[Stanford Type A Acute Aortic Dissection with Leg Ischemia and Visceral Ischemia].

A 52-year-old man developed Stanford type A acute aortic dissection and suffered severe pain in the back and the chest, and numbness of the left lower limb. Contrast-enhanced computed tomography (CT) revealed occlusion of the left iliac artery due to dissection. The celiac artery was also obstructed and the superior mesenteric artery was severely narrowed, but there was no clear sign of organ ischemia. Endovascular treatment in the iliac artery was performed, but the patient complained of right upper abdominal pain 6 hours after the procedure. Serum liver enzyme levels were significantly elevated. Repeat contrast-enhanced CT revealed liver infarction, ischemic cholecystitis, and duodenal ischemia due to decreased collateral flow. We immediately carried out cholecystectomy and revasculariza-tion of the celiac and superior mesenteric arteries using a saphenous vein. The patient underwent central repair for aortic dissection several days after recovery of liver function, and was discharged uneventfully 24 days later.

Spatial memory impairment without apoptosis induced by the combination of beta-amyloid oligomers and cerebral ischemia is related to decreased acetylcholine release in rats.

The purpose of the present study was to examine the effect of beta-amyloid (Abeta) oligomers, not the fibrils that make up Abeta plaques, on spatial memory and the cholinergic system in rats. Recently, several researchers have suggested that small assemblies of Abeta, Abeta oligomers, caused memory loss during the early stages of Alzheimer's disease without showing cell death. In the present study, the combination of Abeta oligomers and cerebral ischemia, but not cerebral ischemia alone, significantly impaired spatial memory without apoptosis in the CA1 region of the hippocampus. Donepezil, an acetylcholinesterase inhibitor, ameliorated this memory impairment. Therefore we examined acetylcholine (ACh) release from the dorsal hippocampus. A microdialysis study showed that spontaneous release of ACh was not significantly decreased by the combination of Abeta oligomers and cerebral ischemia; however, high K(+)-evoked ACh release was decreased. These results suggest that a combination of Abeta oligomers and cerebral ischemia induces memory impairment by cholinergic synapse dysfunction without apoptosis. This model may be useful for developing new drugs for the treatment of early-phase Alzheimer's disease.