Addition of Nitric Oxide to Oxygen Improves Cardiopulmonary Function in Patients With Severe COPD: Outcome
In contrast, pulmonary hemodynamics continued to improve as the NO concentration was increased from 5 through 20 ppm, demonstrating dose dependence. The mechanism appeared to be NO-induced pulmonaiy vasodilatation leading to a reduction of MPAP and improved REF. Because the HR remained unchanged, we surmise that the increase in Cl was due to improved REF. Both the increase in Pa02 and decrease in PVRI demonstrated considerable heterogeneity of response (Table 6).
The observation that patients 15 and 17 had marked decreases in PVRI under NO whereas in patient 2 the decrease was only moderate is in accordance with the international experience suggesting that the higher the pathologic values, the more pronounced the response to NO is likely to be. In patient 2 with an only slightly elevated PVRI, the lesser response to NO is not unexpected.
The variability of the values is probably related to varying endogenous NO deficiency. This has been clearly outlined by the study of Dinh-Xuan et al in which the authors describe the effects of chronic hypoxia on the endothelium-dependent relaxation of pulmonaiy artery rings. Ziesche et al have shown in specimens from COPD patients with pulmonary hypertension that there are considerable differences in the degree of permanent pulmonary inflammation that significantly reduces the expression of NOS-3. Asthma inhalers Reading here The chronic inflammation that causes the downregulation of NOS-3 can partly be attributed to chronic hypoxia, but it also depends on the very different interindividual extent of inflammatory activity in pulmonary vasculature of COPD patients, which can be measured, eg, by quantitative polymerase chain reaction techniques. That means that in addition to factors like hypoxia, smoking, and repeated bacterial infections, the level of the patient’s immune response to the process of chronic inflammation could play a major role in the development and maintenance of pulmonary hypertension.
The explanation for the striking difference between our results and those of Barbera et al may relate to the differential effect of NO on oxygenation and pulmonary vascular resistance. Given the well-established dose dependence of the response of the pulmonary vasculature to NO, it is conceivable that at 40 ppm (but not at <20 ppm), the dose is sufficient to overcome hypoxic pulmonary vasoconstriction and worsen oxygenation.
Table 6—Range of Response to 10 ppm NO