H. Takatsu et al., CARDIAC SYMPATHETIC-NERVE FUNCTION ASSESSED BY [I-131] METAIODOBENZYLGUANIDINE AFTER ISCHEMIA AND REPERFUSION IN ANESTHETIZED DOGS, Journal of nuclear cardiology, 4(1), 1997, pp. 33-41
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiac & Cardiovascular System","Radiology,Nuclear Medicine & Medical Imaging
Background. Accumulation of I-131-labeled metaiodobenzylguanidine ([I-
131]MIBG), a radiolabeled norepinephrine analog, is reduced in infarct
ed myocardium, suggesting loss of cardiac sympathetic nerve viability,
Histopathologic studies, however, indicate that the nerve endings are
morphologically intact, Experiments were therefore designed to determ
ine the mechanism of reduced MIBG accumulation. Methods and Results. D
esipramine, a specific blocker of neuronal norepinephrine reuptake, wa
s used to separate the portions of total myocardial [I-131]MIBG accumu
lation attributable to neuronal and nonneuronal uptake mechanisms, Six
teen dogs underwent circumflex coronary artery occlusion for 60 minute
s followed by a 5-hour reperfusion, [I-131]MIBG was injected intraveno
usly 1 hour after reperfusion, The left ventricle was removed and incu
bated in triphenyltetrazolium chloride to identify infarcted and viabl
e myocardium within the zone at risk, Preliminary studies in sham-oper
ated dogs showed that pretreatment with desipramine (5 mg/kg) reduced
[I-131]MIBG accumulation 4 hours after injection to 38.9% of untreated
controls, Chemical sympathectomy by topical phenol resulted in a simi
lar decrease in [I-131]MIBG accumulation (to 45.7% of normal), and des
ipramine did not produce further inhibition of [I-131]MIBG accumulatio
n over that produced by phenol alone, indicating that the inhibitory e
ffect of desipramine on neuronal accumulation of [I-131]MIBG was essen
tially complete, In dogs undergoing ischemia-reperfusion, myocardial s
amples from infarcted and viable postischemic areas showed 64.5% +/- 1
1.8% and 84.7% +/- 9.1% of normal [I-131]MIBG activity, respectively (
both, p < 0.01 vs normal area, n = 9), With desipramine pretreatment (
n = 7), accumulation of [I-131]MIBG decreased in all areas. Neuronal a
ccumulation was reduced uniformly in infarcted, viable postischemic, a
nd normal areas by 30% to 35% compared with sham-operated controls, In
contrast, nonneuronal accumulation was only 39.3% in infarcted areas
and 84.6% in viable postischemic areas compared with normal areas, and
these decreases accounted entirely for the reduced total [I-131]MIBG
accumulation. Conclusions. Reduced [I-131]MIBG accumulation in infarct
ed myocardium after 60 minutes of ischemia and 5 hours of reperfusion
is attributable to a deficit in nonneuronal accumulation and not to de
creased accumulation by sympathetic nerves.