Mechanism of action of aspirin
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Effects on cyclooxygenase
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There are at least two different cyclooxygenase
Newer NSAID drugs called
Effects on prostaglandins and thromboxanes
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Prostaglandins are local chemical messengers that exert multiple effects including but not limited to the transmission of pain information to the brain, modulation of the hypothalamic thermostat, and inflammation. They are produced in response to the stimulation of phospholipids within the plasma membrane of cells resulting in the release of arachidonic acid (prostaglandin precursor).[11] Thromboxanes are responsible for the aggregation of
Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation.[13]
This antiplatelet property makes aspirin useful for reducing the incidence of heart attacks;[13] heart attacks are primarily caused by blood clots, and their reduction with the introduction of small amounts of aspirin has been seen to be an effective medical intervention.[citation needed] A dose of 40 mg of aspirin a day is able to inhibit a large proportion of maximum thromboxane A2 release provoked acutely, with the prostaglandin I2 synthesis being little affected; however, higher doses of aspirin are required to attain further inhibition.[14]
A side-effect of aspirin mechanism is that the ability of the blood in general to clot is reduced, and excessive bleeding may result from the use of aspirin.[15]
Other methods of action
Aspirin has been shown to have three additional modes of action. It uncouples
Additionally, aspirin induces the formation of NO-radicals in the body, which have been shown in mice to have an independent mechanism of reducing inflammation. This reduces leukocyte adhesion, which is an important step in immune response to infection. There is currently insufficient evidence to show that aspirin helps to fight infection.[17]
More recent data also suggests that salicylic acid and its derivatives modulate signaling through NF-κB.[18] NF-κB is a transcription factor complex that plays a central role in many biological processes, including inflammation.
Reye's syndrome
Reye's syndrome is a potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain and liver, as well as causing hypoglycemia.[19] The exact cause is unknown, and while it has been associated with aspirin consumption by children with viral illness, it also occurs in the absence of aspirin use.
The disease causes
Early diagnosis is vital; while most children recover with supportive therapy, severe brain injury or death are potential complications.
See also
References
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- ^ Sherwood L (2013). Human Physiology: from Cells to Systems. Belmont, CA: Brooks/Cole, Cengage Learning. p. 758.
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- ^ a b "Aspirin in Heart Attack and Stroke Prevention". American Heart Association. Archived from the original on 1 November 2004.
The American Heart Association recommends aspirin use for patients who've had a myocardial infarction (heart attack), unstable angina, ischemic stroke (caused by blood clot) or transient ischemic attacks (TIAs or "little strokes"), if not contraindicated. This recommendation is based on sound evidence from clinical trials showing that aspirin helps prevent the recurrence of such events as heart attack, hospitalization for recurrent angina, second strokes, etc. (secondary prevention). Studies show aspirin also helps prevent these events from occurring in people at high risk (primary prevention).
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- ^ "Reye syndrome" at Dorland's Medical Dictionary
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