Hemodynamic changes in early pregnancy in chronically instrumented,
conscious rats.
Slangen, Brigitte F. M., Iris C. M. Out, Carla M. Verkeste, Louis L.
H. Peeters.
Department of Obstetrics and Gynecology, University of Limburg,
6200 MD Maastricht, The Netherlands
APStracts 2:0539H, 1995.
To explore the onset of, and the interrelationship between maternal
hemodynamic changes in pregnancy, serial hemodynamic measurements
were performed in chronically instru mented, conscious rats by using
electromagnetic flow probes around the ascending aorta and arterial
catheters. The rats were studied daily from day 4 until day 12, and
on day 14, 18 and 20 of pregnancy. Nonpregnant (NP) rats, matched for
age and days postsurgery served as controls. In the pregnant (P)
group, the hematocrit started to decrease by postconceptional day 6
(day of implantation) to reach a value of 9 +/- 3% below the initial
level, by day 8. In these 2 days cardiac output (CO) increased by 9
+/- 4%, as a result of a rise in stroke volume (SV). No changes in
mean arterial pressure were observed. In both groups, heart rate (HR)
had decreased by day 7. Aortic flow acceleration and peak aortic
flow, indicators of myocardial contractility, increased from day 10
on, only in the P group. In this context it should be emphasized that
the results of this study do not allow differentia tion between the
contractile properties of the cardiac muscle and the contractile
changes as a result of the altered preload and afterload. By day 12
and day 18, CO had increased by 20 +/- 5% and 29 +/- 9%,
respectively, above the initial value. CO had increased by 25% and
40%, respectively, above the value observed in the NP group, by day
12 and day 18. The rise in CO after day 14 was accomplished by a
concomitant increase in HR and SV and was accompanied by a further
increase in myocardial performance. We conclude that hemodynamic
changes can already be identified by day 8 of rat pregnan cy, 2 days
after implantation. The rise in CO in early pregnancy results from a
selective increase in SV and is accompanied by a rise in myocardial
performance.
Received 11 July 1995; accepted in final form 22 November 1995.
APS Manuscript Number H640-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95