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stimulates alveolar liquid clearance during intestinal
ischemia-reperfusion in rats
1 Department of Surgery, Lund University Hospital, SE-221 85 Lund; and 2 Department of Animal Physiology, Lund University, SE-223 62 Lund, Sweden
Intestinal ischemia-reperfusion commonly occurs
in critically ill patients and may lead to the development of remote
organ injury, frequently involving the lungs. In the present study, alveolar liquid clearance was studied in ventilated, anesthetized rats
subjected to 45 min of intestinal ischemia followed by 3 h of
reperfusion. An isosmolar 5% albumin solution was instilled into the
lungs, and alveolar liquid clearance was measured from the increase in
alveolar protein concentration as water was reabsorbed over 45 min.
Intestinal ischemia-reperfusion resulted in a 76% increase in
alveolar liquid clearance compared with the control value (P < 0.05). The stimulated alveolar liquid clearance seen after
intestinal ischemia-reperfusion was not inhibited by
propranolol, indicating stimulation through a
noncatecholamine-dependent pathway. Intestinal
ischemia-reperfusion did not result in increased intracellular cAMP levels. Amiloride inhibited similar fractions in animals subjected
to ischemia-reperfusion and control animals. Administration of
a neutralizing polyclonal anti-tumor necrosis factor-
antibody before induction of intestinal ischemia completely inhibited
the increased alveolar liquid clearance observed after intestinal ischemia-reperfusion. In conclusion, our results suggest that intestinal ischemia-reperfusion in rats leads to stimulation of alveolar liquid clearance and that this stimulation is mediated, at
least in part, by a tumor necrosis factor--dependent mechanism.
tumor necrosis factor-; endothelium; epithelium; lung; lung
injury; pulmonary edema
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