HYPERTONIC SALINE TREATMENT OF ACID ASPIRATION-INDUCED LUNG INJURY

Citation
R. Rabinovici et al., HYPERTONIC SALINE TREATMENT OF ACID ASPIRATION-INDUCED LUNG INJURY, The Journal of surgical research, 60(1), 1996, pp. 176-180
Citations number
32
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
60
Issue
1
Year of publication
1996
Pages
176 - 180
Database
ISI
SICI code
0022-4804(1996)60:1<176:HSTOAA>2.0.ZU;2-M
Abstract
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.