Effect of defibrinogenation on lung water accumulation after pulmonary microembolism in dogs.

We determined the effects of chronic fibrinogen depletion on the development of pulmonary edema after pulmonary microembolization. Dogs were defibrinogenated with a purified fraction of Malayan pitviper venom (ancrod). Studies were made in four groups: control untreated (group I); emboli untreated (group II); control defibrinogenated (group III); and emboli defibrinogenated (group IV). Fibrinogen decreased (P < 0.05) from 570.6 +/- 100.9 to 5.3 +/- 3.1 mg/100 ml in the ancrod-treated groups. Pulmonary arterial pressure was increased to similar levels in both embolized groups after infusion of 100-mug-diam nonsiliconized glass beads into the right atrium. Pulmonary vascular resistance and pulmonary perfusion pressure were initially increased to similar levels in both embolized groups, but by 75 min postembolization (PE) both parameters were higher (P < 0.05) in the defibrinogenated group. The extravascular lung water-to-bloodless dry lung ratio at 75 min PE of 4.53 +/- 0.24 in group II was greater than the control value of 2.84 +/- 0.22 in group I (P < 0.05). In contrast, the extravascular lung water-to-bloodless dry lung ratio of 3.64 +/- 0.09 in group IV was not different from the control value of 3.38 +/- 0.04 in group III, but was less than 4.53 +/- 0.24 in group II (P < 0.05). Therefore, chronic defibrinogenation in dogs prevented the development of pulmonary edema after pulmonary microembolization. The protective effect may be due to inhibition of the increase in lung vascular permeability and to a time-dependent reduction in pulmonary microvascular pressure.