[Experimental studies on the effects of alpha-tocopherol in small intestinal ischemia and reperfusion injury].

In the present study, we quantified the biochemical [thiobarbituric acid (TBA) reactants, superoxide dismutase (SOD) and vitamin E] and histologic changes in the small intestinal tissue after ischemia and/or reperfusion. Sixty-seven Wistar rats were divided into 7 groups; N group: control, A-I group: 30 min. ischemia, A-II group: 120 min. ischemia, B-I group: Declamp after 30 min. ischemia, B-II group: 30 min. reperfusion after 30 min. ischemia, B-III group: 30 min. reperfusion after 120 min. ischemia, E group: vitamin E administration 30 min. reperfusion after 30 min. ischemia. The levels of TBA reactants were significantly different between A-II and B-II, B-II and E (all p less than 0.01). For SOD, there were significant differences between N and B-I (p less than 0.01), N and E (p less than 0.05). For vitamin E, there were significant differences between A-I and B-I, A-I and B-I, B-II and E (all p less than 0.01). Histologic changes showed that the grade of tissue injury was more severe in B-I and B-II than in A-I, and was less in E than in B-II. It is suggested that vitamin E protected cells from injury due to oxygen free radicals.

Buerger's colour.

Cyanosis of the hands and feet in Buerger's disease is known as 'Buerger's colour'. This characteristic skin colour is produced by the subpapillary venous plexus. The reactions of the subpapillary venous plexus in patients with Buerger's disease were observed by analysing the fractional blood volume of tissue using a visible light reflective spectrophotometer. Capillary morphology was investigated using an intravital video-microscopic system. Twenty-seven subjects, comprising 13 normals and 14 patients with Buerger's disease, were studied. In the nailbeds of patients with Buerger's disease, an increase in the number of loops, cyanotic colour change and dilatation were observed. In this condition there was incompetence of venular tonus and regurgitation at venular valves. Buerger's colour is probably due to excessive congestion of venous blood in the subpapillary venous plexus which is produced by these mechanisms.

[Clinical reevaluation of continuous intravenous infusion of 5-fluorouracil--plasma concentrations and clinical dose by continuous intravenous and 60-min infusions].

Daily and intermittent continuous intravenous infusions [by gravity drip, (IVG) or infusion pump, (IVP)] and intermittent short-time intravenous drip infusion of 5-FU were carried out on advanced cancer patients. The MTD and dose-limiting toxicity were investigated in relation to the plasma concentrations of 5-FU determined by HPLC. Responses in eleven patients receiving IVG administration daily at 8-21 mg/kg/day were NC, but those given 5-FU alone showed no adverse reactions. Plasma concentrations were too low to be determined. In 9 patients receiving IVG or IVP administration weekly at 60 mg/kg for 24 hr, 1 of the 5 evaluable patients showed reduced hepatic metastatic lesions. One of 4 patients receiving IVP administration weekly at 120 mg/kg for 48 hr showed a disappearance of metastatic lesions in the skeletal muscle, but bone marrow suppression was observed as dose-limiting toxicity. Pharmacokinetics were more stable in IVP than in IVG with less individual difference in the plasma concentrations. Among the outpatients receiving short-time iv, IVG administration once or twice a week, 2 patients given weekly administrations at 20 mg/kg for 60 min showed slight adverse reactions. In 6 patients given high-dose administrations, bone marrow suppression was observed. When pharmacokinetics in the patients given 5-FU for 60 min were compared between the IVG and IVP groups, there were individual differences in plasma concentrations, but the differences were not significant. It was concluded from above results that the following practical dose schedules would be recommendable: 60 mg/kg for 24hr/week by IVP for inpatients and 20 mg/kg for 60 min/week by IVG for outpatients.

[Surgical treatment in dissecting aneurysm of the infrarenal abdominal aorta--report of two cases].

In this paper, we present two cases of dissecting aneurysm in the infrarenal abdominal aorta and a review of this type of lesion. DeBakey's classification has found wide acceptance since it combines both anatomical description and a basis for management. However, there is another type of the aneurysm, omitted in this classification, which involves the infrarenal segment of the abdominal aorta, the intimal tear being distal to the renal arteries. Its clinical manifestation, therefore, differs from dissecting aneurysm of the thoracic aorta. The incidence of dissecting aneurysm in the lower abdominal aorta in the literature is 2-14%. Sixteen cases of atraumatic dissecting aneurysm in the abdominal aorta, including our two, have been reported in Japan. Radioimaging techniques such as ultrasound, computerized tomography with contrast enhancement and conventional angiography, allow diagnosis of dissecting aneurysm. Computerized tomography with contrast enhancement has led to more frequent preoperative diagnosis of dissecting aneurysm in the abdominal aorta. However, precise visualization of the intimal defect together with the site of entry is a prerequisite of operation. Angiography remains the most suitable method of achieving this end. Although both abdominal and thoracic aortic dissection share a common management in respect to hypotensive therapy, we believe that surgical intervention is required, especially in dissection of the abdominal aorta, with prosthetic replacement of the infrarenal segment and obliteration of any proximal or distal false lumen.