Catecholamine release from isolated guinea pig lungs during sympathetic stimulation with varied ventilation and perfusion

This study was performed to elucidate catecholamine release in the pulmonary circulation of isolated lungs due to the sympathetic nerve stimulation and to assess the experimental conditions which can modify the release, i.e., stimulus intensify, ventilation state of the lung and flow rate of perfusion. In artificially ventilated lungs, electrical stimulation of stellate ganglions evoked large noradrenaline efflux from the lung, but adrenaline efflux was below the detection limit, and dopamine was not detected in any case. In the unventilated preparations, the lung parenchyma were not bleached and the arterial pressure was significantly higher than in ventilated preparations. Noradrenaline efflux from the unventilated group was significantly lower than that from the ventilated preparations. The effect of the perfusion flow rate was investigated under pressure-operated ventilation. The pulmonary arterial pressure (Pa) was not varied at 5-10 ml min(-1), but it was increased significantly at 20 ml min(-1). Noradrenaline efflux was also increased significantly at 20 mi min(-1). These results indicate that noradrenaline was the catecholamine exclusively released from pulmonary vasculature due to the sympathetic nerve stimulation, and that both ventilation and the perfusion flow rate could affect the release. The concomitant increase in arterial pressure indicates that noradrenaline efflux would be affected by the alteration in resistive small arteries. Circulatory change in these arteries is supposed to be one of the factors that modify noradrenaline release from the lungs. The analysis of noradrenaline should be a useful method to evaluate the sympathetic effect on the pulmonary vasculature.