TY - JOUR
T1 - Role of nitric oxide in lung injury associated with experimental acute pancreatitis
AU - O'Donovan, D. A.
AU - Kelly, C. J.
AU - Abdih, H.
AU - Bouchier‐Hayes, D.
AU - Watson, R. W.G.
AU - Redmond, H. P.
AU - Burke, P. E.
AU - Bouchier‐Hayes, D. A.
PY - 1995/8
Y1 - 1995/8
N2 - This study evaluated the effect of varying the synthesis of nitric oxide with sodium nitroprusside or N‐nitro‐L‐arginine methyl ester (L‐NAME) in a pancreatitis‐lung injury model. Rats (n = 45) were randomized to control or caerulein‐induced pancreatitis groups, treated with saline, sodium nitroprusside (0·4 μg/kg) or L‐NAME (10 mg/kg). Myeloperoxidase activity was used as a measure of neutrophil infiltration. Wet to dry (W:D) lung weight and bronchoalveolar lavage (BAL) protein concentrations were used to assess vascular leakage. Pancreatitis was shown to induce pulmonary neutrophil influx: mean(s.e.m.) myeloperoxidase activity 6·79(0·5) units/g in caerulein‐treated animals versus 2·08(0·5) units/g in controls (P < 0·001). Animals with pancreatitis showed increased microvascular leakage compared with controls (mean(s.e.m.) W:D lung weight 7·01(0·5) versus 2·85(0·2), P < 0·001; BAL protein concentration 2539(222) versus 347(32) μg/ml, P < 0·001). Compared with the saline‐treated pancreatitis group, these changes were reduced by sodium nitroprusside (mean(s.e.m.) myeloperoxidase activity to 2·5(0·4) units/g, P < 0·001; W:D lung weight to 3·8(0·37), P < 0·001; BAL protein concentration 1389(182) μg/ml, P < 0·05). L‐NAME exacerbated the pancreatitis‐induced pulmonary oedema (W:D lung weight increased to 11·96(0·6), P < 0·001), protein leakage (BAL protein concentration rose to 3707(309) μg/ml, P < 0·05) and neutrophil infiltration (myeloperoxidase activity increased to 9·01(0·3) units/g, P < 0·05). These data suggest that, in vivo, nitric oxide inhibits pancreatitis‐induced lung injury, possibly in part by inhibiting pulmonary neutrophil influx.
AB - This study evaluated the effect of varying the synthesis of nitric oxide with sodium nitroprusside or N‐nitro‐L‐arginine methyl ester (L‐NAME) in a pancreatitis‐lung injury model. Rats (n = 45) were randomized to control or caerulein‐induced pancreatitis groups, treated with saline, sodium nitroprusside (0·4 μg/kg) or L‐NAME (10 mg/kg). Myeloperoxidase activity was used as a measure of neutrophil infiltration. Wet to dry (W:D) lung weight and bronchoalveolar lavage (BAL) protein concentrations were used to assess vascular leakage. Pancreatitis was shown to induce pulmonary neutrophil influx: mean(s.e.m.) myeloperoxidase activity 6·79(0·5) units/g in caerulein‐treated animals versus 2·08(0·5) units/g in controls (P < 0·001). Animals with pancreatitis showed increased microvascular leakage compared with controls (mean(s.e.m.) W:D lung weight 7·01(0·5) versus 2·85(0·2), P < 0·001; BAL protein concentration 2539(222) versus 347(32) μg/ml, P < 0·001). Compared with the saline‐treated pancreatitis group, these changes were reduced by sodium nitroprusside (mean(s.e.m.) myeloperoxidase activity to 2·5(0·4) units/g, P < 0·001; W:D lung weight to 3·8(0·37), P < 0·001; BAL protein concentration 1389(182) μg/ml, P < 0·05). L‐NAME exacerbated the pancreatitis‐induced pulmonary oedema (W:D lung weight increased to 11·96(0·6), P < 0·001), protein leakage (BAL protein concentration rose to 3707(309) μg/ml, P < 0·05) and neutrophil infiltration (myeloperoxidase activity increased to 9·01(0·3) units/g, P < 0·05). These data suggest that, in vivo, nitric oxide inhibits pancreatitis‐induced lung injury, possibly in part by inhibiting pulmonary neutrophil influx.
UR - https://www.scopus.com/pages/publications/0029096162
U2 - 10.1002/bjs.1800820838
DO - 10.1002/bjs.1800820838
M3 - Article
C2 - 7648171
AN - SCOPUS:0029096162
SN - 0007-1323
VL - 82
SP - 1122
EP - 1126
JO - British Journal of Surgery
JF - British Journal of Surgery
IS - 8
ER -