The Changes Of Proinflammatory Cytokines In The Circulation Following Acute Pulmonary Thromboembolism In Dogs

Histological examination of acute lung injury associated with sepsis often revealed thromboembolic lesions in the pulmonary microcirculation. Several inflammatory mediators such as platelet activating factor,thromboxane,and endothelins have also been implicated in the pathogenesis of acute pulmonary thromboembolism(APTE). Objective In the present study we examined the roles of three proinflammatory cytokines, tumor necrosis factor- a (TNF- a ), interleukin 1 (IL-1 ), and IL-8 in the early phase of APTE, and analysis the impaction of these cytokines on the systemic circulation. Methods APTE was induced in 7 anesthetized dogs by injecting the thrombus of oneself body into right jugular vein. Seven animals that received only warm sterile saline served as controls. Arterial serum samples were collected regularly(0h,0.5h,1h,2h,4h,6h) so that cytokine levelscould be measured later by radio-immunity assay. Results Administration of clots caused significant increase in the mean pulmonary arterial pressure (from 17 1.9 to 28.8 8.4 mmHg, P< 0.05, 0.5h) and decrease in PaO2 (from 99.1 5.7 to 66.8 15.3 mmHg, P<0.05, 0.5h) ,and these changes remained throughout the experiments. Mean arterial blood pressure remained comparable after initial fluid resuscitation. Cardiac output was increased lasting 2 hours. Plasma levels of TNF- a IL-1 , and IL-8 were not significantly increased in the APTE group when compared with their baseline values or the control group. Conclusion APTE is associated with pulmonary hypertension and deterioration of gas exchange but not with the systemic release of TNF- a , IL-1 or IL-8. These cytokines have minimal impact on the systemic circulation during APTE.