Microcirculatory perfusion is improved with plasma, but not with crystalloids, in a rat polytraumatic shock model

Traumatic shock is associated with microcirculatory dysfunction. Plasma resuscitation for traumatic shock outside the context of bleeding may exert benefit by augmenting intravascular volume and inhibiting endotheliopathy. However, its effects on microcirculatory perfusion and tissue oxygenation in trauma remain poorly understood.

Following polytraumatic injury and shock induction with controlled bleeding, rats (n = 11) received crystalloids or plasma until mean arterial pressure (MAP) was 65 mmHg for 2 h, after resuscitation was stopped. Total vessel density (TVD), functional capillary density (FCD), proportion of perfused vessel density (PPV), and tissue red blood cell perfusion (tRBCp) were evaluated. Microcirculatory oxygen availability (μHbO_2sat) was measured by tissue spectroscopy. Plasma hyaluronan and sVCAM were assessed for endothelial integrity.

After resuscitation, MAP was restored in both groups. However, TVD, FCD, and tRBCp were impaired in the crystalloid group as compared to the sham (p < 0.05), which did not occur in the plasma group. tRBCp was significantly improved by plasma resuscitation compared to crystalloid (p < 0.05). After resuscitation had stopped, TVD, FCD, and tRBCp remained significantly higher in the plasma group compared to the crystalloid group (p < 0.05). sVCAM decreased significantly by plasma compared to crystalloid (p < 0.05). There was no significant change in hyaluronan and μHbO_2sat levels.

Plasma, but not crystalloids, preserved microcirculatory diffusion and perfusion, which was associated with correction of endothelial functionality in rats requiring fluids following traumatic shock. Results suggest that plasma may be used in traumatic shock patients with persistent need of volume after bleeding has been contained.