Objective: To observe the effects of exogenous normal lymph on myeloperoxidase (MPO) and adenosine triphosphatase (ATPase) activities of lung homogenate in rats with endotoxic shock caused by lipopolysaccharide (LPS), and to preliminarily discuss its mechanisms.
Methods: Forty male Wistar rats were randomly divided into four groups: endotoxin group, lymph group, plasma group and control group. The rats in the preceding three groups were injected intravenously with LPS (5 mg/kg. bw, iv) to replicate endotoxic shock model. LPS was replaced by equal volume of normal saline in the control group. Fifteen minutes later, lymph without cell components was infused in lymph group. The amount of lymph was 1/15 of blood volume. In plasma group, lymph was replaced by plasma, and in normal and endotoxin groups, lymph were replaced by normal saline. Four hours after the infusion of LPS, lung homogenate in a concentration of 10% was prepared. The activities of MPO and ATPase were determined in lung homogenate.
Results: Compared with control group, the activities of MPO in lung homogenate of endotoxin group and plasma group were significantly increased while the activities of ATPase were significantly lower (P<0.05 or P<0.01). The activity of MPO in lung homogenate of lymph group was significantly higher, while Na(+)-K(+)-ATPase activity was significantly lower than those of control group (both P<0.05). The activities of Ca(2+)-ATPase, Mg(2+)-ATPase and Ca(2+)-Mg(2+)-ATPase in lymph group showed no statistically significant differences compared with those of control group (all P>0.05), but when compared with the endotoxin group and plasma group, the activity of MPO in lung homogenate was significantly lower (both P<0.01) and the activities of 4 kinds of ATPase were significantly higher (P<0.05 or P<0.01).
Conclusion: The results demonstrate that exogenous normal lymph could ameliorate the lung injury as a result of endotoxic shock, and its mechanism might relate to reduction of activity of the polymorphonuclear leucocyte (PMN) and enhancement of the activity of ATPase.