Pan-Dong Ryu

Primo vascular system (PVS) discovered in 1960s is now considered as a novel vascular system composed of nodes and vessels. Previously we observed that the size of the organ surface PVS tissue samples and the number of red-colored tissue are larger in the rats with heart failure (HF) [1], or hemolytic anemia [2]. Based on these and other previous observation [3], we hypothesized that the reduced tissue perfusion in both disease models induces sympathetic hyperactivation which in turn brings the morphological changes in the PVS tissues. Here, we first examined whether exercise training also inhibit the HF-induced-morphological changes in the PVS since exercise training is known to reduce the elevated sympathetic tone in HF [4]. HF model rats were prepared by ligating the left descending coronary artery. In HF rats, we observed an increase in the size of the primo nodes (p<0.01), the number of the PVS tissue samples per rat (p<0.05), the proportion of PVS tissue samples with red chromophore (p<0.001), and the number of RBCs (p<0.001) in the primo nodes. Exercise training ameliorated these HF-induced changes in the PVS. Blocking sympathetic activity with 6-hydroxydopamine, a chemical sympathectomy agent dramatically reduced the number of samples per rat in normal rats. In the rats with hemolytic anemia induced by phenylhydrazine, the treatment of 6-hydroxydopamine also normalized the enlarged primo node size (p<0.05) and the elevated proportion of the tissues with red chromophore (p<0.001). The increase in the size and number of the samples per rat was induced by administration of noradrenaline via subcutaneous osmotic pump. In contrast, the incidence of the tissue with red chromophore was not altered by noradrenaline. The noradrenaline-induced enlargement of the PVS tissue were blocked in the rat treated with propranolol (b-adrenoceptor antagonist), but not with phentolamine (a-adrenoceptor antagonist). Taken together, the results indicate that sympathetic stimulation may induce the enlargement of PVS tissue via b -adrenoceptor in the rats with heart failure or hemolytic anemia. This study newly provides experimental evidence for sympathetic modulation of the PVS tissue and will help understand the pathophysiological roles of the PVS in health and disease states.