• P J Schenarts, H G Bone, L D Traber, and D L Traber.
• Department of Anesthesiology, University of Texas Medical Branch, Galveston 77555, USA.
• Shock. 1996 Sep 1;6(3):201-5.

AbstractMultiple nonpulmonary organ dysfunction is frequently associated with acute lung injury; however, the mechanisms underlying the pathogenesis of this process are not completely understood. Decreased oxygen delivery to distant organs due to maldistribution of blood flow may be a contributing factor. We examined the effects of acute lung injury induced by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary artery, and left atrial catheters. After a 5 day recovery period, a tracheostomy was performed, followed by insufflation with 48 breaths of cool cotton smoke. Determination of microvascular blood flow using colored microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. Animals were resuscitated to maintain left atrial pressure at +/- 2 mmHg of the baseline value and FiO2 was adjusted to maintain Sao2 at > 90%. After 48 h, sheep were killed and an autopsy was performed. Samples of trachea, left ventricle, ileum, colon, spleen, pancreas, and cortex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, while blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was not statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h after injury. These decreases were independent of changes in cardiac output or systemic oxygen delivery. It is likely that alteration in microvascular blood flow may contribute to the development of nonpulmonary organ dysfunction after acute lung injury.

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