Cardiac denervation in mice infected with Trypanosoma cruzi

E. Rodrigues, E. Liberti, L. Maifrino, R. D. de Souza
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引用次数: 12

Abstract

Abstract The neuronal features of the hearts of mice that were acutely or chronically infected with the Y strain of Trypanosoma cruzi were compared with those of control hearts from uninfected mice. Whole-mount preparations of the murine atria, isolated by microdissection, were stained to reveal neurons with NADH-diaphorase activity. Counts, by a microscopist who was blind to the infection status of the donor mouse, revealed that there were significantly (38%) fewer such neurons in the atria from the acutely infected mice than in the atria from the control hearts. The ganglia of the infected mice were also irregularly distributed, severely damaged ganglia being found beside slightly degenerated or morphologically normal ones. Although the ganglia contained small, medium and large neurons, the apparent destruction caused by T. cruzi was confined to the large ones. As neuron counts in preparations of hearts from mice with chronic infections were 32% lower than those in the control hearts, there appears to be no additional loss of cardiac neurons as the acute infection in mice progresses to the chronic phase.
克氏锥虫感染小鼠心脏失神经支配的研究
摘要对急性和慢性克氏锥虫Y株感染小鼠心脏的神经元特征与未感染小鼠心脏的神经元特征进行比较。通过显微解剖分离的小鼠心房的全载制剂,染色显示具有NADH-diaphorase活性的神经元。由一名不知道供体小鼠感染状况的显微镜学家进行的计数显示,急性感染小鼠心房中的此类神经元明显少于对照小鼠心房(38%)。感染小鼠的神经节分布也不均匀,除了轻微退化或形态正常的神经节外,还可发现严重受损的神经节。虽然神经节包含小、中、大神经元,但克氏锥虫对神经节的明显破坏仅限于大神经元。由于慢性感染小鼠心脏的神经元计数比对照心脏的神经元计数低32%,因此随着小鼠急性感染进展到慢性期,似乎没有心脏神经元的额外损失。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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