Aspirin appears to produce analgesia by virtue of both a peripheral and CNS effect. Peripherally, aspirin acts by inhibiting the synthesis and release of prostaglandins. Acting centrally, it would appear to produce analgesia at a hypothalamic site in the brain, although the mode of action is not known. Aspirin's antipyretic activity may also be related to inhibition of synthesis and release of prostaglandins. Uncoated aspirin at a dosage of three 5-grain tablets given three times a day caused an average fecal blood loss of 4.33 ml per day.
Aspirin tablets are enteric coated.
This coating acts to prevent the release of aspirin in the stomach but permits the tablet to dissolve with resultant absorption in the upper portion of the small intestine. This reduces any gastric irritation that may occur with uncoated aspirin but does delay the onset of action. A direct correlation between salicylate plasma levels and clinical analgesic effectiveness has not been definitely established, but effective analgesia is usually achieved at plasma levels of 15 to 30 mg per 100 ml. Effective antiinflammatory activity is usually achieved at salicylate plasma levels of 20 to 30 mg per 100 ml. There is also poor correlation between toxic symptoms and plasma salicylate concentrations, but most patients exhibit symptoms of salicylism at plasma salicylate levels of 35 mg per 100 ml.