Subchronic endotoxin inhalation causes persistent airway disease.

The endotoxin component of organic dusts causes acute reversible airflow obstruction and airway inflammation. To test the hypothesis that endotoxin alone causes airway remodeling, we have compared the response of two inbred mouse strains to subchronic endotoxin exposure. Physiological and biological parameters were evaluated after 1 day, 5 days, or 8 wk of exposure to endotoxin [lipopolysaccharide (LPS)] in endotoxin-sensitive (C3HeB/FeJ) and endotoxin-resistant (C3H/HeJ) mice. After 5 days or 8 wk of LPS exposure, only C3HeB/FeJ had elevated airway hyperreactivity to inhaled methacholine. Only the C3HeB/FeJ mice had significant inflammation of the lower respiratory tract after 1 day, 5 days, or 8 wk of LPS exposure. Stereological measurements of small, medium, and large airways indicated that an 8-wk exposure to LPS resulted in expansion of the submucosal area only in the C3HeB/FeJ mice. Cell proliferation as measured by bromodeoxyuridine incorporation contributed to the expansion of the submucosa and was only significantly elevated in C3HeB/FeJ mice actively exposed to LPS. C3HeB/FeJ mice had significantly elevated levels of interleukin-1beta protein in whole lung lavage after 1 day and 5 days of LPS exposure and significantly elevated protein levels of total and active transforming growth factor-beta1 in whole lung lavage fluid after 5 days of LPS exposure. Our findings demonstrate that subchronic inhalation of LPS results in the development of persistent airway disease in endotoxin-responsive mice.

Bilateral persistent complete sciatic artery.

A case with persistent sciatic artery (PSA) was found in a cadaver of a 65-year-old female during a medical gross anatomy course. The artery was bilateral and complete and provided the major blood supply to both lower extremities. The vessel arose from the internal iliac artery that was extremely large bilaterally. The sciatic artery passed out of the pelvis through the infrapiriform foramen and descended posterior to the sciatic nerve through the gluteal region. The sciatic nerve was considerably flattened out under the artery. Large articular branches arose from the part of the artery at the buttock just below the piriform muscle. The artery descended along the back of the thigh and was crossed obliquely posteriorly by the long head of the biceps femoris muscle. The sciatic artery continued as the popliteal artery located very superficially in the popliteal fossa. A companion vein, i.e., the sciatic vein, accompanied each artery. The right sciatic vein entered the pelvis posteriorly through the infrapiriform foramen, whereas the left perforated the quadriceps muscle from behind and joined the femoral vein anteriorly. There was a gracile superficial femoral artery bilaterally. The deep femoral arteries of both lower limbs were hypoplastic with slender circumflex branches. There were no macroscopic connections between the sciatic and the deep or superficial femoral arteries on either side. This anomaly should be kept in mind in the evaluation of patients with sciatic or buttock pain or palpable "pulsating" buttock mass. Persistent sciatic artery also could be a potential hazard during orthopedic manipulations, hip joint surgery, and renal transplant surgery.