{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T23:25:29Z","timestamp":1791156329503,"version":"4.1.0"},"reference-count":31,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Applied Physiology"],"published-print":{"date-parts":[[2010,1]]},"abstract":"<jats:p> Rapid infusion of intravenous saline, a model of pulmonary interstitial edema, alters the distribution of pulmonary perfusion, raises pulmonary capillary blood volume, and increases bronchial wall thickness in humans. We hypothesized that infusion would disrupt pulmonary gas exchange by increasing ventilation\/perfusion (V\u0307a\/Q\u0307) inequality as opposed to a diffusive impairment in O<jats:sub>2<\/jats:sub> exchange. Seven males (26 \u00b1 3 yr; FEV1: 110 \u00b1 16% predicted.) performed spirometry and had V\u0307a\/Q\u0307 mismatch measured using the multiple inert gas elimination technique, before and after 20 ml\/kg iv of normal saline delivered in \u223c30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% ( P &lt; 0.0001) and left FVC unchanged but reduced expiratory flows (FEF<jats:sub>25\u201375<\/jats:sub> falling from 5.1 \u00b1 0.4 to 4.2 \u00b1 0.4 l\/s, P &lt; 0.05). However, V\u0307a\/Q\u0307 mismatch as measured by the log standard deviation of the ventilation (LogSDV\u0307) and perfusion (LogSDQ\u0307) distributions remained unchanged; LogSDV\u0307: 0.40 \u00b1 0.03 pre, 0.38 \u00b1 0.04 post, NS; LogSDQ\u0307: 0.38 \u00b1 0.03 pre, 0.37 \u00b1 0.03 post, NS. There was no significant change in arterial Po<jats:sub>2<\/jats:sub> (99 \u00b1 2 pre, 99 \u00b1 3 mmHg post, NS) but arterial Pco<jats:sub>2<\/jats:sub> was decreased (38.7 \u00b1 0.6 pre, 36.8 \u00b1 1.2 mmHg post, P &lt; 0.05). Thus, infusion compressed small airways and caused a mild degree of hyperventilation. There was no evidence for a diffusive limitation to O<jats:sub>2<\/jats:sub> exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at Fi<jats:sub>O<\/jats:sub><jats:sub>2<\/jats:sub> = 0.125 (4.3 \u00b1 1.0 pre, 5.2 \u00b1 1.0 post, NS). After infusion, the fraction of perfusion going to areas with V\u0307a\/Q\u0307 &lt; 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 \u00b1 0.06 (Fi<jats:sub>O<\/jats:sub><jats:sub>2<\/jats:sub> = 0.21), 0.80 \u00b1 0.06 (Fi<jats:sub>O<\/jats:sub><jats:sub>2<\/jats:sub> = 0.30), P &lt; 0.05] with similar effects on ventilation in the face of unchanged V\u0307a and Q\u0307. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences. <\/jats:p>","DOI":"10.1152\/japplphysiol.00787.2009","type":"journal-article","created":{"date-parts":[[2009,11,12]],"date-time":"2009-11-12T22:19:51Z","timestamp":1258064391000},"page":"53-59","source":"Crossref","is-referenced-by-count":32,"title":["Rapid intravenous infusion of 20 ml\/kg saline does not impair resting pulmonary gas exchange in the healthy human lung"],"prefix":"10.1152","volume":"108","author":[{"given":"G. 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