EFFECT OF SEVERE SMOKE-INHALATION INJURY ON SYSTEMIC MICROVASCULAR BLOOD-FLOW IN SHEEP

Multiple 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 deliv ery to distant organs due to maldistribution of blood flow may be a co ntributing factor. We examined the effects of acute lung injury induce d by smoke inhalation on microvascular blood flow to various organs in sheep. Seven sheep were prepared with arterial, venous, pulmonary art ery, and left atrial catheters, After a 5 day recovery period, a trach eostomy was performed, followed by insufflation with 48 breaths of coo l cotton smoke. Determination of microvascular blood flow using colore d microspheres, standard hemodynamic measures, and blood gas analysis were performed before and at 12 h intervals after smoke inhalation. An imals were resuscitated to maintain left atrial pressure at +/-2 mmHg of the baseline value and FiO(2) was adjusted to maintain Sao(2) at >9 0%. After 48 h, sheep were killed and an autopsy was performed. Sample s of trachea, left ventricle, ileum, colon, spleen, pancreas, and cort ex from both kidneys were obtained for determination of microvascular blood flow. Blood flow to the trachea was substantially increased, whi le blood flow to the kidneys was preserved near baseline levels. Left ventricular blood flow decreased slightly; however, this decline was n ot statistically significant. Blood flow to ileum, colon, spleen, and pancreas was significantly decreased, particularly at 36 and 48 h afte r injury. These decreases were independent of changes in cardiac outpu t or systemic oxygen delivery. It is likely that alteration in microva scular blood flow may contribute to the development of nonpulmonary or gan dysfunction after acute lung injury.