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Articles in PresS, published online ahead of print December 5, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00626.2002
Submitted on July 19, 2002
Accepted on November 25, 2002
1 Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, OR, USA
2 Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, OR, USA; Department of Medicine (Cardiology), Portland VA Medical Center, Portland, OR, USA
3 Department of Comparative Medicine, Oregon Health and Science University, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: brooksv{at}ohsu.edu.
Pregnant animals are less able to maintain mean arterial pressure (MAP) during hemorrhage compared to nonpregnant animals, but the hemodynamic basis of this difference is unknown. The hypothesis that pregnancy attenuates responses of cardiac output, as well as total peripheral resistance (TPR) and femoral conductance, to hemorrhage was tested in conscious rabbits in both the pregnant (P) and nonpregnant (NP) state (n=10). During continuous, slow blood loss (2% of the initial blood volume per min), MAP was maintained initially in both groups. However, MAP then abruptly decreased to below 45 mmHg in all animals, but after a smaller percentage of the initial blood volume was removed in P compared to NP rabbits (43.6±1.7%, NP; 29.6±2.2%, P; p<0.005). The more rapid transition to hypotension exhibited by P rabbits was associated with greater initial falls in cardiac output (-56±10 ml/min, NP; -216±33 ml/min, P; p<0.005) and stroke volume (0.8±0.1 ml/beat, NP; -1.3±0.1 ml/beat, P; p<0.05). In addition, the increase in TPR as a function of the decrease in cardiac output was markedly attenuated (p<0.0001) during pregnancy. While femoral conductance decreased in NP rabbits, it did not change significantly in P animals. In conclusion, the lesser ability of conscious, pregnant rabbits to maintain MAP during hemorrhage is due largely to a greater decrease in cardiac output, but also to inadequate reflex increases in TPR, possibly in part in the femoral vascular bed.
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