• C O Corso, S Okamoto, R Leiderer, and K Messmer.
• Institute for Surgical Research, Munich University, Munich, D-81366, Germany.
• J. Surg. Res. 1998 Dec 1; 80 (2): 210-20.

BackgroundHemorrhagic shock severely compromises hepatic microcirculation and function with tendency to promote hepatic insufficiency and multiple organ failure.Material And MethodsThe aim of the study was to evaluate the effects of small volume resuscitation on liver microcirculation (intravital fluorescence microscopy and electron microscopy) and function (arterial ketone body ratio (AKBR) and bile flow), in a rat model of traumatic-hemorrhagic shock. One hour after hemorrhage (MAP 40 mm Hg) the rats were resuscitated with HSD (7.2% NaCl/10% dextran 60, 10% of shed blood/2 min, n = 8); DEX (6% dextran 60, 100% of shed blood/5 min, n = 8); or RL (Ringer lactate, 400% of shed blood/20 min, n = 6).ResultsHSD yielded a better recovery of sinusoidal perfusion (17.8 +/- 0.8% nonperfused sinusoids) than DEX (21.8 +/- 0. 7%, P < 0.05) and RL (23.9 +/- 0.9%, P < 0.01). Hemorrhagic shock produced a moderate increase of mean sinusoidal endothelial cell thickness, which was further enhanced by DEX and RL (P < 0.05 vs baseline), whereas HSD reduced the mean endothelial cell thickness toward baseline (P < 0.05 vs DEX and RL). Both AKBR and bile flow were profoundly reduced after 1 h shock. Resuscitation with DEX and RL produced a weak recovery, still remaining at shock level, while HSD infusion allowed a significant improvement of AKBR and bile flow (P < 0.05 vs shock).ConclusionReduction of mean endothelial cell thickness after HSD is very likely the mechanism for the amelioration of sinusoidal perfusion, resulting in a significant improvement of hepatic energetic status and excretory function.Copyright 1998 Academic Press.

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