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D E Rannels

Publications and source records attributed to D E Rannels.

113 records · Page 7Linked to original sources
PubMedDate not supplied

Postpneumonectomy lung growth following thyroparathyroidectomy.

Hormonal regulation of compensatory lung growth is not well understood, but it may be similar to that during compensatory growth of other organs. Liver regeneration is blocked by hypocalcemia in thyroparathyroidectomized (TPX) animals. Although calcium status is an important regulator of growth in many biological systems, the effect of TPX on compensatory lung growth is unknown. In male Sprague-Dawley rats, TPX lowered blood ionized calcium by 42% (p < .01) within two days; it remained depressed for at least one additional week. Thyroid-intact and TPX animals were therefore subjected either to sham thoracotomy or to left pneumonectomy on post-TPX day 2. Growth of the right lung was assessed on day 9 when, in pneumonectomized animals, lung mass had increased 23% (p < .01). TPX had no effect on right lung mass in sham animals. Similarly, TPX had no effect on the postpneumonectomy increase in right lung mass, which reached 118% (p < .01) of that in TPX controls. Analysis of right lung DNA, RNA, and protein concentrations on day 9 revealed that tissue macromolecule content increased postoperatively in both PNX and TPX/PNX rats in proportion to lung growth. These results demonstrate that postpneumonectomy compensatory growth of the lung is not blocked in the thyroparathyroprivic hypocalcemic rat.

Animals↗
PubMedDate not supplied

Factors accounting for growth and atrophy of the heart.

Growth of the rat heart was induced by intrathoracic aortic banding, while atrophy followed hypophysectomy. During the early phase of hypertrophy, RNA concentration increased markedly. During the period of atrophy, RNA concentration was reduced. These changes in RNA concentration seemed to account for either the increased or the decreased rates of protein synthesis that was observed during hypertrophy or atrophy, respectively. Rates of protein degradation were unaffected during changes in heart size. These findings suggest that alterations in synthesis, processing, or degradation of RNA play a key role in modification of heart size.

Aging↗