SESSION TITLE: ARDS/Lung Injury
SESSION TYPE: Original Investigation Slide
PRESENTED ON: Monday, October 27, 2014 at 04:30 PM - 05:30 PM
PURPOSE: Fat embolism (FE) after long bone trauma, cosmetic procedure (liposuction) or related orthopedic surgery will lead to respiratory insufficiency but only few studies have been performed on long term effects of FE in experimental models or on humans with documented FE. Our study ascertained the persistence of lung damage after FE using the response of pulmonary vessel components (media, adventitia) to FE, as well as the extent of pulmonary fibrosis at 10 weeks. Based on preliminary work, we hypothesize that FE involves input of the renin-angiotensin system in our chronic model. The current experiment tests this hypothesis in vivo by adding losartan to half the FE group and saline controls.
METHODS: 28 SD male rats, 2 groups of 14, were administered triolein (FE model) or saline I.V. at 0 time. At 6 weeks, losartan was given to half of each group as i.p. loading dose then in drinking water to week 10. At necropsy (10 weeks), tissue was frozen or fixed in formalin. Histology was studied from H&E and trichrome stained slides, 4-5 photos at 400X of each lung section were taken. Lumen - media ratio and media-adventitia ratios were calculated and compared using Statistica parametric comparison. The image J program was used to measure trichrome stain for quantification of pulmonary fibrosis.
RESULTS: The study showed significantly (p=0.006) increased lumen patency in both groups treated with losartan after saline (77.6 ± 2.6) or triolein (76.3 ± 2.5) compared to saline and triolein groups not receiving losartan (72.2 ± 5.6) and (67.9 ± 5.7). Image-J analysis showed significantly (p=0.018) increased fibrosis % in the triolein group (15.3 ± 3.5) % when compared to control (5.9 ± 0.05) %. It also showed a trend (p=0.08) to decreased fibrosis % in (triolein+ losartan) group (12.5 ± 2.1) % when compared to (triolein+ saline) group (15.3 ± 3.5) %. Vessel adventitia ratios, depressed by triolein, did not respond to losartan.
CONCLUSIONS: In the fat embolism model, persistent pathology included reduced lung patency and fibrosis at 10 weeks. Lung pathology was generally reduced or blocked by the angiotensin II receptor blocker, losartan.
CLINICAL IMPLICATIONS: The results support the possibility of using angiotensin blockade in clinical situations where FE is suspected. Data also suggest that use of angiotensin blockade after incidence of FE should be further investigated.
DISCLOSURE: The following authors have nothing to disclose: Shehabaldin Alqalyoobi, Darwish Naji, Devin Bass, Betty Herndon, Agostino Molteni, Gary Salzman
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