Effect of Sympathetic Nerve Stimulation on Net Transvascular Movement of Fluid in Canine Adipose Tissue

Abstract

Net transvascular movement of fluid has been studied in the isolated, autoperfused subcutaneous adipose tissue of the dog, during and after sympathetic nerve stimulation (1-15 Hz) and during infusion of 50% glucose i.a. Net fluid movement was calculated as the difference between change in tissue volume and change in blood volume. Tissue volume was measured by plethysmography and blood volume by external monitoring of circulating 131I-albumin. No net fluid movement of statistical significance was found during or after nerve stimulation except during the first minute of stimulation at 15 Hz when a small net absorption (p less than 0.05) was obtained. In contrast, infusion of glucose at 25-75 mOsm/kg H2O produced a dose-dependent net absorption lasting several minutes, amounting maximally to 0.30 ml x min-1 x 100 g-1. The absence of prolonged net absorption in subcutaneous adipose tissue during nerve stimulation as well as the absence of net filtration after stimulation may be explained by an essentially unaltered mean hydrostatic capillary pressure. The results indicate that adipose tissue does not contribute to the fluid homeostasis of the body via sympathetic resetting of the pre-postcapillary resistance ratio. Thus, mobilisation of fluid from the interstitial space in adipose tissue into the blood does not seem to occur by nerve activity.

Neural innervation of white adipose tissue and the control of lipolysis

“…Regarding the former, although there clearly is parenchymal sympathetic innervation of WAT [51;267;306] in addition to its innervation of WAT vasculature [267;305;306], it seems likely that some of the PRV tract tracing of the SNS outflow to WAT also includes this sympathetic blood vessel innervation. From a functional standpoint, the ability of the sympathetic WAT denervation to decrease or block lipolysis also could have, as part of its mechanism, a decrease in SNS-induced capillary permeability [185;186]. Thus, although the sympathetic innervation of WAT vasculature might appear to contribute caveats to the interpretations of the viral transneuronal tract tracing of the SNS outflow from the brain to WAT and to sympathetic denervation-induced decreases in lipid mobilization, neither caveat creates an interpretational nightmare.…”