Takatsu H, Uno Y, Fujiwara H
Second Department of Internal Medicine, Gifu University School of Medicine, Japan.
J Nucl Med. 1995 Jun;36(6):1055-61.
Genetically inbred cardiomyopathic hamsters were examined to investigate the mechanism of reduced myocardial accumulation of metaiodobenzylguanidine (MIBG) in the cardiomyopathic heart.
Bio 14.6 Syrian hamsters (hypertrophic stage: n = 15, early heart failure stage: n = 17) and control F1b strain golden hamsters (n = 36) were injected with 296 kBq of [125I] MIBG and killed 30 min or 4 hr later. Thirty-three of these hamsters were pretreated with 10 mg/kg of desipramine to determine non-neuronal MIBG accumulation. To evaluate the nonexocytotic MIBG release from nerve endings, desipramine was administered to four Bio 14.6 hamsters 15 min after [125I]MIBG injection. To determine the role of the activated renin-angiotensin system (RAS) in MIBG washout from sympathetic nerve terminals in cardiomyopathy at early heart failure stage, 10 mg/kg/day cilazapril, an angiotensin-converting enzyme inhibitor, was given orally to 7 controls and 16 cardiomyopathic hamsters for 16 wk.
In the absence of desipramine pretreatment, left ventricular [125I]MIBG accumulation 4 hr after injection was 0.376% +/- 0.015 %kg dose/g (mean +/- s.e.m.) in the hypertrophic hamsters (versus 0.418 +/- 0.019 in controls of the same age; ns), and 0.195 +/- 0.025 in early heart failure hamsters. Treatment with cilazapril partially restored MIBG accumulation in the Bio 14.6 hamsters but did not affect the controls.
Decreased [125I]MIBG accumulation in cardiomyopathic hamsters during the early heart failure stage is caused by neuronal release which is partially modulated by the activated RAS.
对基因纯合的心肌病仓鼠进行检查，以研究心肌病心脏中去甲碘苄胍（MIBG）心肌蓄积减少的机制。
给Bio 14.6叙利亚仓鼠（肥厚期：n = 15，早期心力衰竭期：n = 17）和对照F1b品系金黄仓鼠（n = 36）注射296 kBq的[125I]MIBG，30分钟或4小时后处死。其中33只仓鼠用10 mg/kg的地昔帕明预处理，以确定非神经元性MIBG蓄积。为评估神经末梢非胞吐性MIBG释放，在[125I]MIBG注射15分钟后给4只Bio 14.6仓鼠给予地昔帕明。为确定激活的肾素-血管紧张素系统（RAS）在早期心力衰竭期心肌病交感神经末梢MIBG洗脱中的作用，给7只对照仓鼠和16只心肌病仓鼠口服10 mg/kg/天的西拉普利（一种血管紧张素转换酶抑制剂），持续16周。
在未用地昔帕明预处理的情况下，肥厚仓鼠注射后4小时左心室[125I]MIBG蓄积为0.376%±0.015 %kg剂量/g（平均值±标准误）（同龄对照为0.418±0.019；无显著性差异），早期心力衰竭仓鼠为0.195±0.025。西拉普利治疗可部分恢复Bio 14.6仓鼠的MIBG蓄积，但对对照仓鼠无影响。
早期心力衰竭期心肌病仓鼠[125I]MIBG蓄积减少是由神经元释放引起的，且部分受激活的RAS调节。
