Alterations in systemic arterial mechanical properties during septic shock: role of fluid resuscitation. Cholley, Bernard P., Roberto M. Lang, David S. Berger, Claudia Korcarz, Didier Payen, Sanjeev G. Shroff. Cardiology Section, Department of Medicine, University of Chicago, Chicago, Illinois 60637 and Laboratoire de Recherche en Anesth[acute]esie -R[acute]eanimation, H[circumflex]opital Lariboisi[grave]ere, 2, rue Ambroise Par[acute]e, 75010, Paris, France
APStracts 2:0026H, 1995.
The effects of septic shock (endotoxin) on arterial mechanical properties were studied in anesthetized rabbits, both in the absence (EDTX-alone) and presence (EDTX+Fluids) of fluid resuscitation. Aortic pressure-flow (n=20) and pressure-diameter (n=10) measurements were used to calculate systemic arterial and regional aortic mechanical properties. At three hours of endotoxin shock, EDTX-alone rabbits had elevated total peripheral resistance (TPR, +30%, P<0.05), reduced cardiac output (CO, -40%, P<0.05), and increased aortic characteristic impedance (Zc, +78%, P<0.05). In contrast, EDTX+Fluids group responded with decreased TPR (-30%, P<0.05), a tendency to increase cardiac output (CO, +23%), and elevated Zc (+46%, P<0.05). A reduction in aortic diameter (-20%, P<0.05) and an increase in elastic modulus (+50%, P<0.05) and water content (+23%, P<0.02) of the aortic wall were observed following endotoxemia. Thus, following endotoxin: (1) "hyperdynamic" septic shock profile (i.e., low TPR, high CO) was observed only when concomitant fluid replacement was provided; (2) aortic wall stiffening was present, due to both increased smooth muscle tone and vessel wall edema; and (3) fluid resuscitation resulted in discordant changes in TPR and Zc, suggesting differential flow-induced vasodilation between arteriolar and aortic smooth muscle.

Received 20 October 1994; accepted in final form 27 January 1995.
APS Manuscript Number H937-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 24 February 1995.