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The contribution of the intrapulmonary lobar veins to the increase in pulmonary vascular resistance in response to sympathetic stimulation was studied under conditions of controlled blood flow in the anesthetized dog in which vascular pressures were measured simultaneously in the perfused lobar artery, an intrapulmonary lobar vein 2-3 mm in diameter and in the left atrium. Stimulation of the stellate ganglia at 3, 10, and 30 cycles/s increased pressure in the lobar artery and small vein in a stimulus-related manner but decreased pressure in the left atrium. Injection of norepinephrine into the perfused lobar artery also increased pressure in the lobar artery and small vein but decreased pressure in the left atrium. The increase in lobar arterial and venous pressure in response to either injected norepinephrine or to nerve stimulation was antagonized by an alpha receptor blocking agent. The rise in pressure in both labor artery and small vein with nerve stimulation but not administered norepinephrine was inhibited by an adrenergic nerve terminal blocking agent. The results suggest that under conditions of steady flow, sympathetic nerve stimulation increases the resistance to flow in the lung by constricting pulmonary veins and vessels upstream to the small veins, and that at each stimulus-frequency studied approximately 50% of the total increase in resistance may be due to venoconstriction. It is concluded that the increase in resistance to flow in the lung in response to nerve stimulation is thre result of activation of alpha adrenergic receptors by norephinephrine liberated from adrenergic nerve terminals in venous segments and in vessels upstream to samll veins, presumed to be small arteries.

Influence of sympathetic stimulation and vasoactive substances on the canine pulmonary veins.