Mefenamic acid

enzymatic and nonenzymatic reactions result in the conversion of these highly unstable prostaglandins to more stable and physiologically important prostanoids, including prostaglandin H2, prostacyclin (PGI2) and thromboxane A2. Arachidonic acid is a 20 carbon, unsaturated fatty acid found in membrane phospholipids. It can be cleaved from these phospholipids through the actions of phospholipase A> or phospholipase C, whereupon it can react with cyclooxygenase to form prostanoids. One of the mechanisms through which glucocorticoids reduce inflammation is by inhibiting this phospholipase-mediated liberation of arachidonic acid from membrane phospholipids. Prostaglandins contribute to the inflammatory process primarily by causing relaxation of vascular smooth muscle around arterioles, thereby increasing blood flow. While prostaglandins themselves cause only minor changes in the permeability of blood vessels, the increase in blood flow they produce results in a synergistic increase in plasma exudation (edema formation) caused by other mediators, such as histamine and bradykinin. In doing so, prostaglandins contribute to three of the cardinal signs of inflammation, namely, redness, swelling and heat.

Prostaglandins also contribute to the pain associated with inflammation. Prostaglandins themselves are not particularly potent at inducing a pain response when applied, for example, to the base of a blister in human skin. However, they can produce a state of prolonged hyperalgesia and increase the sensitivity of peripheral pain receptors to chemical and mechanical stimuli. For example, the presence of prostaglandins at a site of inflammation or injury will greatly increase the sensitivity of pain receptors to mediators such as bradykinin and histamine. By inhibiting prostaglandin synthesis, NSAIDs remove this hyperalgesic component of an inflammatory reaction. NSAIDs exert analgesic effects both peripherally and centrally, although it is the peripheral action that predominates.

Prostaglandins also play a key role in the generation of fever. There is strong evidence that prostaglandins are produced in the hypothalamus in response to interleukin 1 (IL-1). These prostaglandins mediate the resetting of temperature-regulating systems in the hypothalamus. Blockade of prostaglandin synthesis by NSAIDs results in a blockade of this effect of IL-1 and other pyrogenic substances. Interestingly, acetaminophen (paracetamol) shares this ability to inhibit prostaglandin synthesis in the hypothalamus and therefore reduce fever, but this drug is a poor inhibitor of prostaglandin synthesis in the periphery, so is not an effective anti-inflammatory drug.

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