Nitric oxide and pulmonary arterial pressures in pulmonary hypertension.
Decreased production of vasodilator substances such as nitric oxide (NO) has been proposed as important in development of pulmonary arterial hypertension (PAH). We hypothesize that NO measured over time serves as a non invasive marker of severity of PAH and response to therapy. We prospectively and serially measured exhaled NO and carbon monoxide (CO), a vasodilator and anti-inflammatory product of heme oxygenases, in 17 PAH patients in conjunction with hemodynamic parameters over 2 years. Although pulmonary artery pressures and NO were similar in all patients at entry to the study, NO increased in the 12 individuals who survived to complete the study, and correlated with change in pulmonary artery pressures. In contrast, CO did not change or correlate with hemodynamic parameters. Investigation of NO-oxidant reaction products in PAH in comparison to controls suggests that NO synthesis is impaired in the lung and that reactive oxygen species may be involved in the pathophysiology of pulmonary hypertension. Endogenous NO is inversely related to pulmonary artery pressure in PAH, with successful therapy of PAH associated with increase in NO.
Machado
Roberto F
RF
Department of Pulmonary and Critical Care Medicine, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Londhe Nerkar
Medha-Vini
MV
Dweik
Raed A
RA
Hammel
Jeffrey
J
Janocha
Allison
A
Pyle
Jacqueline
J
Laskowski
Daniel
D
Jennings
Constance
C
Arroliga
Alejandro C
AC
Erzurum
Serpil C
SC
D001794:Blood Pressure / Q000502:physiology*; D002248:Carbon Monoxide / Q000378:metabolism; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000378:metabolism* / Q000503:physiopathology* / Q000628:therapy; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*; D011446:Prospective Studies; D011651:Pulmonary Artery / Q000378:metabolism* / Q000503:physiopathology*; D013997:Time Factors
D009569:Nitric Oxide; D002248:Carbon Monoxide