Aortic distensibility and compliance in conscious pregnant rats.

Abstract

In pregnancy, complex hormonal and hemodynamic changes develop. In this study, we tested the hypothesis that these pregnancy-associated changes are accompanied by an alteration of the compliance of central conduit vessels. To this end, we determined in awake, restrained pregnant rats the distensibility (DC) and compliance (CC) coefficients of the descending thoracic aorta. End diastolic aortic diameter (d) and changes in aortic diameter during the cardiac cycle (delta d) were measured noninvasively by ultrasound, simultaneously with diastolic aortic blood pressure (Pdia) and pulse pressure (delta P) through a chronically implanted catheter. From these parameters, DC and CC (expressed as the relative and the absolute increase, respectively, in lumen cross-sectional area for a given increase in P) were calculated. Nine rats were studied before pregnancy and, on days 4, 8, 10, and 18 of pregnancy, were matched for age and days postsurgery with eight nonpregnant rats. On day 20, the animals were killed and the thoracic aorta was isolated for morphometric analysis. In the pregnant group, Pdia decreased from 109 +/- 5 mmHg on day 4 to 98 +/- 9 mmHg on day 18 (means +/- SD), whereas d did not change. delta d increased from 242 +/- 20 microm on day 4 to 271 +/- 29 microm on day 18. delta P did not change. Both DC and CC increased in early pregnancy to a plateau reached by day 10. The increase in DC and CC preceded the fall in Pdia. On day 20, neither cross-sectional area nor thickness of the aortic media had changed significantly, when compared with the nonpregnant group. In the nonpregnant group, none of the variables changed consistently during the study period. On the basis of these results, we conclude that CC of the thoracic aorta increases in early pregnancy. We speculate that the increased aortic CC and DC and the decreased total peripheral resistance develop in early pregnancy in response to the increase in stroke volume, thus preventing a concomitant rise in arterial wall stress.