Fat Embolism In Rabbits Research Articles

EFFECTS OF APROTININ ON PULMONARY FUNCTIONS IN EXPERIMENTAL FAT EMBOLISM: CHANGES IN ARTERIAL BLOOD GAS LEVELS AND SCINTIGRAPHIC FINDINGS

Purpose: To assess the effects of aprotinin on the formation and resolution of fat embolism of the lungs. Methods: The changes in arterial blood gas levels and perfusion scintigraphy were studied by forming experimental standardized fat embolism in rabbits with autogenous fat obtained from their femur medullas. Two groups, each consisting of 14 albino rabbits, were used in this study. Group 1, which received intravenous saline solution, was the control group. Group 2, which received aprotinin, was referred to as the aprotinin group. Autogenous femoral medullary content was used for embolization procedures. Arterial blood gas levels were recorded 72 hours before and 1, 24, 72 hours and 10 days following the embolization procedure. Pulmonary perfusion scintigraphies were performed 72 hours before the embolization procedure and on the first and 72nd hours, and the 10th day. Results: Fat embolism was achieved in all rabbits. Seven rabbits in the control group and one rabbit in the aprotinin group died within an hour after the embolization procedure. According to blood gas levels and perfusion scintigraphic findings, the aprotinin group significantly had less pulmonary fat embolism and recovered faster than the control group, especially during the first 24 hours. There was no significant difference in regression of pulmonary dysfunction between the two groups. Conclusion: The correlation between the blood gas levels and scintigraphic findings suggested that the administration of aprotinin for prophylactic purposes had favorable effects on the development of pulmonary gas exchange disturbance and perfusion defect in fat embolism.

Effects of Aprotinin on Pulmonary Functions in Experimental Fat Embolism Changes in Arterial Blood Gas Levels and Scintigraphic Findings

Purpose: To assess the effects of aprotinin on the formation and resolution of fat embolism of the lungs. Methods: The changes in arterial blood gas levels and perfusion scintigraphy were studied by forming experimental standardized fat embolism in rabbits with autogenous fat obtained from their femur medullas. Two groups, each consisting of 14 albino rabbits, were used in this study. Group 1, which received intravenous saline solution, was the control group. Group 2, which received aprotinin, was referred to as the aprotinin group. Autogenous femoral medullary content was used for embolization procedures. Arterial blood gas levels were recorded 72 hours before and 1, 24, 72 hours and 10 days following the embolization procedure. Pulmonary perfusion scintigraphies were performed 72 hours before the embolization procedure and on the first and 72nd hours, and the 10th day. Results: Fat embolism was achieved in all rabbits. Seven rabbits in the control group and one rabbit in the aprotinin group died within an hour after the embolization procedure. According to blood gas levels and perfusion scintigraphic findings, the aprotinin group significantly had less pulmonary fat embolism and recovered faster than the control group, especially during the first 24 hours. There was no significant difference in regression of pulmonary dysfunction between the two groups. Conclusion: The correlation between the blood gas levels and scintigraphic findings suggested that the administration of aprotinin for prophylactic purposes had favorable effects on the development of pulmonary gas exchange disturbance and perfusion defect in fat embolism.

Pulmonary Fat Embolism Induced Intravenous Injection of Autologous Bone Marrow in Rabbit: CT and Pathologic Correlation

Purpose : To evaluate the correlation between CT and pathologic findings of pulmonary fat embolism in rabbits. Materials and Methods : In 16 rabbits, pulmonary fat embolism was induced by intravenous injection of autol-ogous bone marrow(mean 3.3 mL). Chest CT scans were obtained immediately(within 1 hour), and 1, 3, and 7 days after embolization. The rabbits were divided into four groups. Group 1 underwent CT scanning immedi-ately after embolization, group 2 immediately and 1 day after embolization, group 3 immediately, 1 day and 3 days after embolization, group 4 immediately, 1 day, 3 days and 7 days after embolization. Pathologic speci-mens were obtained immediately after the last CT scan. Results : The earliest CT findings of pulmonary fat embolism in rabbits were peripheral lung lucency(16/16, 1 00 %), perivascular ground-glass (12/16, 75.0 %) and enlargement of the central pulmonary artery(11/16, 6 8 .8 %). Pathologically, perivascular ground-glass opacity correlated with extensive perivascular alveolar con-gestion and enlargement of the central pulmonary artery correlated with perivascular connective tissue edema and reactive pulmonary arterial engorgement. Peripheral lung lucency was probably caused by embolic occlu-sion of the pulmonary artery and decreased perfusion and air trapping induced by arterial and bronchial s-pasm associated with hypoxia. CT scans obtained 1 and 3 days after embolization showed nodules and patchy ground-glass opacity and consolidation. Aggregation of nodules resulted in patch opacities. Pathologically, pul-monary nodules correlated with focal inflammation surrounding an artery and parenchymal opacity correlat-ed with parenchymal consolidation and hemorrhagic edema. CT scans and pathologic specimens obtained 7 days after embolization showed improvement of parenchymal lung abnormalities. Conclusion : Pulmonary fat embolism in rabbits show CT and pathologic findings which vary with dynamic change. Typical earliest findings of pulmonary fat embolism were peripheral lung lucency, perivascular ground-glass opacity and enlargement of the central pulmonary artery.

