Loss Of Glycocalyx Barrier Properties Impairs Insulin-Mediated Recruitment Of Microvascular Blood Volume In Rat Hind Limb Muscle

Experimental data suggest that a rapid increase in capillary blood volume underlies the insulin-mediated glucose uptake in skeletal muscle. We hypothesize that loss of glycocalyx properties impairs the ability of insulin to increase microvascular blood volume in skeletal muscle. In anesthetized rats, the hind limb muscle microcirculation was visualized with a Sidestream Dark Field camera before and during a 30 minute infusion of insulin (6mU/min/kg). Median values and dynamic range of red blood cell (RBC) column widths were measured to determine functional microvascular diameters and glycocalyx barrier function, respectively. In control rats (n=5), insulin infusion increased within five minutes the dynamic range of RBC width with 0.56 μm ± 0.19 μm (mean ± SEM) (P<0.05). Hereafter, microvascular diameter increased with 0.69 μm ± 0.22 μm (P<0.05), while the dynamic range of RBC width returned to pre-insulin values. In rats, in which the glycocalyx was degraded with a bolus of hyaluronidase (500U; n=7), the dynamic range was already increased at baseline levels with 0.30 μm ± 0.02 μm (p<0.05), with no further effect of insulin. Rapid insulin-mediated increases in microvascular blood filling in rat skeletal muscle appear to be preceeded by an attenuation of glycocalyx barrier properties. This ability of insulin is impaired after enzymatic degradation of the glycocalyx. Supported by DFN 2006.00.027 and NHF 2005T037