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Ann Thorac Surg 2003;75:1450-1456
© 2003 The Society of Thoracic Surgeons

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Original article: cardiovascular

Development of abnormal tissue architecture in transplanted neonatal rat myocytes

^a Department of Emergency Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA
^b Department of Internal Medicine, University of Cologne, Cologne, Germany
^c Heart Institute, Good Samaritan Hospital, Los Angeles, California, USA
^d Institute for Genetic Medicine Los Angeles, CA, USA
^e Department of Medicine, University of Southern California, Los Angeles, California, USA

Accepted for publication December 4, 2002.

^* Address reprint requests to Dr Whittaker, University of Massachusetts Medical School, Department of Emergency Medicine, 55 Lake Avenue North, Worcester, MA 01655, USA
e-mail: peter.whittaker{at}umassmed.edu

BACKGROUND: Most myocardial cell transplant studies focus on demonstration of improved function; however, such improvement depends on the development of appropriate tissue structure. Thus, our aim was to assess the architectural changes that occurred after cell transplant into normal and infarcted myocardium.

METHODS: Male neonatal cells (1 to 2 days old) were injected into the left ventricular free wall of adult female rats. The tissue was examined 0 to 1 days and 1 to 2, 4 to 6, and 12 weeks later in noninfarcted hearts and 6 months after transplant into infarcts. In histologic sections, we assessed the cells’ retardation of polarized light (to measure development of contractile elements), two-dimensional cell orientation, cell nuclear morphology, and collagen content.

RESULTS: The transplant cells’ retardation of polarized light gradually increased to 81% of that of host cells after 6 months (p < 0.001). The transplant cells were disorganized and although their nuclei increased in size, they always had a rounded appearance. Collagen content in the transplant was 210% to 430% higher than in host tissue (p < 0.01). In addition, scar collagen always separated transplant and host cells.

CONCLUSIONS: One architectural feature, the rounded nuclei, provided a distinctive marker to identify transplanted cells. Nevertheless, the transplants’ inhibited muscle development together with disorganization, separation from the host muscle, and a substantial increase in collagen resulted in a structure unlikely to play an active role in systolic function.

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