Chronic cerebral vasospasm was induced in monkeys by placement of an autologous blood clot after the basal cisterns had been opened over the arteries of the circle of Willis on one side. The experimental protocol was detailed in Part 1 of this paper. Twenty of the 30 monkeys studied from both groups (one receiving placebo and the other nimodipine) underwent cerebral fixation (Day 14) at controlled pressure by intra-arterial perfusion. The arteries at the base of the brain were studied by light microscopy and scanning (SEM) and transmission electron microscopy (TEM). Cerebral angiography on Day 7 showed that vasospasm was significantly more common (p less than 0.0001) and more severe (p less than 0.01) on the clot side compared to the control or non-clot side. Vasospasm was less severe on Day 14, just before sacrifice. On SEM, 80% of the 20 middle cerebral artery (MCA) specimens that had been in spasm (Day 7) showed marked corrugation , and in some the endothelium had a fish-scale appearance. All of the 10 MCA's on the clot side examined by TEM that had been in spasm (Day 7) showed marked changes such as endothelial swelling, subendothelial proliferation, corrugation of the elastic lamina, and myonecrosis. With few exceptions, none of the basilar arteries or MCA's on the non-clot (control) side showed any abnormalities. The pathological findings of vessels in spasm were considered to be slightly less severe in the nimodipine group; however, the trial drug (1 mg/kg/8 hrs) did not prevent such abnormalities from occurring. The ultrastructural changes in the arterial walls of specimens from both placebo and nimodipine groups in vasospasm are described. Since dramatic changes are present in the vessel walls even after radiologically visible vasospasm has almost completely abated, we believe that vasospasm is due to long-lasting smooth-muscle constriction and not to vessel wall thickening caused by a cellular or subcellular infiltrate.
Proteinuria developed in 5 of 75 rheumatoid arthritis patients treated with gold salts. In 2 of these 5 patients criteria for the nephrotic syndrome were fulfilled. Two other cases of gold‐induced nephrotic syndrome are also reported. Blood and urine gold levels were measured on 27 of the 75 patients and no difference was found between the 2 patients who eventually developed the nephrotic syndrome and the 25 who did not. Light, electronmicroscopic and histochemical studies revealed no difference in the site or degree of gold deposition in the 4 cases with nephrotic syndrome, as compared with 1 patient who did not have proteinuria. Eventual clearing of the proteinuria was fairly closely related to the degree of glomerular basement membrane thickening, as judged by light microscopy.
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