and collagen fibrils at gastric ulcers. ET-1 also stimulates migration and proliferation of gastric myofibroblasts and enhances the release of growth factors, angiogenic factors, and PGE2. Thus ET-1 has important roles not only in ulcer formation but also in ulcer healing via mobilizing myofibroblasts and inducing production of stroma-derived factors.

scholarly journals Effect of Laser Irradiation at Different Wavelengths (940, 808, and 658 nm) on Pressure Ulcer Healing: Results from a Clinical Study

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
J. Taradaj ◽  
T. Halski ◽  
M. Kucharzewski ◽  
T. Urbanek ◽  
U. Halska ◽  
...  
Keyword(s):  
Laser Therapy ◽  
Ulcer Healing ◽  
Healing Rate ◽  
Pressure Ulcers ◽  
Maximum Output Power ◽  
Maximum Output ◽  
Average Dose ◽  
Radiation Emission ◽  
Group I ◽  
Ulcer Healing Rate

The aim of the study was to assess the efficacy of laser therapy (at different wavelengths: 940, 808, and 658 nm) for treating pressure ulcers. The primary endpoint in this trial included both the percentage reduction of the ulcer surface area and the percentage of completely healed wounds after one month of therapy (ulcer healing rate). The secondary endpoint was the ulcer healing rate at the follow-up evaluation (3 months after the end of the study). In total, 72 patients with stage II and III pressure ulcers received laser therapy once daily, 5 times per week for 1 month using a (GaAlAs) diode laser with a maximum output power of 50 mW and continuous radiation emission. Three separate wavelengths were used for the laser treatment: 940 nm (group I), 808 nm (group II), and 658 nm (group III). An average dose of 4 J/cm2was applied. In group IV, a placebo was applied (laser device was turned off). The laser therapy at a wavelength of 658 nm appeared to be effective at healing pressure ulcers. The wavelengths of 808 and 940 nm did not have any effect in our study.

Ankle Motility is a Risk Factor for Healing of Chronic Venous Leg Ulcers

2001 ◽  
Vol 16 (1) ◽  
pp. 38-40 ◽  
Author(s):  
J. R. Barwell ◽  
M. Taylor ◽  
J. Deacon ◽  
C. Davies ◽  
M. R. Whyman ◽  
...  
Keyword(s):  
Risk Factor ◽  
Pump Power ◽  
Ulcer Healing ◽  
Independent Risk Factor ◽  
Healing Rate ◽  
Leg Ulcer ◽  
Venous Leg Ulcer ◽  
Compression Bandaging ◽  
Venous Ulcers ◽  
Ulcer Healing Rate

Objective: To investigate the effect of ankle motility on chronic venous leg ulcer healing, and to relate this to calf pump function and muscle bulk. Methods: This was a prospective cohort study undertaken in a leg ulcer clinic. Ankle motility, calf-ankle circumference ratio and calf pump power (derived from digital photoplethysmography) were assessed as to their effect on ulcer healing rate. Thirty consecutive patients undergoing multi-layer compression bandaging for open chronic venous ulcers were included. Results: Ankle motility was an independent risk factor for ulcer healing ( p = 0.001, hazard ratio 1.08, 95% CI 1.03–1.13). Ankle motility correlated with calf-ankle circumference ratio ( r = 0.48, p<0.01). No relationship was found between photoplethysmography-derived calf pump power, ankle motility or ulcer healing rate. Conclusions Ulcers in legs with poor ankle motility are slower to heal and this may be related to reduced calf muscle bulk. Ankle exercises or physiotherapy could be considered in such patients.

EFFECT OF SUPPORT SURFACE ON PRESSURE ULCER HEALING RATE*

2004 ◽  
Vol 31 (Supplement) ◽  
pp. S2
Author(s):  
Rachel Ochs ◽  
Susan Horn ◽  
Randall Smout ◽  
Lia van Rijswijk
Keyword(s):  
Pressure Ulcer ◽  
Ulcer Healing ◽  
Healing Rate ◽  
Support Surface ◽  
Ulcer Healing Rate ◽  
Effect Of Support

Angiogenesis, cell proliferation and apoptosis in gastric ulcer healing. Effect of a selective cox-2 inhibitor

2004 ◽  
Vol 505 (1-3) ◽  
pp. 187-194 ◽  
Author(s):  
Susana Sánchez-Fidalgo ◽  
Inés Martín-Lacave ◽  
Matilde Illanes ◽  
Virginia Motilva
Keyword(s):  
Cell Proliferation ◽  
Gastric Ulcer ◽  
Ulcer Healing ◽  
Gastric Ulcer Healing ◽  
Healing Effect ◽  
Proliferation And Apoptosis ◽  
Cox 2
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