Nitric oxide

• NO is produced by iNOS, eNOS, nNOS
• eNOS = endothelial NO synthase (constitutive)
• iNOS = induced NO synthase (increased expression)
• iNOS produces NO at high levels during inflammation
• eNOS produces NO to relax blood vessels
• nNOS produces NO to inhibit neurotransmitter release from neurons
• nNOS = neuronal NO synthase (constitutive)
• iNOS = inducible NO synthase (inducible)
• Nitric oxide (NO) is used as a selective pulmonary vasodilator in pulmonary hypertension.
• Nitric oxide (NO) is an inorganic gas.
• Nitric oxide (NO) is presented in aluminium cylinders containing 100/800 ppm of NO and nitrogen; the cylinders may contain either 353 l at standard temperature and pressure (STP) of NO in nitrogen or 1963 l at STP.
• Pure NO is toxic and corrosive.
• Nitric oxide (NO) can also be supplied via stainless steel medical gas piping.
• Nitric oxide (NO) is a potent vasodilator that mediates the hypotension and significant vascular leak characteristic of septic shock.
• Inhaled NO is a selective pulmonary vasodilator, since it is avidly bound to haemoglobin and thereby inactivated before reaching the systemic circulation.
• Nitric oxide (NO) released from the vascular endothelium inhibits platelet aggregation and attenuates platelet and white cell adhesion.
• Nitric oxide (NO) inhibits hypoxic pulmonary vasoconstriction and preferentially increases blood flow through well-ventilated areas of the lung, thereby improving ventilation:perfusion relationships.
• Nitric oxide (NO) increases the cerebral blood flow and appears to have a physiological role as a neurotransmitter within the autonomic and central nervous systems.
• Nitric oxide (NO) may play a role in the regulation of renin production and sodium homeostasis in the kidney.
• Nitric oxide (NO) is the physiological mediator of penile erection.
• Nitric oxide (NO) is highly lipid-soluble and diffuses freely across cell membranes.
• Following inhalation, NO combines with oxyhaemoglobin that is 60–100% saturated, producing methaemoglobin and nitrate.
• Nitric oxide (NO) has a half-life of <5 seconds.
• During the first 8 hours of NO exposure, methaemoglobin concentrations increase.
• The main metabolite of nitric oxide (NO) is nitrate (70%) which is excreted by the kidneys.
• Prolonged inhalation (up to 27 days) of the gas appears safe and is not associated with tachyphylaxis.
• Abrupt cessation of NO can cause a profound decrease in PaO2 and increase in pulmonary artery pressure, possibly via downregulation of endogenous NO production or guanylate cyclase activity.
• The dose of nitric oxide (NO) should be reduced slowly to avoid this from occurring, even in patients who may not have clinically responded to NO therapy.
• During treatment, concentrations of nitrogen dioxide must be monitored.
• Nitric oxide (NO) therapy is contraindicated in neonates known to have circulations dependent on a right-to-left shunt or significant left-to-right shunts.
• Development of methaemoglobinaemia usually rapidly resolves on discontinuation of treatment over several hours.
• Persistent methaemoglobinaemia can be treated using methylthioninium chloride.
• Mortality does not appear to be affected by the administration of NO in ARDS.