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Is β-adrenergic receptor stimulation crucial for splanchnic O2availability in septic shock?


Septic shock is characterized by arterial hypotension despite adequate fluid resuscitation, and treatment with vasopressors is current practice [1]. Vasopressors, however, may impair capillary exchange capacity in the splanchnic region [2]. Therefore we tested the effect of replacing noradrenaline (NOR) by phenylephrine (PHE) on splanchnic hemodynamics and O2 kinetics in septic shock.


In up to now four patients with hyperdynamic septic shock (CI ≥ 41/min/m2) all requiring NOR (0.25 ± 0.22 μg/kg min) to maintain mean arterial pressure NOR was replaced by PHE (4.2 ± 3.9 μg/kg min) adjusted to achieve similar systemic hemodynamics. In addition to global oxygen delivery (DO2sys) and uptake (VO2sys) (indirect calorimetry) we measured gastric intramucosal pH (pHi) as well as splanchnic blood flow (Qspl), O2 delivery (DO2spl) and uptake (VO2spl) using the indocyanine-green steady state-infusion technique corrected for hepatic dye extraction. Data were obtained after at least 2 h of stable hemodynamic conditions.


See table.


Replacing NOR by PHE selectively reduced Qspl and DO2spl without influencing pHi. Since VO2sys remained constant, this fall in Qspl, however, was unlikely to be to due to reduced regional O2 demands resulting from decreased β-adrenergic receptor-mediated thermogenesis [3]. Suppression of β-receptor stimulation, hence, may cause supply-dependency of VO2spl in septic shock.



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Reinelt, H., Kiefer, P., Fischer, G. et al. Is β-adrenergic receptor stimulation crucial for splanchnic O2availability in septic shock?. Crit Care 1 (Suppl 1), P080 (1997).

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