Resuscitation with hypertonic saline dextran reduces endothelial cell swelling and improves hepatic microvascular perfusion and function after hemorrhagic shock

Background. Hemorrhagic shock severely compromises hepatic microcirculation and function with tendency to promote hepatic insufficiency and multiple o rgan failure. Material and methods. The aim of the study was to evaluate the effects of s mall volume resuscitation on liver microcirculation (intravital fluorescenc e microscopy and electron microscopy) and function (arterial ketone body ra tio (AKBR) and bile flow), in a rat model of traumatic-hemorrhage shock. On e 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), Results. HSD 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 an d 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 how were profoundly reduced after 1 h shock. Resuscitation with DEX and RL prod uced a weak recovery, still remaining at shock level, while HSD infusion al lowed a significant improvement of AKBR and bile flow (P < 0.05 vs shock). Conclusion. Reduction of mean endothelial cell thickness after HSD is very likely the mechanism for the amelioration of sinusoidal perfusion, resultin g in a significant improvement of hepatic energetic status and excretory fu nction. (C) 1998 Academic Press.