Endotoxin-induced increased alveolar capillary membrane permeability.
In an attempt to define the effects of endotoxin on the permeability of the pulmonary alveolar capillary membrane (ACM) to a variety of substances [molecular weight (MW) varying from 60 to 69,000], we studied the movement of specific molecular species from the pulmonary capillary blood to the saline-filled "alveolus," employing an in vivo dog lung model. Following endotoxin injection (2-2.5 mg/kg) baseline T1/2 values (time, in minutes, for 50% equilibration of the specific solute between the blood and the saline-filled lung) decreased as follows (compared to baseline values): urea (MW 60) - 42.5 +/- 24 to 21.3 +/- 18; sucrose (MW 360) - 201 +/- 72 to 76 +/- 53; 3,000 MW dextran - 1,275 +/- 746 to 686 +/- 433; 10,400 MW dextran - 1,871 +/- 845 to 1,052 +/- 630 (all p less than 0.05). Neither 20,000 MW dextran nor albumin (MW 69,000) showed an increased permeability following endotoxin injection. Histamine analysis revealed a significant increase in all lung liquid samples post-endotoxin injection without a significant increase in blood histamine values. We conclude that, acutely (within 4 hr of injection), endotoxin causes an increase in permeability of the ACM for substances up to 10,400 MW. The role of histamine in this increased permeability remains controversial.
D000818:Animals; D002199:Capillary Permeability; D003911:Dextrans / Q000378:metabolism; D004285:Dogs; D004927:Escherichia coli Infections / Q000378:metabolism; D006439:Hemodynamics; D006632:Histamine / Q000378:metabolism; D008168:Lung / Q000032:analysis; D008970:Molecular Weight; D011650:Pulmonary Alveoli / Q000098:blood supply*; D012772:Shock, Septic / Q000378:metabolism* / Q000503:physiopathology; D013395:Sucrose / Q000378:metabolism; D014508:Urea / Q000378:metabolism
D003911:Dextrans; D013395:Sucrose; D006632:Histamine; D014508:Urea