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This Article Full Text Full Text (PDF) All Versions of this Article: 286/2/H693    most recent 00888.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Dodd-o, J. M. Articles by Pearse, D. B. Search for Related Content PubMed PubMed Citation Articles by Dodd-o, J. M. Articles by Pearse, D. B.

Effect of bronchial artery blood flow on cardiopulmonary bypass-induced lung injury

¹Department of Anesthesia and Critical Care, ²Division of Pulmonary and Critical Care Medicine, Department of Medicine, and ³Division of Cardiac Surgery, Department of Surgery, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21224

Submitted 16 September 2003 ; accepted in final form 13 October 2003

Cardiovascular surgery requiring cardiopulmonary bypass (CPB) is frequently complicated by postoperative lung injury. Bronchial artery (BA) blood flow has been hypothesized to attenuate this injury. The purpose of the present study was to determine the effect of BA blood flow on CPB-induced lung injury in anesthetized pigs. In eight pigs (BA ligated) the BA was ligated, whereas in six pigs (BA patent) the BA was identified but left intact. Warm (37°C) CPB was then performed in all pigs with complete occlusion of the pulmonary artery and deflated lungs to maximize lung injury. BA ligation significantly exacerbated nearly all aspects of pulmonary function beginning at 5 min post-CPB. At 25 min, BA-ligated pigs had a lower arterial PO₂ at a fraction of inspired oxygen of 1.0 (52 ± 5 vs. 312 ± 58 mmHg) and greater peak tracheal pressure (39 ± 6 vs. 15 ± 4 mmHg), pulmonary vascular resistance (11 ± 1 vs. 6 ± 1 mmHg·l^–1·min), plasma TNF- (1.2 ± 0.60 vs. 0.59 ± 0.092 ng/ml), extravascular lung water (11.7 ± 1.2 vs. 7.7 ± 0.5 ml/g blood-free dry weight), and pulmonary vascular protein permeability, as assessed by a decreased reflection coefficient for albumin (_alb; 0.53 ± 0.1 vs. 0.82 ± 0.05). There was a negative correlation (R = 0.95, P < 0.001) between _alb and the 25-min plasma TNF- concentration. These results suggest that a severe decrease in BA blood flow during and after warm CPB causes increased pulmonary vascular permeability, edema formation, cytokine production, and severe arterial hypoxemia secondary to intrapulmonary shunt.

pulmonary edema; reflection coefficient; pig; ischemia; extracorporeal perfusion; tumor necrosis factor-; interleukin-6

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