Airway acid aspiration leads to severe microvascular lung injury and p
ulmonary edema. Recent studies have demonstrated that other conditions
associated with microvascular injury such as sepsis and burns can be
effectively treated with low-volume hypertonic saline (HTS). Thus, the
present study aimed to test whether HTS attenuates aspiration-induced
lung injury in the rat. Intratracheal administration of 0.2 mi of 0.1
N HCl (n = 7) induced pulmonary leukosequestration [myeloperoxidase (
MPO) activity +446 +/- 34%, P < 0.05; bronchoalveolar lavage (BAL) flu
id neutrophil count +1.78 +/- 23%, P < 0.05], edema (+43 +/- 6%, P < 0
.01), and microvascular permeability defect (BAL protein concentration
+675 +/- 34%, P < 0.01). These changes were associated with tissue hy
poxia (skeletal muscle PO2, 49 +/- 8 mm Hg, P < 0.05) and elevated ser
um TNF alpha (750 +/- 38 pg/ml, P < 0.01). HTS (2400 mosmole/liter) at
5 ml/kg, administered 20 min after aspiration (n = 7), reduced lung p
ulmonary edema by 58 +/- 7% (P < 0.05) and improved tissue oxygen tens
ion (PO2, 85 +/- 7 mm Hg, P < 0.05) but failed to alter lung MPO and B
AL fluid protein and leukocyte count response. Also, HTS did not reduc
e TNF alpha response to aspiration. These data point to a potential th
erapeutic role for low-volume HTS in treating aspiration-induced lung
injury. In addition, our data suggest that HTS is acting by rapidly sh
ifting fluid from the pulmonary interstitium to the intravascular comp
artment because it did not inhibit the inflammatory response to aspira
tion. (C) 1996 Academic Press, Inc.