• Burns · Dec 2001

    Comparative Study

    Role of nitric oxide in myocardial dysfunction after combined burn and smoke inhalation injury.

    • K Soejima, F C Schmalstieg, L D Traber, C Szabo, A Salzman, and D L Traber.
    • Department of Plastic and Reconstructive Surgery, Tokyo Women's Medical University, 8-1 Kawada-cho, Shinjuku-ku, 162-8666, Tokyo, Japan. kasoejim@prs.twmu.ac.jp
    • Burns. 2001 Dec 1;27(8):809-15.

    AbstractThis study tested the hypothesis that nitric oxide (NO) synthesized from inducible NO synthase (iNOS) is responsible for the cardiac dysfunction observed after burn and smoke inhalation injury. Twelve sheep received 40% third-degree burn and smoke inhalation under halothane anesthesia. The animals were divided into two groups: a MEG group [iNOS was inhibited with mercaptoethylguanidine (MEG), a selective inhibitor of iNOS, n=6] and a control group (n=6). The control group showed a significant increase in NO(2)(-)/NO(3)(-) (NO(x)) concentration, metabolite of NO, in plasma after 24 h, whereas the MEG group did not. In the control group, cardiac depression was observed immediately after injury associated with hemoconcentration. Cardiac function returned to a normal level within 6 h following injury. In the control group cardiac dysfunction was observed again after 24 h although the hemoconcentration peaked at 24 h after injury and then began to resolve. In the MEG group, cardiac depression and hemoconcentration were not observed. The present data suggest that cardiac depression seen with this combination injury consists of two phases and that the later phase is mediated by iNOS-NO.

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