| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Anesthesia and Critical Care, Johns Hopkins University, Baltimore, MD, USA
2 Medicine, Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD, USA
3 Surgery, Division of Cardiac Surgery, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: dpearse{at}jhmi.edu.
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 this study was to determine the effect of BA blood flow on CPB-induced lung injury in anesthetized pigs. In 8 pigs (BA-ligated), the BA was ligated whereas in 6 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. Bronchial artery ligation significantly exacerbated nearly all aspects of pulmonary function beginning at 5 min post-CPB. At 25 min, BA-ligated pigs had a lower PaO2 on FIO2 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-1), extravascular lung water (11.7 ± 1.2 vs. 7.7 ± 0.5 ml.g-1 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 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.
This article has been cited by other articles:
|
|
 |
|
  H. Imura, M. Caputo, K. Lim, M. Ochi, M.-S. Suleiman, K. Shimizu, and G. D. Angelini Pulmonary injury after cardiopulmonary bypass: Beneficial effects of low-frequency mechanical ventilation. J. Thorac. Cardiovasc. Surg., June 1, 2009; 137(6): 1530 - 1537. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E Hirleman and D. Larson Cardiopulmonary bypass and edema: physiology and pathophysiology Perfusion, November 1, 2008; 23(6): 311 - 322. [Abstract] [PDF]
|
|
|
|
|
|
T. C. Lisle, L. M. Gazoni, L. G. Fernandez, A. K. Sharma, A. M. Bellizzi, G. D. Schifflett, V. E. Laubach, and I. L. Kron Inflammatory lung injury after cardiopulmonary bypass is attenuated by adenosine A(2A) receptor activation. J. Thorac. Cardiovasc. Surg., November 1, 2008; 136(5): 1280 - 1288. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. M. Dodd-o, L. E. Welsh, J. D. Salazar, P. L. Walinsky, E. A. Peck, J. G. Shake, D. J. Caparrelli, R. C. Ziegelstein, J. L. Zweier, W. A. Baumgartner, et al. Effect of NADPH oxidase inhibition on cardiopulmonary bypass-induced lung injury Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H927 - H936. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
