肠道病毒71型脑干脑炎患儿与去甲肾上腺素心脏毒性猫的心力衰竭比较。

Comparison of heart failure in children with enterovirus 71 rhombencephalitis and cats with norepinephrine cardiotoxicity.

作者信息

Fu Y-C, Chi C-S, Lin N-N, Cheng C-C, Jan S-L, Hwang B, Hsu S-L, Gong C-L, Chen Y-T, Chiu Y-T

机构信息

Department of Pediatrics, Taichung Veterans General Hospital, Taichung, 407 Taiwan, Republic of China.

出版信息

Pediatr Cardiol. 2006 Sep-Oct;27(5):577-84. doi: 10.1007/s00246-005-0915-6.

DOI:10.1007/s00246-005-0915-6

PMID:16933070

Abstract

The mechanism of heart failure in patients with enterovirus 71 rhombencephalitis (brain stem encephalitis) remains unknown. Our previous reports hypothesized that a catecholamine storm induced by rhombencephalitis may account for the heart failure. The aim of this study was to develop a novel feline model of norepinephrine cardiotoxicity and compare the resulting heart failure to that in children with enterovirus 71 rhombencephalitis. Nine of 75 children (12%) with enterovirus 71 rhombencephalitis (5 boys and 4 girls; age, 4-28 months; median age, 16 months) were complicated with left ventricular hypokinesia (ejection fraction, 31 +/- 9%). Six cats (weight, 3.03 +/- 0.64 kg) were administered intravenous norepinephrine 30 microg/kg/min for 3 hours. Echocardiography assessed the left ventricular diameter and function before and after the administration of norepinephrine. Pathology studies included hematoxylin and eosin stain and in situ terminal deoxyribonucleotidyl transferase-mediated dUTP nick end-labeling assay. In the feline model, norepinephrine induced significant left ventricular dilatation (end diastolic diameter from 1.18 +/- 0.19 to 1.62 +/- 0.22 cm, p = 0.001; endsystolic diameter from 0.54 +/- 0.09 to 1.36 +/- 0.32 cm, p = < 0.001) and hypokinesia (ejection fraction from 87.5 +/- 4.1 to 35.2 +/- 16.3%, p = 0.001). Heart specimens from 4 patients and six cats showed similar pathology findings, including myocardial hemorrhage, cardiomyocyte apoptosis, and coagulative myocytolysis, which is characterized by sarcoplasmic coagulation, granulation, vacuolization, myofibrillar waving, and disruption. Both groups showed no significant inflammatory reaction. In conclusion, heart failure in patients with enterovirus 71 rhombencephalitis is similar to that in cats with norepinephrine cardiotoxicity. Norepinephrine cardiotoxicity may play a role in the pathogenesis of heart failure in enterovirus 71 rhombencephalitis.

摘要

肠道病毒71型所致菱形脑炎（脑干脑炎）患者发生心力衰竭的机制尚不清楚。我们之前的报告推测，菱形脑炎诱发的儿茶酚胺风暴可能是导致心力衰竭的原因。本研究的目的是建立一种新型的去甲肾上腺素心脏毒性猫模型，并将由此导致的心力衰竭与肠道病毒71型菱形脑炎患儿的心力衰竭进行比较。75例肠道病毒71型菱形脑炎患儿中有9例（12%）（5例男孩，4例女孩；年龄4 - 28个月；中位年龄16个月）并发左心室运动功能减退（射血分数为31±9%）。6只猫（体重3.03±0.64 kg）静脉注射去甲肾上腺素30μg/kg/min，持续3小时。超声心动图评估去甲肾上腺素给药前后的左心室直径和功能。病理研究包括苏木精-伊红染色和原位末端脱氧核苷酸转移酶介导的dUTP缺口末端标记分析。在猫模型中，去甲肾上腺素引起显著的左心室扩张（舒张末期直径从1.18±0.19 cm增加到1.62±0.22 cm，p = 0.001；收缩末期直径从0.54±0.09 cm增加到1.36±0.32 cm，p = < 0.001）和运动功能减退（射血分数从87.5±4.1%降至35.2±16.3%，p = 0.001）。4例患者和6只猫的心脏标本显示出相似的病理表现，包括心肌出血、心肌细胞凋亡和凝固性肌溶解，其特征为肌浆凝固、颗粒形成、空泡化、肌原纤维波动和破坏。两组均未显示明显的炎症反应。总之，肠道病毒71型菱形脑炎患者的心力衰竭与去甲肾上腺素心脏毒性猫的心力衰竭相似。去甲肾上腺素心脏毒性可能在肠道病毒71型菱形脑炎心力衰竭的发病机制中起作用。