Cyclooxygenase pathways model

Prostacyclin is increased in response to ischemia and reperfusion through activation of the cyclooxygenase-2 pathway. Inhibition of cyclooxygenase-2 by celecoxib or meloxicam resulted in a concentration dependent exacerbation of the myocardial dysfunction and damage in a perfused rabbit heart model of ischemia and reperfusion, indicating a cardioprotective role for prostacyclin.104... 

Fig. (9). Simplified model of the possible relationships between NO, SA, ROS and ethylene. NO and ROS trigger SA synthesis and SA might also enhance NO and ROS synthesis. SA, NO and ROS may act synergistically by similarly modulating the activity of common targets (for example, aconitase, ACC oxidase and cyclooxygenase). This amplification process favours the SA-dependent pathway. By contrast, NO- and SA-mediated ACC oxidase inhibition prevent ethylene synthesis and consequently the ethylene pathway (SA-independent pathway). SA may also counteract some of the NO effects and may prevent NO deleterious damage (for example accumulation of NO inhibits electron transport through cytochrome c oxidase while SA activates the alternative oxidase [18]).

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