1992年 · 第08卷第05期

The effects of normal sera and uraemic sera on insulin release in neonatal rat pancreatic islet beta-cell monolayer cultures were compared. Sera were obtained from 12 patients with newly-diagnosed uraemia and healthy subjects. Pancreatic islet cells from neonatal rats were cultured in monolayer for 5 days. Insulin relesae was significantly inhibited after 50-h pre-incubation in the media containing 50 per cent of uraemic sera compared with containing 50 per cent of normal sera (insulin release: 31.19±3.65 vs 35.44±1.49 μU/ml. 90min, p<0.01);

Experimental rats were divided as follows: diabetic control (DC, N=9), captopril-treating group (DT, N=12) and normal controls (NC).

Results: moderate hyperglycemia were maintained in diabetic groups throughout the experiment period. There was no difference of blood glucose levels before and after the treatment, HbA1c levels was similar between DT and DC at end of 6th month of the experiment. The increased urinary protein (IUP) in DC and DT groups was significantly higher than that in NC. IUP in DS was significantly lower than that in DC. MGV in DC and DT groups was bigger than that in NC (p<0.05). MGV in DT was smaller than in DC, but the difference was not significant. Creatinine clearance rate (CCr) in DC and DT was significantly increased; CCr in DC was higher than that in DT.

Histology: light microscope showed no significant morphological changes in DC and DT. However, enlargement of mesangial cells and matrix, thickening of glomerular basement membrance were observed in both DC and DT under electric microscope. The glomerular lesion in DC was prominent as compared wiht that in DT. NC showed no glomerular morphological lesions.

The results mentioned above reveal that the disorder of glucose metabolism could cause renal function and structure injury and that administration of captopril in the early stage of experimental diabetic may delay the formation of the diabetic glomerulopathy.

Immediately after right nephrectomy, 18 mongrel dogs were randomly divided into 3 groups. Group A (n=6) served as saline treated controls. Group B (n=6) was treated with postischemic intravenous ATP-MgCl₂30μmol/kg in saline 6ml/kg and group C (n=6) with inosine 150mg/kg. Acute renal failure (ARF) was induced by occluding the left renal artery for 1 hour under general anaesthesia. Renal function changes has been observeb for 5 hours

after reperfusion. And renal structure damages was observed with electronic microscope.

It is concluded that postischemic infusion of inosine, similar to ATP-MgCl₂, can enhance recovery of renal function and structure damage, accelerate regeneration of sublethally injured tubular cells and has no side-effect of ATP -MgCl₂ which reduces blood pressure. It is suggested that major dose of inosine can be used in hemorrhagic and traumatic shock to prevent ARF from initiation or aggravation.

The distribution of GBM negative charge in 10 membranous nephropathy (MN) and 2 normal renal biopsied specimens was observed by Müller's colloidal iron staining. Out of the 10 MN the colloidal iron staining showed that GBM negative charge was decreased in MN stage I-II and significantly decreased or disappeared in MN stage III. This result suggested that the decrease of GBM negative charge are correspondence with the degrees of renal lesions. The colloidal iron staining was a simple and convenient method and was easy to operate and popularize.