BP59. Nifedipine and halothane as treatment for experimental acute pulmonary fat embolism in rabbits

BP59. Nifedipine and halothane as treatment for experimental acute pulmonary fat embolism in rabbits

Pulmonary fat embolism in rabbits induced by forced immobilization.

In the study reported here, rabbits were used to develop an experimental model for inducing pulmonary fat embolism by forced immobilization. The emboli were quantitated by a computerized system. The activity of lipoprotein lipase in post-heparin plasma (PHP-LPL) and concentrations of free fatty acids (FFA) were measured. Also, blood gases were analyzed and pulmonary morphology and ultrastructure were observed. Forced immobilization for 5 hours was found to induce pulmonary embolism. This was accompanied by elevation of PHP-LPL and FFA levels in the blood, hypocapnia, and a tendency for insufficiency of pulmonary surfactant. The results suggest that the disorder of homeostasis caused by immobilization is strong enough to bring about pulmonary embolism without bone fracture.

The Role of Hypovolemic Stress in the Production of Fat Embolism in Rabbits*: 2. Changes in Arterial Blood Gas Levels and Static Compliance

The purpose of this study was to assess the possible role of hypovolemia as a factor in the production of impaired pulmonary function in pulmonary fat embolizaiton. Iv vivo static lung compliance was measured by inflating the lungs with known volumes of air and recording the transpulmonary pressure, monitoring intraesophageal pressure as an index of intrapleural pressure. Arterial blood was drawn from the central artery of the ear. Embolization was produced by the intravenous injection of homologous fat cells either as the sole experimental procedure or in conjunction with hypovolemic shock. Two types of shock were studied. In one, 20 percent of the blood volume was removed, producing hypovolemia associated with hemodilution, and in the other a tourniquet was applied to induce hypovolemia and hemoconcentration. The results indicate that embolization is associated with significantly greater impairment of pulmonary function if it develops on a background of shock than if it occurs in an otherwise healthy animal. These pathophysiologic findings parallel the results of a morphologic study.

The Role of Hypovolemic Stress in the Production of Fat Embolism in Rabbits: 1. Morphologic Alterations of the Lungs

In rabbits, an experimental model of fat embolism was produced that simulates the course of events in the clinical situation. Small doses of fat-cell suspension (0.075 ml/kg of body weight), prepared by collagenase treatment of homologous adipose tissue, were injected intravenously. Concomitantly, hypovolemia was produced in two animal groups by either withdrawing 20 percent of the estimated blood volume or by application of a hind-limb ischemic tourniquet for 90 minutes. The presence of pathoanatomic characteristics typical of fat embolism was evaluated by recording lung/body weights, macroscopic appearance, and semiquantitative microscopic estimation in the lungs of edema, hemorrhage, atelectasis, intravascular coagulation, and leukocytic thrombi. Mean indices of lung/body weight were higher in all animals receiving injections of fat-cell suspension, as compared to controls. The score for microscopic generalized pulmonary damage was significantly higher in rabbits exposed to both fat-cell injections and hypovolemia than in controls or after fat-cell injections alone. It is concluded that hypovolemia enhances the development of fat embolism in rabbits subjected to small doses of fat-cell suspension.

Pulmonary pathophysiological and clotting factor alterations in experimental fat embolism in rabbits

Cotev, S.; Hershko, H.; Rosenmann, E.; Shafrir, E.; Ben-Natan, F.; Davidson, J. T. Author Information

Induced Fat Embolism in Rabbits: Effects of Defibrinogenation and Thrombocytopenia

Fat embolism was induced in rabbits by giving an intravenous injection of radioactively labelled homologous retroperitoneal fat. One group was defibrinogenated by Arvin. A second group was made thrombocytopenic by treatment with Busulphan. After the animals had been made thrombocytopenic and had been defibrinogenated, respectively, fat embolism was induced. Macroscopic and histologic examinations were carried out, as well as recordings of wet weight and radioactivity content of the lung. There was a highly significant increase in the pulmonary wet weight of thrombocytopenic animals compared with controls. Macroscopic as well as histologic examination revealed a massive interstitial and alveolar oedema. Half of the specimens showed moderate to massive bleedings. Defibrinogenated animals did not differ from controls. Under the given circumstances, the results suggest that platelets are protective to the endothelial lining of the pulmonary capillaries during embolism. The presence or absence of fibrinogen initially does not seem to be of major importance for the pulmonary damage induced by fat injection.

Fat embolism and intravascular coagulation.

The association between intravascular clotting and fat embolism in rabbits, following the intravenous injection of two doses of lipopolysaccharide, and in mice following the intravenous injection of trypsin is reported. Intravascular fibrin in the absence of fat emboli was seen after injection of Liquoid. It is suggested that the two findings may have a common aetiology, and that their association may be more frequent than appears from the literature.

The production of fat embolism in rabbits by feeding high fat meals

Plastic and Reconstructive Surgery and the Transplantation Bulletin: April 1960 - Volume 25 - Issue 4 - p 389

Fat embolism

On the basis of the presence of fat in the urine, we found fat embolism in half of 109 persons moderately or severaly injured. The incidence after moderate injuries did not differ significantly from that after severe injuries. It was most common after fractures and burns but occurred in about one-fourth of other soft tissue injuries. The demonstration of free fat in the sputum was found to be an unreliable test for fat embolism. Neither a change in the emulsion of the circulating fat nor fat embolism occurred after a simulated “alarm reaction” in rabbits. Tween 80 did not have a significant effect in the treatment of fat embolism in rabbits.