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1. The effect of heart rate on right ventricular output was examined in six lambs during a period extending from 126 to 139 days of gestation. The fetuses had been surgically instrumented at least four days previously with a main pulmonary artery flow probe, right ventricular dimension transducers and left and right atrial pacing electrodes. 2. During spontaneous variations in heart rate, rate was correlated positively with right ventricular output (P less than 0.0001) and end-diastolic dimension (P less than 0.0001) among the lambs considered as a group, but no significant effect of rate on stroke volume was found. When individual responses were examined, output increased significantly with rate in sixteen out of seventeen observations. 3. With left atrial pacing, heart rate did not affect output. With right atrial pacing, rate correlated negatively with output (P less than 0.0001). With pacing from either site, rate correlated negatively with end-diastolic dimension (P less than 0.0001) and stroke volume (P less than 0.0001). 4. The introduction of a longer period interval during each pacing rate inhibited the rate-related decrease in dimension and allowed the ventricle to fill to the same end-diastolic dimension. The systole following these longer intervals had a greater stroke volume than did the preceding systoles with smaller end-diastolic dimension. The faster the preceding paced rate, the greater was the increase in stroke volume (P less than 0.001). 5. Right ventricular dimensions and volumes were measured in vitro, and the relationship was found to be linear using regression analysis. 6. This study demonstrates that experimentally induced variations in heart rate produce changes in end-diastolic volume and contractility which prominently affect right ventricular stroke volume. As a consequence, rate has, over a broad range, either no significant effect on output or a negative one. With spontaneous variations in rate, additional changes in contractility and venous return occur which affect stroke volume and end-diastolic volume and enhance right ventricular output. These relationships are similar to those in the adult heart, and demonstrate the absence of a maturational change in the effects of rate on ventricular function from the fetus to the adult.
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
January 1976,
American journal of obstetrics and gynecology,
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
May 1983,
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P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
November 1981,
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P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
January 1984,
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P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
June 2012,
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P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
July 1959,
American journal of obstetrics and gynecology,
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
November 1976,
Obstetrics and gynecology,
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
January 2016,
Fetal diagnosis and therapy,
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
August 1975,
The American journal of physiology,
P A Anderson, and
A P Killam, and
R D Mainwaring, and
A E Oakeley
November 1985,
American journal of obstetrics and gynecology,
