• R E Carlin, D J McGraw, E M Camporesi, and T S Hakim.
• Department of Surgery, SUNY Health Science Center at Syracuse 13210, USA.
• J. Surg. Res. 1997 May 1; 69 (2): 362-6.

AbstractAcute hemorrhage is associated with a variety of physiologic and metabolic alterations, including vascular hyporeactivity and endothelial cell dysfunction. The lung is a major target organ during hemorrhagic shock. The effect of acute hemorrhage on NO production in the lung is not well described. In the present study we examined the effect of acute hemorrhage on exhaled NO (NOe), and studied how changes in blood volume and flow affect NOe. Anesthetized and mechanically ventilated rabbits were used. The effect of acute hemorrhage by slow exsanguination on NOe was examined using chemiluminescence. Because hemorrhagic shock is associated with decreased pulmonary blood flow, we established an isolated lung preparation perfused with autologous blood (Hct = 17.4%) and studied the effect of pulmonary flow rate on NOe independent of metabolic changes. In order to separate the effect of flow from the effect of changes in blood volume, we examined the effect of flow in isolated lungs perfused with a blood-free albumin solution (PAS). In the isolated lung, ventilation was similar to that used in the intact animal, and temperature, pH, pCO2, and PO2 were kept normal. Prior to exsanguination, baseline NOe in the intact animal was 24 +/- 3 ppb. At 5, 10, 15, and 20 min after initiating the hemorrhage, NOe rose to 31 +/- 3, 51 +/- 7, 94 +/- 10, and 154 +/- 16 ppb, respectively (P < 0.05). During baseline conditions in the blood-perfused isolated lungs (200 ml/min), NOe was 35 +/- 3 ppb. When flow was decreased to 70 and 0 ml/min, NOe increased to 37 +/- 3 and 56 +/- 6 ppb, respectively (P < 0.001). During baseline conditions in the PAS-perfused lungs (70 ml/min), NOe was 94 +/- 13 ppb and was unaffected by changes in flow. The perfusion pressure in the isolated lungs was in the normal range. Reduction in blood flow rate in the isolated lung was associated with less than twofold increase in NOe. This was attributed to reduction in red blood cell volume and not due to changes in blood flow rate. Reduction in flow in the intact animal during hemorrhage generated more than threefold increase in NOe, suggesting that neurohumoral mediators, in addition to changes in flow, play an important role in determining. NOe in the intact condition. NOe began to rise immediately after exsanguination began, and therefore may be a useful early marker of acute hemorrhagic shock and hypovolemia. This information may be useful in the intensive care setting.

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