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Soichiro Inoue, MD; Akimasa Nakao, MD; Wakahiko Kishimoto, MD; Hiroya Murakami, MD; Koichi Itoh, MD; Takafumi Itoh, MD; Akio Harada, MD; Toshiaki Nonami, MD; Hiroshi Takagi, MD

Arch Surg. 1995;130(1):93-98.

Abstract
Objective
To examine the role of activated neutrophils in microvascular injury after severe acute pancreatitis. We used the polyclonal anti–rat neutrophil antibody (PoAb) to deplete peripheral neutrophil counts and the anti–rat monoclonal antibody (MoAb) CD18 to block neutrophil adherence functions.

Design
Prospective, controlled trial.

Setting
Laboratory.

Participants
Anesthetized male Wistar breeder rats, in which necrotizing pancreatitis was induced by injecting necrotizing agents into the pancreatic duct.

Interventions
Treatment groups received an infusion of PoAb, 8 mL/kg, before induction of pancreatitis or MoAb CD18, 2 mg/kg, after induction of pancreatitis. Control animals received 2 mL of rabbit serum or 1 mL of saline solution.

Main Outcome Measures
Survival rate, white blood cell count, levels of serum amylase and lipase, myeloperoxidase activity in the lung, lipid peroxide levels in the pancreas, and results of histological studies.

Results
The survival rate of rats treated either with PoAb before or MoAb CD18 after induction of sepsis improved significantly (P<.01). Histologically and according to the levels of neutrophil myeloperoxidase in their lungs, rats treated with the antibodies 24 hours after inducing pancreatitis improved significantly (P<.05). Moreover, the serum lipase concentrations and lipid peroxide levels in the pancreas of these rats decreased significantly (P<.05).

Conclusions
Both the depletion of peripheral neutrophils by PoAb and blocking of neutrophil adherence functions by MoAb CD18 may help to prevent acute lung injury caused by severe acute pancreatitis in this model.

(Arch Surg. 1995;130:93-98)

Author Affiliations
From the Department of Surgery II, Nagoya University School of Medicine, Nagoya, Japan.

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