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加利福尼亚海狮(Zalophus californianus)中与软骨藻酸毒性相关的退行性心肌病的特征描述。

Characterization of a degenerative cardiomyopathy associated with domoic acid toxicity in California sea lions (Zalophus californianus).

作者信息

Zabka T S, Goldstein T, Cross C, Mueller R W, Kreuder-Johnson C, Gill S, Gulland F M D

机构信息

Marine Mammal Center, GGNRA, Sausalito, CA, USA.

出版信息

Vet Pathol. 2009 Jan;46(1):105-19. doi: 10.1354/vp.46-1-105.

DOI:10.1354/vp.46-1-105
PMID:19112124
Abstract

Domoic acid, produced by marine algae, can cause acute and chronic neurologic sequela in California sea lions (Zalophus californianus) from acute toxicity or sublethal exposure. Eight sea lions, representing acute and chronic cases, both sexes, and all age classes, were selected to demonstrate a concurrent degenerative cardiomyopathy. Critical aspects of characterizing the cardiomyopathy by lesion distribution and morphology were the development of a heart dissection and tissue-trimming protocol and the delineation of the cardiac conducting system by histomorphology and immunohistochemistry for neuron-specific protein gene product 9.5. Histopathologic features and progression of the cardiomyopathy are described, varying from acute to chronic active and mild to severe. The cardiomyopathy is distinguished from other heart lesions in pinnipeds. Based on histopathologic features, immunopositive staining for cleaved caspase-3, and comparison with known, similar-appearing cardiomyopathies, the proposed pathogenesis for the degenerative cardiomyopathy is the primary or at least initial direct interaction of domoic acid with receptors that are suspected to exist in the heart. l-Carnitine, measured in the heart and skeletal muscle, and troponin-I, measured in serum collected at the time of death from additional animals (n = 58), were not predictive of the domoic acid-associated cardiomyopathy. This degenerative cardiomyopathy in California sea lions represents another syndrome beyond central neurologic disease associated with exposure to domoic acid and may contribute to morbidity and mortality.

摘要

由海藻产生的软骨藻酸,可因急性毒性或亚致死性暴露,在加利福尼亚海狮(Zalophus californianus)中引发急性和慢性神经后遗症。选取了八只海狮,代表急性和慢性病例、不同性别及所有年龄组,以证明同时存在的退行性心肌病。通过病变分布和形态来表征心肌病的关键方面包括制定心脏解剖和组织修剪方案,以及通过组织形态学和针对神经元特异性蛋白基因产物9.5的免疫组织化学来描绘心脏传导系统。描述了心肌病的组织病理学特征和进展情况,从急性到慢性活动期,从轻到重各不相同。这种心肌病与鳍足类动物的其他心脏病变有所区别。基于组织病理学特征、裂解的半胱天冬酶-3的免疫阳性染色,以及与已知的、外观相似的心肌病进行比较,推测退行性心肌病的发病机制是软骨藻酸与心脏中疑似存在的受体发生原发性或至少是初始的直接相互作用。在心脏和骨骼肌中测量的左旋肉碱,以及在另外58只动物死亡时采集的血清中测量的肌钙蛋白I,均不能预测与软骨藻酸相关的心肌病。加利福尼亚海狮的这种退行性心肌病代表了除与接触软骨藻酸相关的中枢神经系统疾病之外的另一种综合征,可能会导致发病率和死亡率上升。

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