Difference between revisions of "AUTOREGULATION-PGI2 vs TXA2"
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==Reference(s)== | ==Reference(s)== | ||
Barrett, K.E., Barman, S.M | Barrett, K.E., Barman, S.M., Brooks, H.L., X, J. and Ganong, W.F. (2019). Ganong’s review of medical physiology. 26th ed. New York: Mcgraw-Hill Education | ||
[[Category:Autoregulation]] | [[Category:Autoregulation]] | ||
[[Category:Physiology]] | [[Category:Physiology]] |
Latest revision as of 02:30, 21 March 2023
SUMMARY
PGI-2
1. Prostacylin (PGI-2) produced by endothelial & smooth muscle cells in blood vessels
2. PGI-2 inhibits platelet aggregation & promote vasodilation.
TXA-2
3. Thromboxane A2 (TXA-2) released from platelets, derived from arachnidonic acid via COX pathway.
4. TXA-2 promotes platelet aggregation & vasoconstriction, thus promoting ‘plug’ formation.
BALANCE!
5. Balance between the 2 controls localized clot formation, while maintaining distal blood flow.
6. Aspirin shift this balance towards PGI-2 by irreversible inhibition of cyclooxygenase.
Reference(s)
Barrett, K.E., Barman, S.M., Brooks, H.L., X, J. and Ganong, W.F. (2019). Ganong’s review of medical physiology. 26th ed. New York: Mcgraw-Hill Education