Abstract
The nitric oxide/cyclic guanosine monophosphate (NO/cGMP) pathway has a significative influence in hemodynamic changes that occur in transplants. Classically, the ischemia-reperfusion syndrome (IRS) is characterized by hypotension and low vascular resistance, when cGMP and nitric oxide (NO) are increased, contributing to oxidative stress, within an inflammatory context. These mechanisms occur in several types of transplants, such as liver, heart, lungs, kidney, which are a therapeutic choice in several clinical conditions when conventional treatments failed. It is well known the significant relation between graft dysfunction or rejection and ischemia-reperfusion injury that is linked to inflammatory response and NO/cGMP pathway activation. This review aims to study the NO/cGMP pathway in solid organ transplants. Finally, we inquire whether physicians do not underestimate the NO/cGMP pathway.
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