多巴酚丁胺诱导的内脏血流增加对感染性休克患者肝脏代谢活性的影响。

Effects of a dobutamine-induced increase in splanchnic blood flow on hepatic metabolic activity in patients with septic shock.

作者信息

Reinelt H, Radermacher P, Fischer G, Geisser W, Wachter U, Wiedeck H, Georgieff M, Vogt J

机构信息

Sektion Operative Intensivmedizin, Universitätsklinik für Anästhesiologie, Klinikum der Universität, Ulm, Germany.

出版信息

Anesthesiology. 1997 Apr;86(4):818-24. doi: 10.1097/00000542-199704000-00012.

DOI:10.1097/00000542-199704000-00012

PMID:9105226

Abstract

BACKGROUND

Septic shock leads to increased splanchnic blood flow (Qspl) and oxygen consumption (VO2spl). The increased Qspl, however may not match the splanchnic oxygen demand, resulting in hepatic dysfunction. This concept of ongoing tissue hypoxia that can be relieved by increasing splanchnic oxygen delivery (DO2spl), however, was challenged because most of the elevated VO2spl was attributed to increased hepatic glucose production (HGP) resulting from increased substrate delivery. Therefore the authors tested the hypothesis that a dobutamine-induced increase in Qspl and DO2spl leads to increased VO2spl associated with accelerated HGP in patients with septic shock.

METHODS

Twelve patients with hyperdynamic septic shock in whom blood pressure had been stabilized (mean arterial pressure > or = 70 mmHg) with volume resuscitation and norepinephrine received dobutamine to obtain a 20% increase in cardiac index (CI). Qspl, DO2spl, and VO2spl were assessed using the steady-state indocyanine green clearance technique with correction for hepatic dye extraction, and HGP was determined from the plasma appearance rate of stable, non-radio-active-labeled glucose using a primed-constant infusion approach.

RESULTS

Although the increase in CI resulted in a similar increase in Qspl (from 0.91 +/- 0.21 to 1.21 +/- 0.34l.min-1.m2; P < 0.001) producing a parallel increase of DO2spl (from 141 +/- 33 to 182 +/- 44 ml.min-1.m2; P < 0.001), there was no effect on VO2spl (73 +/- 16 and 82 +/- 21 ml.min-1.m2, respectively). Hepatic glucose production decreased from 5.1 +/- 1.6 to 3.6 +/- 0.9 mg.kg-1.min-1 (P < 0.001).

CONCLUSIONS

In the patients with septic shock in whom blood pressure had been stabilized with volume resuscitation and norepinephrine, no delivery-dependency of VO2spl could be detected. Oxygen consumption was not related to the accelerated HGP either, and thus the concept that HGP dominates VO2spl must be questioned in well-resuscitated patients with septic shock.

摘要

背景

感染性休克会导致内脏血流量（Qspl）和氧耗量（VO2spl）增加。然而，增加的Qspl可能无法满足内脏的氧需求，从而导致肝功能障碍。然而，这种持续组织缺氧的概念可通过增加内脏氧输送（DO2spl）来缓解，这一观点受到了挑战，因为大部分升高的VO2spl归因于底物输送增加导致的肝脏葡萄糖生成（HGP）增加。因此，作者检验了以下假设：在感染性休克患者中，多巴酚丁胺诱导的Qspl和DO2spl增加会导致VO2spl增加，并伴有HGP加速。

方法

12例高动力型感染性休克患者，经液体复苏和去甲肾上腺素治疗后血压已稳定（平均动脉压≥70 mmHg），给予多巴酚丁胺以使心脏指数（CI）增加20%。使用稳态吲哚菁绿清除技术并校正肝脏染料摄取来评估Qspl、DO2spl和VO2spl，采用首剂-恒速输注法通过稳定的、非放射性标记葡萄糖的血浆出现率来测定HGP。

结果

尽管CI增加导致Qspl出现类似程度的增加（从0.91±0.21升至1.21±0.34 l·min-1·m2；P<0.001），DO2spl也随之平行增加（从141±33升至182±44 ml·min-1·m2；P<0.001），但对VO2spl没有影响（分别为73±16和82±21 ml·min-1·m2）。肝脏葡萄糖生成从5.