PubMed · 4685514
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J N Baird, R L Thompson, K DeVoe. 1973-02-15. "Shock lung".. https://doi.org/10.1016/0002-9378(73)90417-1
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The objective of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model of ventilator-induced lung injury. Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either during or after injurious ventilation, with a solution containing the membrane-impermeant label propidium iodide. In lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with plasma membrane wounds, both permanent and transient, whereas in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with permanent plasma membrane wounds. Hypercapnia minimized the adverse effects of high-volume ventilation on vascular barrier function, whereas hypocapnia had the opposite effect. Despite CO2-dependent differences in lung mechanics and edema the number of injured subpleural cells per alveolus was similar in the three groups (0.48 +/- 0.34 versus 0.51 +/- 0.19 versus 0.43 +/- 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively). However, compared with normocapnia the probability of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p < 0.02). This finding was subsequently confirmed in alveolar epithelial cell scratch models. The potential relevance of these observations for lung inflammation and remodeling after mechanical injury is discussed.
BACKGROUND/PURPOSE: This study was aimed at determining whether intraoperative intratracheal pulmonary ventilation (ITPV) could prevent/treat respiratory complications of laparoscopy in a model of pediatric pulmonary insufficiency. METHODS: Severe lung injury was induced in 0- to 2-month-old lambs (n = 5) by endotracheal saline lavage. Animals then underwent establishment of CO2 pneumoperitoneum. Intraperitoneal pressures were progressively raised from 0 to 15 mm Hg, at intervals of 5 mm Hg. At each interval, blood gas and hemodynamic data were recorded, 20 minutes after initiation of both conventional ventilation and pure ITPV. All ventilatory parameters were constant and identical on both modes of ventilation. RESULTS: On conventional ventilation, severe respiratory acidosis and hypoxemia ensued at intraperitoneal pressures of 5 mm Hg and 10 mm Hg or more, respectively. Compared with conventional ventilation, ITPV led to statistically significant decreases in PCO2 at intraperitoneal pressures of 5 mm Hg (43.2 +/- 5.2 vs 56.1 +/- 6.6 mm Hg) and 10 mm Hg (45.1 +/- 3.2 vs 61 +/- 6.3 mm Hg) and to significant increases in PO2 at 10 mm Hg (92 +/- 10.2 vs 61 +/- 8.1 mm Hg), resolving the acidosis and hypoxemia at those pressure levels. CONCLUSIONS: Compared with conventional ventilation, ITPV improves both CO2 removal and oxygenation during CO2 pneumoperitoneum in a pediatric lung injury model. Intratracheal pulmonary ventilation may be a safer intraoperative mode of ventilation for neonates and children with respiratory failure who require laparoscopy.