Histopathological and biochemical changes following fat embolism with administration of corn oil micelles A NEW ANIMAL MODEL FOR FAT EMBOLISM SYNDROME
ABSTRACT Several experimental models have been used to produce intravascular fat embolism. We have developed a simple technique to induce fat embolism using corn oil emulsified with distilled water to form fatty micelles. Fat embolism was produced by intravenous administration of these fatty micelles in anaesthetised rats, causing alveolar oedema, haemorrhage and increased lung weight. Histopathological examination revealed fatty droplets and fibrin thrombi in the lung, kidney and brain. The arteriolar lumen was filled with fatty deposits. Following fat embolism, hypoxia and hypercapnia occurred. The plasma phospholipase A(2), nitrate/nitrite, methylguidanidine and proinflammatory cytokines were significantly increased. Mass spectrometry showed that the main ingredient of corn oil was oleic acid. This simple technique may be applied as a new animal model for the investigation of the mechanisms involved in the fat embolism syndrome.
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- "The vehicle group received DMSO 100 μg/g lung weight. In the FE group, corn oil 0.6 ml with distilled water 0.2 ml was added into the lung perfusate [5,6]. The FE+PMA group received corn oil micelles with PMA (4 μg/g lung weight) [27,28]. "
ABSTRACT: Fat embolism syndrome (FES) associated with acute lung injury (ALI) is a clinical condition following long bone fracture. We have reported 14 victims due to ALI with FES. Our laboratory has developed an animal model that produced fat emboli (FE). The major purpose of this study was to test whether neutrophil activation with phorbol myristate acetate (PMA) and inhibition with sivelestat (SVT) exert protection on the lung. The lungs of Sprague-Dawley rats were isolated and perfused. FE was produced by addition of corn oil micelles into the lung perfusate. PMA and SVT were given simultaneously with FE. Parameters such as lung weight/body weight ratio, LW gain, exhaled nitric oxide (NO), protein concentration in bronchoalveolar lavage relating to ALI were measured. The neutrophil elastase (NE), myeloperoxidase, malondialdehyde and phopholipase A₂ activity were determined. We also measured the nitrate/nitrite, methyl guanidine (MG), and cytokines. Pulmonary arterial pressure and microvascular permeability were assessed. Lung pathology was examined and scored. The inducible and endothelial NO synthase (iNOS and eNOS) were detected. FE caused ALI and increased biochemical factors. The challenge also resulted in pulmonary hypertension and increased microvascular permeability. The NE appeared to be the first to reach its peak at 1 hr, followed by other factors. Coadministration with PMA exacerbated the FE-induced changes, while SVT attenuated the effects of FE. The FE-induced lung changes were enhanced by PMA, while SVT had the opposite effect. Sivelestat, a neutrophil inhibitor may be a therapeutic choice for patients with acute respiratory distress syndrome (ARDS) following fat embolism.Journal of Biomedical Science 01/2012; 19(1):3. DOI:10.1186/1423-0127-19-3 · 2.76 Impact Factor
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- "An animal model using Sprague Dawley rats was used for this study. Many studies have utilized rats as a model for fat embolism [13-17]. Most of them used external infusion of fatty acids to simulate fat embolism. "
ABSTRACT: Fat Embolism is a complication of long bone fractures, intramedullary fixation and joint arthroplasty. It may progress to fat embolism syndrome, which is rare but involves significant morbidity and can occasionally be fatal. Fat Embolism can be detected at the time of embolization by transoesophageal echocardiography or atrial blood sampling. Later, a combination of clinical signs and symptoms will point towards fat embolism but there is no specific test to confirm the diagnosis. We investigated serum Interleukin-6 (IL-6) as a possible early marker for fat embolism. An animal study was conducted to simulate a hip replacement in 31 adult male Sprague Dawley rats. The procedure was performed under general anesthesia and the animals divided into 3 groups: control, uncemented and cemented. Following surgery and recovery from anaesthesia, the rats allowed to freely mobilize in their cages. Blood was taken before surgery and at 6 hours, 12 hours and 24 hours to measure serum IL-6 levels. The rats were euthanized at 24 hours and lungs removed and stained for fat. The amount of fat seen was then correlated with serum IL-6 levels. No rats in the control group had fat emboli. Numerous fat emboli were seen in both the uncemented and cemented implant groups. The interleukin levels were raised in all groups reaching a peak at 12 hours after surgery reaching 100 pg/ml in the control group and around 250 pg/ml in the uncemented and cemented implant groups. The IL-6 levels in the control group were significantly lower than any of the implant groups at 12 and 24 hours. At these time points, the serum IL-6 correlated with the amount of fat seen on lung histology. Serum IL-6 is a possible early marker of fat embolism.Journal of Orthopaedic Surgery and Research 07/2009; 4(1):18. DOI:10.1186/1749-799X-4-18 · 1.39 Impact Factor
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ABSTRACT: Future high-luminosity experiments make serious demands on detector technologies and have prompted a “chain” of inventions of new high-rate gaseous detectors: Microstrip Gas Counters (MSGC's), Microgap Chambers (MGC's), Compteur A Trou (CAT's), Micromesh Gas Structure (MICROMEGAS), and Gas Electron Multipliers (GEM's). We report results from a systematic study of breakdown mechanisms in these and other gaseous detectors recently chosen or considered as candidates for high-luminosity experiments. It was found that, for all the detectors tested, the maximum achievable gain before breakdown appeared, dropped dramatically with rate, sometimes inversely proportional to it. Further, in the presence of alpha particles, typical of the backgrounds in high-energy experiments, additional gain drops of 1-2 orders of magnitude were observed for some detectors. We discovered that the breakdown in these detectors was through a previously unknown mechanism for which we give a qualitative explanation. We also present possible ways of increasing the value of the maximum achievable detector gain at high rates and have verified these experimentallyIEEE Transactions on Nuclear Science 07/1999; 46(3-46):321 - 325. DOI:10.1109/23.775537 · 1.28 Impact Factor