A 61-year-old man, who had previously undergone quadruple coronary artery bypass graft surgery, was successfully treated for proximal descending aortic aneurysm using hypothermic circulatory arrest via a left thoracotomy. Preoperative angiograms revealed that the left internal thoracic artery bypass graft to the LAD was patent, and that the aneurysm was located at the descending aorta just distal to the left subclavian artery. Operative procedures were as follows. A left thoracotomy incision was made through the 4th intercostal space. The common femoral artery and vein were cannulated, and the venous cannula was positioned in the right atrium. The patient was cooled by partial cardiopulmonary bypass until the EEG was isoelectric (24°C rectal temperature), and then circulation was arrested. Left ventricular decompression was not performed. After opening of the aneurysm, proximal anastomosis was performed first at the aorta just distal to the left subclavian artery. Another arterial cannula, connected to the Y-shaped arterial line, was inserted into the graft, and perfusion to the brain was restored through this cannula. Distal anastomosis was then completed, and routine cardiopulmonary bypass was reestablished. After the heart was defibrillated, the patient was rewarmed to 34°C before discontinuing the bypass. Circulatory arrest time and total cardiopulmonary bypass time were 17 minutes and 139 minutes, respectively. Postoperative recovery was uneventful.

We have treated 12 popliteal aneurysms in ten patients from 1965 to 1989. There were seven men and three women, aged 34 to 78 years (mean, 61.5 years). Two patients had bilateral aneurysms. The chief complaint was pain at rest, claudication, coldness, etc. in eight patients, a mass or induration at the popliteus in two patients, peroneal nerve or vein compression in one patient each. Angiography showed thrombotic obstruction in six legs and distal occlusion in one leg. Ten of aneurysms of eight patients were treated surgically. In two patients, the operation was done on emergency basis. Amputation was not necessary in any case. The operative method was usually excision of the aneurysm. Reconstruction was made with artificial vessels in the first patient who underwent bilateral aneurysm surgery. Auto-saphenous vein were used in other seven patients. All vein grafts were patent at follow-up (mean follow-up period, 4 years and 3 months). Arteriosclerotic changes were histologically observed in all aneurysms. Complications such as thrombotic obstruction and distal occulsion are frequent and leg amputation is necessary in some cases. Arterial reconstruction with an auto-saphenous vein is necessary for popliteal aneurysm.

OBJECTIVESMucosal immunity plays a pivotal role for body defense against infection and allergy. The aim of this study was to clarify the effects of 2,3,7,8-tetraclorodibenzo-p-dioxin (TCDD) on mucosal immunity in the gut.

METHODSFecal IgA level and oral tolerance induction were examined in TCDD-treated mice. Flow cytometric and histological analyses were also performed.

RESULTSSingle oral administration of low dose 2,3,7,8-TCDD resulted in a marked decrease in IgA secretion in the gut without any effects on the cellular components of gut-associated lymphoid tissues (GALT) including Peyer's patches (PPs) and mesenteric lymph nodes (LNs). Decressed IgA secretion by TCDD was not observed in aryl hydrocarbon receptor (AhR)-deficient mice. Flow cytometric analysis revealed that IgA B cells in PPs and the mesenteric LNs remained unchanged in the TCDD-treated mice. An immunofluorescence study also demonstrated that a significant number of cytoplasmic IgA cells were present in the lamina propria of the gut in the TCDD-treated mice. Furthermore, oral tolerance induction by ovalbumin (OVA) was impaired in the TCDD-treated mice and OVA-specific T cell proliferation occurred in the peripheral lymphoid tissues including the spleen and LNs.

CONCLUSIONSThese results suggest that a relatively low dose of TCDD impairs mucosal immunity in the gut and induces systemic sensitization by oral antigens.