PATHOLOGICAL STUDY ON PHLEBOSCLEROSIS

Abstract

In order to study the morphogenesis of phlebosclerosis and subsequently to obtain fundamental knowledges for understanding the genesis of arteriosclerosis, morphological studies were performed on the portal, splenic, and superior mesenteric vein, as well as the inferior vena cava under several conditions. The investigated 81 autopsy cases included 4 groups, that is, 1. cases in which luminal pressure of the portal vein or inferior vena cava was elevated, 7. cases with intense atherosclerosis particularly in the aorta, 3. with severe anemia and 4. controls without such diseases. The findings obtained were compared with experimental phlebosclerosis prcduced by investing the rabbit's portal vein with a silver cuff to increase its pressure. Results obtained from this study were as follow. 1. In the controls intimal thickening occurred initially in the inferior vena cava in the forties, and became visible also in the portal and superior mesenteric vein with advance in age. The thickening, however, measured below 20μ. 2. With increased venous pressure, cellulofibrous intimal thickening, consisting mainly of smooth muscle cells, fibroblast-like intimal cells, and collagenous and elastic fibers, was observed in the venous wall. Both venous hypertension and it's duration were important in the genesis of this intimal thickening. 3. Thrombus and intimai hemorrhage secondarily enhanced venous intimal thickening, but were not primary causes of the thickening. 4 Smooth muscle cells in the thickened intima of the vein were considered to be derived from both fibroblast-like intimal cells which were formed by endothelial cells dropped off, and medial muscle cells. 5 Human phlebosclerosis was different from arteriosclerosis in the following points. 1) Phlebosclerosis did not show atheroma, aggregation of foam cells, fatty swelling of collagenous fibers and calcification. However, foam cells were visible in the partially organiged thrombus. 2) In phlebosclerosis, the thickened intima was abundant with capillaries, and rich in intercellular ground-substance, but fibrosis was relatively poor. 3) Elastosis was poorer in phlebosclerosis than in arteriosclerosis, and such lamellar elastosis as seen in the renal artery was not observed in phlebosclerosis. 4) In contrast to arteriosclerosis, phlebosclerosis was accompanied by thrombus more frequently despite the absence of atheroma. These differences are considered to result probably because in tht vein as compared with the artery, the luminal pressure is lower, blood flow is slower, the wall is rich in vasa vasorum, the wall structure is relatively looser, and moreover the duration of which the high blood pressure stimulates on the vascular wall is shorter. 6. when the rabbit's portal vein was constricted by investment, intimal thickening resembling human phlebosclerosis was produced in both proximal and distal ends of the constricted part and in a site a little away to distal from it At periods of 24 days after operation swelling and proliferation of endothelial cells were observed, and on the 7th day after operation smooth muscle cells were seen in the intima 7. When the portal vein was constricted in cholesterol fed rabbits, foam cells appeared in the intima of the portal vein, but not formation of atheroma.