Alterations in systemic arterial mechanical properties during septic shock: role of fluid resuscitation.
The effects of septic shock (endotoxin; EDTX) 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 3 h of EDTX 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, the EDTX + fluids group responded with decreased TPR (-30%, P < 0.05), a tendency to increase 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 EDTX 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.
Cholley
B P
BP
Department of Medicine, University of Chicago, Illinois 60637, USA.
Lang
R M
RM
Berger
D S
DS
Korcarz
C
C
Payen
D
D
Shroff
S G
SG
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000502:physiology; D001158:Arteries / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D004548:Elasticity / Q000187:drug effects; D004731:Endotoxins / Q000494:pharmacology; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D011817:Rabbits; D012039:Regional Blood Flow; D012151:Resuscitation; D012772:Shock, Septic / Q000139:chemically induced / Q000503:physiopathology*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction
D004731:Endotoxins; D009599:Nitroprusside