Load sensitivity of relaxation in the foetal and newborn rabbit heart
- 1 September 1984
- journal article
- research article
- Published by Oxford University Press (OUP) in Cardiovascular Research
- Vol. 18 (9), 523-527
- https://doi.org/10.1093/cvr/18.9.523
Abstract
Differences in the mechanism of cardiac relaxation and the influence of changes in the stimulation frequency were studied in foetal and newborn rabbit hearts. In the foetal rabbit heart which lacks a well developed sarcoplasmic reticulum, load sensitivity of relaxation was investigated and compared with that observed in the newborn. Load sensitivity was studied by measuring force and shortening length in twitches with increasing afterloads and also when load clamp steps were rapidly imposed during the twitch. Quantification of the load sensitivity was achieved by the measurement of the time to relaxation “tRi” which was linearly related to the relative developed force. The slope (S) of this linear relation quantifies the load sensivity: the higher the slope, the more load sensitive is the relaxation. At a frequency of 24 beats·min−1, S was respectively 0.24 in the foetal heart and 0.36 in the newborn heart showing at both ages the existence of a load sensitivity and its significant increase at birth. No further increase in load sensitivity was observed from 1 day to 21 days afterbirth. Reducing the stimulation frequency from 24 to 10 beats·min−1 abolished the load sensitivity in foetal hearts (S=0.05) while, in the newborn, a significant load sensitivity could still be observed (S=0.25). Thus, in rabbit myocardium, the load sensitivity of cardiac relaxation depended upon the age and the stimulation frequency showing a perinatal development of the structures involved in the control of myocardial relaxation.Keywords
This publication has 2 references indexed in Scilit:
- Changes in intracellular Ca2+ activity with stimulation in sheep cardiac Purkinje strandsAmerican Journal of Physiology-Heart and Circulatory Physiology, 1982
- Load-insensitive relaxation caused by hypoxia in mammalian cardiac muscle.Circulation Research, 1981