Use of indium-111-labeled transferrin to study plasma extravasation during endotoxin shock and the effects of the beta-2 agonist terbutaline.

Endotoxemia and sepsis are common causes of respiratory distress (ARDS), which is characterized by increased pulmonary vascular permeability to plasma proteins resulting in "noncardiac pulmonary edema." The aim of this series was to study the effects of the beta-2 receptor agonist, terbutaline, on plasma extravasation in multiple organs, in sheep exposed to endotoxin shock. A double isotope technique was used and the radioactivity was recorded in different organs (lungs, liver, spleen, kidneys, intestine) by a computerized gamma camera. Tc-99m-labeled erythrocytes were used as a marker for intravascular volume and In-111m-labeled transferrin for tracing extravascular plasma leakage. An organ-transferrin index (organ-TI) was calculated for each organ which corrects for changes in blood distribution. Fourteen sheep were anesthetized and ventilated. After stabilization (t = 0) all animals received E. coli endotoxin 10 micrograms/kg by IV infusion during 30 min. At t = 30, seven animals (group T) received IV infusion of terbutaline, 20 micrograms/kg/hr, during 4 h, while the other seven received normal saline and served as controls (group E). The endotoxin infusion caused an immediate and significant increase in the transferrin index in the lungs and in the liver in both groups. The transferrin index continued to rise in the control group towards the end of the experiment (t = 240), while in group T it reached a maximum 60 min after endotoxin. Four hours after endotoxin the transferrin index was significantly higher in the controls than in the terbutaline treated group, both in the lungs and in the liver (P less than 0.01). No significant changes were recorded in the kidneys or over the intestine.(ABSTRACT TRUNCATED AT 250 WORDS)