under normal physiologic circumstances, defense mechanisms prevent the erosion of the upper gastrointestinal mucosal lining by the acidic intraluminal contents. A glycoprotein mucous layer lines the stomach and forms a physical barrier to hydrogen ion back-diffusion. Bicarbonate is trapped in this protective layer and neutralizes hydrogen ions before they can reach the gastric epithelial layer. Adequate perfusion and oxygen delivery maintain intramural pH and prostaglandin synthesis, which is necessary for maintenance of the protective barrier layer. The pathophysiology of stress-related mucosal disease (SRMD) and stress ulceration is complex and the exact mechanisms remain uncertain. Major factors necessary for ulceration are: 1). Low gastric intraluminal pH 2). Upper gastrointestinal tract intramural acidosis, and 3). Increased permeability of the protective mucosal barrier. Gastric intraluminal acidity (pH
In mine hypothesis (Global Medical Discovery; Stress-induced gastrointestinal motility is responsible for epileptic susceptibility. Nikiforova AS. Med Hypotheses. 2014 Apr;82(4):442-51) it is postulated that the stress develops in two phases: the first one is ischemic stress (an involuntary event), followed by oxidative stress (an voluntary event). The paper outlines that the main cause of epileptic susceptibility is stress-induced ischaemic contractions of the circular muscles during the first phase of stress. During this phase, a positive feedback loop from circular muscles and different brain structures sustains the contractions. Energy then accumulates in the circular muscles during the contractions. The signals created by the ischemic contractions circulate continuously through interconnected peripheral/central structures. Since these signals are prolonged, they are also memorized.
The second phase of stress develops on the sensitive background of the first phase. The phasic contractions of the circular muscles then release the accumulated energy via uncontrolled discharges. This means that circular muscles react as a structural am-plifier. Defining ischemic stress as a main factor for developing epileptic susceptibility provides opportunities to exploit this mechanism and develop suitable therapies for drug-resistant epileptic seizures.
Ischemic and oxidative stress promote different mucosal changes. Some articles that
might be interesting for you:
1. World J Pediatr 2007;3(1):30-35
Childhood gastrointestinal dysfunction and
protection mechanism of intestinal mucosal
barrier
2. Critical Care Medicine:
February 2002 - Volume 30 - Issue 2 - pp 379-384
Laboratory Investigations
3. Cell Biochemistry and Biophysics
1-Aug-2005, Volume 43, Issue 1, pp 167-188
Oxidative stress in pathogenesis of chronic obstructive pulmonary disease