A 30-Minute Supraceliac Aortic Clamping in the Rat Causes Death Due to an Inflammatory Response and Pulmonary Lesions.

BACKGROUND: The treatment of thoracoabdominal aortic aneurysms through an open approach has general and pulmonary consequences of multiple etiologies. Our assumption was that the supraceliac aortic clamping needed for this operation causes a systemic inflammatory response associated with a pulmonary attack. METHODS: We developed a model of 30-min supraceliac aortic clamping in Wistar rats weighing 300 g. After 90 min of reperfusion, the rats were sacrificed. The effects on the digestive tract wall were analyzed by measurement of the mucosal thickness/total thickness ratio. The effects on the mesenteric endothelial function were determined by an ex situ measurement of the arterial pressure/volume curves (third branch). The systemic consequences of the procedure were analyzed by dosing tumor necrosis factor alpha (TNFα), interleukin (IL)1ß, and IL10 in the blood. The pulmonary consequences were analyzed by the measurement of macrophages, polymorphonuclear neutrophils (PNs), T lymphocyte infiltration, pulmonary apoptosis (TUNEL) and active caspase 3. The experimental scheme included 20 rats with ischemia-reperfusion (IR) and 20 control rats. An analysis of survival was carried out on 20 other rats (10 IR and 10 controls). RESULTS: The results were expressed as average ± standard error of the mean. The statistical tests were Student's t-test and Mann-Whitney test. This visceral IR model decreased the ratio of the thickness of the intestinal mucosa compared with that of the control rats (0.77 ± 0.008 vs. 0.82 ± 0.009 [P < 0.001]). This local effect was not accompanied by any mesenteric endothelial dysfunction (P = 0.91). On a systemic level, IR increased TNFα (37.9 ± 1.5 vs. 28.2 ± 0.6 pg/mL; P < 0.0001), IL1ß (67.1 ± 9.8 vs. 22.5 ± 5.6 pg/mL; P < 0.001), and IL10 (753.3 ± 96 vs. 3.7 ± 1.7 pg/mL; P < 0.0001). As regards the lungs, IR increased the parenchymal cellular infiltration by macrophages (6.8 ± 0.8 vs. 4.5 ± 0.4 cells per field; P < 0.05) and PNs (7.4 ± 0.5 vs. 6.2 ± 03 cells per field; P < 0.05). There was no increase in the pulmonary cellular apoptosis measured by TUNEL (P = 0.77) or in the caspase 3 activity (P = 0.59). The mortality of the visceral IR rats was 100% at 36 hr vs. 0% in the animals without IR. CONCLUSIONS: This work showed that the inflammatory response to visceral IR had systemic and pulmonary effects which always results in the death in the rat.

Focal non granulomatous orchitis in a patient with Crohn's disease.

Crohn's disease is a systemic disease and sometimes involves the testicle, usually leading to granulomatous lesions. We report herein a case of focal non-granulomatous orchitis in a 21-year-old patient with active Crohn's disease treated by an anti-tumor necrosis factor monoclonal antibody. This circumscribed testicular lesion mimicked a tumor, leading to orchiectomy. Pre-operative blood tests (i.e. alpha-fetoprotein, lactate dehydrogenase and human chorionic gonadotrophin) were strictly normal Pathological examination of the testicle revealed a focal inflammatory infiltrate predominantly composed of lymphocytes accompanied by few plasma cells, lacking giant cells or granulomas. Importantly, intratubular germ cell neoplasia, atrophy or lithiasis were not observed.After discussing and excluding other plausible causes (burnt-out /regressed germ cell tumor, infection, vascular or traumatic lesions, iatrogenic effects), we concluded that this particular case of orchitis was most likely an extra-digestive manifestation of inflammatory bowel disease. To our knowledge, this is the first described case of focal non-granulomatous orchitis associated with Crohn's disease. Virtual Slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/2117747284160112.