• Critical care medicine · Feb 2012

    Comparative Study

    Tetrastarch sustains pulmonary microvascular perfusion and gas exchange during systemic inflammation.

    • Anke Schuster, Udo Schumacher, Bjoern Winkelmann, and Annika Basedow.
    • Department of Anesthesiology, the Cardiovascular Research Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
    • Crit. Care Med.. 2012 Feb 1;40(2):518-31.

    ObjectiveAccording to Fick's law of diffusion, gas exchange depends on the size and thickness of the blood perfused alveolocapillary membrane. Impairment of either one is tenuous. No data are available concerning the impact of hydroxyethyl starches and saline on pulmonary microperfusion and gas exchange during systemic inflammation.DesignProspective, randomized, controlled experimental study.SettingUniversity research laboratory.SubjectsThirty-two anesthetized rabbits assigned to four groups (n = 8).InterventionsExcept for the control group, systemic inflammation was induced by lipopolysaccharide. Fluid resuscitation was performed with saline alone or in conjunction with tetrastarch or pentastarch. Pulmonary microcirculation was analyzed at 0 hr and 2 hrs using intravital microscopy. Thickness of the alveolocapillary membrane was measured using electron microscopy.Measurements And Main ResultsMacrohemodynamics were stable in all groups. In pulmonary arterioles, lipopolysaccharide reduced the erythrocyte velocity and impeded the microvascular decrease of the hematocrit in the saline and pentastarch group. In contrast, infusion of tetrastarch normalized these perfusion parameters. In capillaries, lipopolysaccharide decreased the functional capillary segment density and the capillary perfusion index, which was prevented by both starches. However, compared with saline and pentastarch, treatment with tetrastarch prevented the lipopolysaccharide-induced reduction of the capillary erythrocyte flux and inversely reduced the erythrocyte capillary transit time. Thickening of alveolocapillary septae after lipopolysaccharide application was solely observed in the saline and pentastarch group. In contrast to pentastarch and saline, the application of tetrastarch prevented the lipopolysaccharide-induced increase of the alveoloarterial oxygen difference.ConclusionsTetrastarch sustains pulmonary gas exchange during experimental systemic inflammation more effectively than saline and pentastarch by protecting the diffusion distance and the size of the microvascular gas exchange surface. Improved capillary perfusion resulting from tetrastarch therapy, which is typically applied to increase blood pressure, may according to the Ohm's law locally decrease hydrostatic perfusion pressures in the pulmonary microvasculature during systemic inflammation.

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