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Publication : Increasing myocardial contraction and blood pressure in C57BL/6 mice during early postnatal development.

First Author  Tiemann K Year  2003
Journal  Am J Physiol Heart Circ Physiol Volume  284
Issue  2 Pages  H464-74
PubMed ID  12414444 Mgi Jnum  J:82056
Mgi Id  MGI:2450790 Doi  10.1152/ajpheart.00540.2002
Citation  Tiemann K, et al. (2003) Increasing myocardial contraction and blood pressure in C57BL/6 mice during early postnatal development. Am J Physiol Heart Circ Physiol 284(2):H464-74
abstractText  Knowledge of the developmental changes of cardiovascular parameters in the genetic background of a mouse strain is important for understanding phenotypic changes in transgenic or knockout mouse models for heart disease. We studied arterial blood pressure and myocardial contractility in mice of the common background strain C57BL/6, aged 21 days [postnatal day 21 (P21)] to 580 days. Heart rate increased during maturation from 396 beats/min at P21 to 551 beats/min at postnatal day 50 (P50), and mean arterial blood pressure increased in parallel from 86 to 110 mmHg and remained constant afterward. Echocardiographically determined left ventricular myocardial wall dimensions (R = 0.79, P < 0.0001) and left ventricular mass calculated using the area-length algorithm correlated strongly with histomorphometrical measurements (R = 0.93, P < 0.001). Sarcomere shortening records from isolated ventricular myocytes used as a measure for myocardial contractility revealed a negative shortening-frequency relation under a pacing frequency of 2 Hz and a positive relation above 2 Hz. Shortening amplitudes recorded from P21 myocytes were smaller, and the shortening-frequency relation was less steep than in adult myocytes. A stimulation pause was followed by a negative 'staircase' at pacing frequency of < or =6 Hz and a positive staircase at > or =6 Hz. P21 myocytes developed positive staircases at 8 and 10 Hz, and adult myocytes also developed them at 6 Hz. Blood pressure increase during maturation until P50 may originate from increasing single cardiomyocyte contractility.
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