Summary
Permanent ligation of the feline aorta at the iliac bifurcation is followed by rapid
opening of pre-existing collateral blood vessels. However, if ligation is combined
with formation of a clot, these protective collateral vessels do not function. This
study was undertaken to determine if drugs which alter serotonin function can improve
collateral blood flow after arterial thrombosis. Permanent ligations were placed at
the iliac bifurcation, circumflex iliac and sixth lumbar arteries in all cats. A clot
was produced in the aorta of 27 cats by injection of 0.1 ml of thromboplastin. Ligated
clot-occluded cats were untreated (10); had blood serotonin depleted using a single
dose of reserpine (0.1 mg/kg i. m.) followed by para-chlorophenylanine (p-CPA) (100
mg/kg orally) every 3 days (9) ; or were treated prior to surgery with a serotonin
antagonist cinanserin HC1 (4 mg/kg i. v.) (8). Control cats (18) were acutely ligated.
9 of these cats were untreated, 5 were cinanserin HC1-treated, and 4 were reserpine/p-CPA-treated.
Extent of collateral development was assessed by aortograms 3 days after occlusion
and by neurologic rating. Aortograms of acutely ligated cats indicated a significant
collateral blood flow around the segment of ligated aorta, while ligated clot-occluded
cats had a severely depressed hind-limb perfusion. Reserpine/p-CPA-treated ligation
clot-occluded cats had aortograms similar to acutely ligated cats. The cinanserin
HC1-treated ligation clot-occluded cats had aortograms which indicated hind-limb perfusion
was not as adequate as the acutely ligated cats. However, the perfusion of these animals
was improved over untreated ligation clot-occluded cats. Neurologic rating correlated
with aortograms. These results suggest: 1) the clinical consequences of arterial thrombosis
cannot be entirely attributed to mechanical occlusion of an artery, but may be due
to depression of protective collateral blood flow induced by thrombosis, 2) serotonin
is an important factor in this depression of collateral blood flow, and 3) isolation
of the factors responsible for collateral inhibition could permit the development
of therapeutic interventions.