**3. Ulcer inducing agents/models**

The pathological mechanisms of SU disease that compromises its functional capability and the structural integrity has been established to arise mainly through either production of too much acid and pepsin, or weakening of the gastric epithelia that consequently results in too little mucosal resistance [2]. **Table 1** shows some of the known ulcerogenic agents/models and the pathological mechanism involved in their ulcer pathogenesis. A good understanding of the pathogenic mechanism of action of these models is crucial to spotting and either managing or preventing ulceration and the associated disorders.


**Table 1.** Commonly used experimental models for ulcer induction.

three decades, the most frequently used H<sup>2</sup>

**2.5. Corticohypothalamic drugs**

**2.6. Proton pump inhibitors (PPIs)**

drugs.

28 Stomach Disorders



ranitidine and famotidine [2]. However, many adverse reactions such as effects on the endocrine, cardiovascular and central nervous systems (CNS) have been associated with these

A role has been established for the CNS in the regulation of gastric secretion and in the pathogenesis of peptic ulcer, although clarification is required in many areas. It is not surprising that drugs which act specifically on the CNS may exert a beneficial effect on SU, which sometimes is significantly better than other drugs. Trimipramine is a tricyclic antidepressant which causes a slight decrease in gastric secretion that is apparently not connected with its anticholinergic action. Like other traditional tricyclic antidepressants, it may have some H<sup>2</sup>

antagonistic effects and may also act on α-adrenoceptors enhancing catecholamine availability at central synapses [18], or may depress central vagal function. However the use of

At present, PPIs are the most commonly prescribed class of antiulcer drugs. Their mode of action involves blockage of the site of gastric acid secretion in the parietal cell of the stomach [19]. However, because the parietal cells are constantly reproducing in millions, effective inhibition of gastric acid secretion is almost unachievable and this partly explains their relative safety compared to other groups of antiulcer drugs. In general, the incidence of short-term adverse effects subsequent to PPI usage is relatively low and this may be the reason for their being well tolerated. Their long-term use has not been frequently studied and the dearth of information in this regards has made it difficult to make definitive statements [20]. For all the PPIs (omeprazole, lansoprazole, dexlanprazole, esomeprazole, pantoprazole, rabeprazole and ilaprazole), the occurrence of adverse effects are similar, though they have been reported more frequently with omeprazole. This may be due to its longer availability. The common adverse effects with PPIs include headache, nausea, diarrhea, abdominal pain, fatigue and dizziness. Infrequent adverse effects may also include rash, itch, flatulence, constipation, anx-

The pathological mechanisms of SU disease that compromises its functional capability and the structural integrity has been established to arise mainly through either production of too much acid and pepsin, or weakening of the gastric epithelia that consequently results in too little mucosal resistance [2]. **Table 1** shows some of the known ulcerogenic agents/models and the pathological mechanism involved in their ulcer pathogenesis. A good understanding of the pathogenic mechanism of action of these models is crucial to spotting and either manag-

trimipramine in non-depressed ulcer patients is questionable.

iety, depression, myopathies and rhabdomyolysis [21].

ing or preventing ulceration and the associated disorders.

**3. Ulcer inducing agents/models**
