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[Can prostaglandins in low cytoprotective doses heal peptic ulcers?].
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Cytoprotection of the gastrointestinal mucosa.
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[Experimental gastric lesions and cytoprotection: role of the retrodiffusion of H+ ions].
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Morphologic correlates of "cytoprotection".
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[Cytoprotection with antacids?].
Prostaglandins in very low concentrations which do not inhibit acid secretion protect the mucosa of the gastrointestinal tract against a great number of noxious agents. The protective action of various antacids is likely to be related to its acid neutralizing capacity. Antacids do not prevent lesions evoked by direct necrotising substances such as concentrated ethanol etc. It remains to be established whether the endogenous prostaglandin system is involved in the antiulcerogenic action of some antacids.
Cytoprotection by prostaglandins.
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Gastric cytoprotection by epidermal growth factor. Role of endogenous prostaglandins and DNA synthesis.
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Cytoprotective effect of prostaglandins.
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[Prostaglandins and gastrointestinal cytoprotection].
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Histochemistry of cytoprotection of the rat liver.
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[Cytoprotection of gastric mucosa: myth or reality?].
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[Cytoprotection. A new fashion or real progress?].
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[Cytoprotection: a new principle in ulcer therapy?].
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[The mechanisms of the cytoprotective action of prostacyclin in acute postoperative parotitis].
Effects of prostaglandin I2 of the content of lipid peroxidation products and the activity of glutathione antioxidative system were studied in 60 dogs in whom acute nonepidemic parotitis was induced. Prostaglandin I2 was found to enhance the reactions of protective inhibition of metabolism with reduction of peroxidation level and activation of the antioxidative system, this permitting the cell to preserve its structural intactness. A conclusion is made about the possibility of using prostaglandin I2 for the prevention and therapy of acute nonepidemic parotitis.
Cytoprotective effects of a stable prostacyclin analog and a calcium channel blocker: a study on isolated rat hepatocytes.
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From antianginal drugs to myocardial cytoprotective agents.
The existing major classes of antianginal drugs improve quality of life in patients with coronary artery disease, but mortality in these patients remains unacceptably high. In order to limit the complications of the disease, it is vital to limit myocyte loss. Potentially, this can be achieved not only by prophylaxis, but also by protection, against ischemia. Any therapy that increases myocardial resistance to ischemia will protect against cell death and prolong the life of the myocyte, and possibly the patient. The mechanisms of cell damage during ischemia, and possible therapeutic interventions, are discussed.
[Therapeutic application of myocardial cytoprotection].
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