Control of Glycogenolysis and Hemodynamics in Perfused Rat Liver by the Sympathetic Innervation. Dependence on Stimulation Frequency and Duration

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Abstract
Perivascular stimulation of the hepatic nerves in the situ perfused rat liver with a constant frequency of 20 Hz over a constant period of 5 min had previously been shown to cause an increase of glucose output, a shift from lactate uptake to release, a reduction in perfusion flow (Hartmann et al. (1982) Eur. J. Biochem. 123, 521-526) and an overflow of noradrenaline into the hepatic vein (Beckh et al. (1982) FEBS Lett. 149, 261-265). In the present study the dependence of the metabolic and hemodynamic effects on the frequency between 1 and 30 Hz and duration of stimulation between 0.5 and 5 min was investigated. 1) Over a constant stimulation period of 5 min the alteration in glucose exchange was maximal with a frequency of 10 Hz and half-maximal with 4 Hz. The corresponding values for the exchange of lactate were 5 Hz and 2 Hz, respectively, and for the perfusion flow 2.5 Hz and 1.5 Hz, respectively. An increase of noradrenaline overflow was not observed with the lower frequencies of 1 and 2.5 Hz: it was maximal at 10 Hz and half-maximal at 6.5 Hz. 2) At a constant frequency of 20 Hz the increase in glucose release was maximal with a total stimulation period of 1 min and half-maximal with a period of 0.4 min. An essentially maximal alteration of lactate exchange and perfusion flow as well as of noradrenaline overflow was also effected by a stimulation period of 1 min. 3) At a constant stimulation period of 5 min the time to peak (maximal alteration) amounted to about 7 min for glucose release and to 1 min for noradrenaline overflow at all frequencies; it decreased for perfusion flow from 4 min at a frequency of 1 Hz to 2 min at 10 Hz. 4) At a constant frequency of 20 Hz the time to peak increased with glucose release from 4 min after a stimulation period of 0.5 min to 7 min after a period of 5 min. It amounted to 2 min for perfusion flow and to 1 min with noradrenaline overflow at all durations of stimulation. 5) The alterations of glucose release and lactate exchange were not correlated to the changes in perfusion flow or in noradrenaline overflow. It is concluded from the present results that in the model of the in situ portally perfused rat liver perivascular stimulation of the hepatic nerves causes metabolic effects within the physiological range of frequencies of nerve discharges and that the model is therefore well suited for in vitro studies of the metabolic effects of hepatic nerves. The findings furthermore suggest that the alterations in glucose and lactate exchange cannot be caused by the hemodynamic changes nor by the noradrenaline overflow from the vascular nerve endings.

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