Segmental arterial mediolysis--an iatrogenic vascular disorder induced by ractopamine.
BACKGROUND
Segmental arterial mediolysis, an uncommon arterial disorder most often occurring in the splanchnic muscular arteries of the abdomen, is a cause of catastrophic hemorrhages. Its histology and initial clinical presentations suggested that it represented a localized norepinephrine-induced vasospastic response to perturbations in vascular tone and blood volume distribution caused by coexisting vasoconstrictor conditions. However, later presentations were at odds with some aspects of this hypothesis.


METHODS
Nine greyhound dogs were administered a single dose of ractopamine. Two dogs developing persistent conduction abnormalities with biochemical evidence of heart injury were euthanized and necropsied--one 4 days and the other 17 days after dosage This report is based on findings and comparisons of the canine abdominal and coronary arteries to segmental arterial mediolysis.


RESULTS
Lesions having features of early-injurious-stage segmental arterial mediolysis were identified in the canine arteries 4 days postractopamine, and arteries examined after 17 days showed alterations typically occurring in reparative-stage segmental arterial mediolysis. It is suspected that ractopamine, a Beta-2 adrenergic agonist, created segmental arterial mediolysis by neuromodulating the peripheral sympathetic nervous system to release norepinephrine from varicosities of efferent nerves serving splanchnic arteries that stimulate alpha-1 receptors to induce injury at the adventitial medial junction and medial muscle apoptosis.


CONCLUSIONS
This finding and other cited examples suggest that segmental arterial mediolysis may be a disorder principally caused by iatrogenic or accidental exposure to alpha-1 adrenergic receptor agonists or Beta-2 agonists able to release norepinephrine from the peripheral nervous system.
Cascade Pathology Group, Legacy Emanuel Hospital and Health Center, Portland, OR 97227, USA. rslavin@lhs.org
Richard E
RE
Slavin
Micheal J
MJ
Yaeger
D000318:Adrenergic beta-Agonists / Q000009:adverse effects*; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D001167:Arteritis / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D003251:Constriction, Pathologic / Q000139:chemically induced / Q000473:pathology; D004108:Dilatation, Pathologic / Q000139:chemically induced / Q000473:pathology; D004195:Disease Models, Animal; D004285:Dogs; D010627:Phenethylamines / Q000009:adverse effects*; D012075:Remission, Spontaneous; D019210:Troponin I / Q000097:blood; D017540:Tunica Media / Q000187:drug effects* / Q000473:pathology
D000318:Adrenergic beta-Agonists; D010627:Phenethylamines; D019210:Troponin I; C060897:ractopamine