Effects of nitric oxide inhalation on pulmonary serial vascular resistances in ARDS.

Abstract

The pulmonary vasculature site of action of nitric oxide (NO) in patients with acute respiratory distress syndrome (ARDS) is still unknown. Seven patients were studied during the early stage of ARDS. The bedside pulmonary artery single-occlusion technique, which allows estimation of the pulmonary capillary pressure (Pcap) and segmental pulmonary vascular resistance, was used without NO or with increasing inhaled NO concentrations (15 and 25 parts per million [ppm]). Systemic circulatory parameters remained unaltered during 15 ppm NO inhalation, whereas 25 ppm NO inhalation slightly decreased mean systemic arterial pressure from 76.7 +/- 5.1 (mean +/- SEM) to 69 +/- 5.2 mm Hg (p < 0.01). Mean pulmonary arterial pressure (Ppam) and mean pulmonary capillary pressure (Pcapm) fell during 25 ppm NO inhalation from 27.4 +/- 3.5 to 21 +/- 2.2 mm Hg (p < 0.001) and from 14.8 +/- 1.5 to 10.7 +/- 1.4 mm Hg (p < 0.001) respectively, the total pulmonary resistance decreased by 28% (p < 0.01). The resistance of the capillary-venous compartment fell during 25 ppm NO inhalation from 100 +/- 16 to 47 +/- 16 dyn x s x m(2) x cm(-5) (p < 0.01), whereas the pulmonary arterial resistance was unchanged. In these patients NO inhalation during the early stage of ARDS reduces selectively Ppam and Pcapm by decreasing the pulmonary capillary-venous resistance. This latter effect may reduce the filtration through the capillary bed and hence alveolar edema during ARDS.

Aerosolized Soluble Nitric Oxide Donor Improves Oxygenation and Pulmonary Hypertension in Acute Lung Injury

“…In contrast, animals treated with nebulized saline exhibited no significant improvement in oxygenation. The oxygenation effects noted with delivery of nebulized DMAEP/NO were similar to those observed in both animals and human subjects given continuously inhaled NO gas (10,16,(32)(33)(34). The improvement in oxygenation in the present study was probably due to improvements in intrapulmonary shunt.…”

Single arterial occlusion to locate resistance in patients with pulmonary hypertension

“…Inhaled NO has been reported in isolated perfused lungs of various species after different vasoconstrictor stimuli either to unalter the longitudinal distribution of resistances [26] or to act predominantly at precapillary level [27]. Inhaled NO did not affect the longitudinal distribution of resistances in experimental micro-embolic PH [28] but decreased the capillary-venous component of PVR in acute respiratory distress syndrome [29]. Inhaled NO diffuses easily through the alveolo-capillary membrane before its inactivation by haemoglobin, and probably dilates the smallest arterioles and venules adjacent to the alveolar space, provided there is a component of active constriction.…”

Fluid Management in Acute Lung Injury and ARDS

“…Some have reported that a reduction in pulmonary water or endothelial permeability could be connected to a decrease in capillary filtration pressure [16]. However, most of the clinical studies in ARDS patients have only shown modest effects by these drugs on pulmonary capillary pressure [22][23][24], and the most recent large studies have not reported prognostic benefit with the systematic use of inhaled NO in cases of acute lung injury or ARDS [25]. Fluid restriction that is more or less associated with a diuretic treatment makes it possible to reduce both pulmonary capillary pressure and central venous pressure.…”