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1 Department of Pharmacology, Universitätsklinik Bonn, 53113 Bonn; 2 Department of Physiology II, Universitätsklinik Bonn, 53115 Bonn; and 3 Medizinische Klinik und Poliklinik II, Universitätsklinik Bonn, University of Bonn, 53105 Bonn, Germany
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
6 Hz and a positive staircase
at
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.
cardiovascular disease models; electrocardiography; echocardiography; sarcomere shortening
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