RENAL LESION AND BLOOD PRESSURE CHANGE BY INJECTION OF SUBMICRON CRYSTALLINE SILICA SUSPENSION INTO RENAL ARTERY
1967 Volume 58 Issue 12 Pages 1237-1253
Details
1967 Volume 58 Issue 12 Pages 1237-1253
Relationship between the renal lesion and the blood pressure change following the injection of submicron crystalline silica suspension (0.02-0.05 micron) into renal artery, was studied in rabbits.
1) In rabbits with injection of the suspension into unilateral renal artery, no hypertension was induced until 7 weeks after.
2) In 4 of the 6 rabbits in which one kidney was removed previously and the suspension was injected into contralateral renal artery, elevation of blood pressure occured within 6 weeks and continued thereafter.
3) In all rabbits in which contralateral kidney was removed 7 weeks after silica injection into unilateral renal artery, continious hypertension was induced within 3 days after the nephrectomy.
4) In all rabbits in which the suspension was injected into contralateral renal artery 6 weeks after unilateral renal artery injection, high blood pressure was developed within 3 days and continued permanently.
5) All rabbits with simultaneous bilateral renal artery injection died within several day.
6) Histological findings: In a few days after injection, the kidneys revealed remarkable congestion. Swelling and cell infiltration in glomeruli, and degeneration of tubules were observed, but no emboli by silica particles was found. About 1 week after injection, the arterioles began to show endothelial reactions which resembled endarteritis obliterans, and subsequently, 4 weeks after injection, multiple small infarcts were resulted by obliteration of small arteries. Furthermore these arteriolar reactions progressed and the infarcts increased in size with the proliferation of interstitial connective tissue, and then old infarcted areas were organized and scarred. One year after injection, the renal tissue lost its normal structures, showing typical scarred kidney.
In short, the main changes began in arterioles in the form of endarteritis obliterans, and progressively spread to larger arteries. The renal infarcts developed gradually by the disturbance of arterial blood flow in the kidney, and this seemed to play an important role in the development of hypertension.
