OBJECTIVE: Arginine vasopressin (AVP) is being used increasingly to treat vasodilatory hypotension, although its effects on hepatosplanchnic perfusion have been debated. DESIGN: Prospective study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: We compared the effect of AVP on systemic, gut, and liver blood flow in anesthetized and ventilated rabbits given either saline or endotoxin. Incremental i.v. boluses of AVP ranging from 1 to 1,000[Symbol: see text]ng were administered 90[Symbol: see text]min post-endotoxin or saline. MEASUREMENTS AND RESULTS: Endotoxin induced a shock state with a transient decrease of mesenteric artery blood flow velocity (pulsed Doppler, in centimeters per second, V(mes)) but had no effect on liver surface microcirculation (laser Doppler in TPU, MicroFl(liver)). Gut microcirculatory (MicroFl(gut)) changes became independent of mean arterial pressure (MAP) after endotoxin. In control rabbits (n = 5), increasing doses of AVP elevated MAP but reduced aortic blood flow (pulsed Doppler, VAo), V(mes), and MicroFl(gut) (p < 0.05). In endotoxic animals (n = 6), AVP produced a similar rise in MAP (p < 0.05), while V(mes) and MicroFl(gut) only decreased for AVP doses above 100[Symbol: see text]ng (p < 0.05). Liver microcirculation was only minimally affected by AVP, although significantly, both in control and endotoxin animals. CONCLUSION: Preservation of mesenteric blood flow as well as gut and liver microcirculation, with therapeutic doses of AVP during endotoxemia, supports its use as a hemodynamic agent during septic shock.
OBJECTIVE:Arginine vasopressin (AVP) is being used increasingly to treat vasodilatory hypotension, although its effects on hepatosplanchnic perfusion have been debated. DESIGN: Prospective study in a university-based experimental research laboratory. SUBJECTS AND INTERVENTIONS: We compared the effect of AVP on systemic, gut, and liver blood flow in anesthetized and ventilated rabbits given either saline or endotoxin. Incremental i.v. boluses of AVP ranging from 1 to 1,000[Symbol: see text]ng were administered 90[Symbol: see text]min post-endotoxin or saline. MEASUREMENTS AND RESULTS: Endotoxin induced a shock state with a transient decrease of mesenteric artery blood flow velocity (pulsed Doppler, in centimeters per second, V(mes)) but had no effect on liver surface microcirculation (laser Doppler in TPU, MicroFl(liver)). Gut microcirculatory (MicroFl(gut)) changes became independent of mean arterial pressure (MAP) after endotoxin. In control rabbits (n = 5), increasing doses of AVP elevated MAP but reduced aortic blood flow (pulsed Doppler, VAo), V(mes), and MicroFl(gut) (p < 0.05). In endotoxic animals (n = 6), AVP produced a similar rise in MAP (p < 0.05), while V(mes) and MicroFl(gut) only decreased for AVP doses above 100[Symbol: see text]ng (p < 0.05). Liver microcirculation was only minimally affected by AVP, although significantly, both in control and endotoxin animals. CONCLUSION: Preservation of mesenteric blood flow as well as gut and liver microcirculation, with therapeutic doses of AVP during endotoxemia, supports its use as a hemodynamic agent during septic shock.
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