TITLE

EXPERIMENTAL ARTERIAL STENOSIS: POST STENOTIC DILATATION AND COLLATERAL BLOOD FLOW

AUTHOR(S)
Flasher, J.; Drury, D. R.; Jacobson, G.
PUB. DATE
February 1951
SOURCE
Angiology;Feb1951, Vol. 2 Issue 1, p60
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
A constricting tie or clip was applied to the left renal artery in 10 rabbits, and the right kidney was either not manipulated at all or it was removed. The renal circulation was then investigated angiographically and by surgical exploration with direct visualization. Dilatation of part or all of the post stenotic portion of the artery occurred in 12 of the rabbits; in 4 it appeared to extend into the primary branches. The degree and extent of the dilatation appeared to be related to the degree of renal tissue ischemia, i.e. to the degree of hypertension. Turbulence of blood flow in the most proximal portion of the post stenotic renal artery is a possible explanation of the relatively greater dilatation noted in that area. Intra-arterial pressure changes, and the accompanying blood flow changes, do not offer an adequate explanation for this post stenotic dilatation. The 4 rabbits that failed to develop a post stenotic dilatation, failed to develop hypertension; we assume that the renal artery constriction was of insufficient degree to produce any or sufficient renal ischemia in these animals. There was no apparent collateral blood flow in relation to the renal artery in the normal rabbit, under the conditions of our experiments. Six of the 12 rabbits that exhibited the post stenotic dilatation were investigated for evidence of a collateral renal circulation; all 6 exhibited evidence of a collateral circulation. Two of the 4 rabbits that were similarly investigated failed to develop the post stenotic dilatation; they exhibited no evidence of a collateral circulation. Therefore, the initiation of a collateral blood flow appears to be related to the presence of renal ischemia. If this flow merely represents the opening up of previously present but non-functioning vessels, then the alteration of pressure gradients, occasioned by the constriction of the renal artery, might, also be an adequate explanation. Our experiments do not indicate whether the above changes are due to a substance produced in the ischemic renal tissue or to defective excretion or absorption of a substance by the ischemic or curtailed renal tissue. The former appears to be the more likely possibility.
ACCESSION #
17857657

 

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