This effect is attributed to the ability of the Paracetamol to cross react with either nitric oxide synthase (NOS) by increasing the synthesis of NO, and with cyclooxygenase (COX), by inhibiting the synthesis of prostaglandin I2 (PGI2-antiplatelet and vasodilator effect) without interfering with the production of Thromboxane A2 (TXA2-powerful vasoconstrictor and pro-thrombogenic) causing an imbalance of endovascular homeostasis.