English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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 ((.)VA/(.)Q) inequality as opposed to a diffusive impairment in O2 exchange. Seven males (26 +/- 3 yr; FEV1: 110 +/- 16% predicted.) performed spirometry and had (.)VA/(.)Q mismatch measured using the multiple inert gas elimination technique, before and after 20 ml/kg iv of normal saline delivered in approximately 30 min. Infusion increased thoracic fluid content from transthoracic impedance by 12% (P &lt; 0.0001) and left FVC unchanged but reduced expiratory flows (FEF(25-75) falling from 5.1 +/- 0.4 to 4.2 +/- 0.4 l/s, P &lt; 0.05). However, (.)VA/(.)Q mismatch as measured by the log standard deviation of the ventilation (LogSD(.)V) and perfusion (LogSD(.)Q) distributions remained unchanged; LogSD(.)V: 0.40 +/- 0.03 pre, 0.38 +/- 0.04 post, NS; LogSD(.)Q: 0.38 +/- 0.03 pre, 0.37 +/- 0.03 post, NS. There was no significant change in arterial PO2 (99 +/- 2 pre, 99 +/- 3 mmHg post, NS) but arterial PCO2 was decreased (38.7 +/- 0.6 pre, 36.8 +/- 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 O2 exchange, with the measured-predicted alveolar-arterial oxygen partial pressure difference being unaltered by infusion at FIO2 = 0.125 (4.3 +/- 1.0 pre, 5.2 +/- 1.0 post, NS). After infusion, the fraction of perfusion going to areas with (.)VA/(.)Q &lt; 1 was increased when a subject breathed a hyperoxic gas mixture [0.72 +/- 0.06 (FIO2 = 0.21), 0.80 +/- 0.06 (FIO2 = 0.30), P &lt; 0.05] with similar effects on ventilation in the face of unchanged (.)VA and (.)Q. These results suggest active control of blood flow to regions of decreased ventilation during air breathing, thus minimizing the gas exchange consequences.

Rapid intravenous infusion of 20 ml/kg saline does not impair resting pulmonary gas exchange in the healthy human lung