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  • Title: Pulmonary microvascular permeability following E. coli endotoxin and hemorrhage.
    Author: Kinnebrew PS, Parker JC, Falgout HJ, Taylor AE.
    Journal: J Appl Physiol Respir Environ Exerc Physiol; 1982 Feb; 52(2):403-9. PubMed ID: 7037715.
    Abstract:
    The effects of hemorrhage and Escherichia coli endotoxin on vascular permeability in the lung were investigated in open-chest dogs. Systemic arterial, pulmonary artery, and left arterial pressures were monitored, and a 30-ml balloon catheter placed in the left atrium. An afferent to the left hilar lymph node was cannulated and lymph flow monitored. Lymph and plasma protein concentrations were measured by refractometry. The animals were divided into three groups: 1) a control group in which left atrial pressure was increased by inflation of the left atrial balloon; 2) a hemorrhagic shock group, bled to a systemic arterial pressure of 35-40 Torr until uptake of 20% of shed blood from the reservoir; and 3) an endotoxin shock group in which 2 or 4 mg/kg E. coli endotoxin was infused and left atrial pressure increased to 18 cmH2O for 2 hr. Permeability was determined by comparing the lymph/plasma protein ratios as a function of pulmonary lymph flow for the three groups at base line and increased left atrial pressures. There were no significant differences in lymph protein "wash down" between hemorrhage and control, and there was a minimal but significant difference between endotoxin and control groups. Postmortem extravascular lung water was not increased in the hemorrhage and endotoxin groups when compared to control. Therefore, there were no acute changes in lung vascular permeability within 2 hr after severe hemorrhage, but a minimal increase in permeability following endotoxin.
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