Key result
Fluid resuscitation during endotoxin-induced septic shock in rabbits produced a hyperdynamic profile with decreased total peripheral resistance and increased cardiac output.
Why the study?
Does fluid resuscitation alter systemic arterial mechanical properties in anesthetized rabbits with endotoxin-induced septic shock?
Does fluid resuscitation alter systemic arterial mechanical properties in anesthetized rabbits with endotoxin-induced septic shock?
Fluid resuscitation in endotoxin-induced septic shock produces a hyperdynamic profile but results in discordant changes in TPR and aortic characteristic impedance, indicating differential vasodilation.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for differential vasodilation in septic models; leaves open translation to human arterial mechanics and 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.
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Cholley et al. (1995) studied Septic shock (n=30). Fluid resuscitation vs. Endotoxin (EDTX) alone was evaluated on Total peripheral resistance (TPR) percent change (p=<0.05). Fluid resuscitation during endotoxin-induced septic shock in rabbits produced a hyperdynamic profile with decreased total peripheral resistance and increased cardiac output.
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