2121258a0Nature212506719661210125812590028-0836196610.1038/2121258a0ukNatureNatureNATUREnatureNature is a weekly international journal publishing the finest peer-reviewed research in all fields of science and technology on the basis of its originality, importance, interdisciplinary interest, timeliness, accessibility, elegance and surprising conclusions. Nature also provides rapid, authoritative, insightful and arresting news and interpretation of topical and coming trends affecting science, scientists and the wider public./nature/journal/v212/n5067issueJournal homeArchiveCurrent issueAdvance online publicationPrivacy policySubscribeNature Publishing GroupCurrent issue2121258a0Vascular Lesions due to Obstruction of the Vasa Vasorum
AU  - NAKATA, YUKIFUMI
AU  - SHIONOYA, SHIGEHIKOFirst Department of Surgery, Nagoya University School of Medicine, Nagoya, Japan.DISTURBANCE of the vasa vasorum is probably a major factor in the aetiology of various vascular lesions such as cervical rib syndrome, medionecrosis, arteriosclerosis, and pulseless disease1. Various experimental methods of destroying the vasa vasorum have been reported2,3. These involve crushing or dissecting the adventitia, or applying acids and thermocautery to the outside of the vascular wall. We have found no references to any method involving disturbance of the vasa vasorum alone, however. This communication describes an experimental procedure designed to obstruct the vasa vasorum alone.Fifty-eight young mongrel dogs weighing about 10 kg were used. The abdominal aorta was clamped between the renal arteries and the aortic bifurcation, and all branches arising from this abdominal segment were clamped as well. A mixture of 2,000 u of thrombin and 2 g of e-amino-caproic acid in 50 ml. of 10 per cent gelatine-saline was injected into the abdominal aorta at a pressure of 150-200 mm of mercury over 2-3 min at 38 C. Five min after the injection the fluid in the aortic lumen was flushed out through an incision at the distal end of the aorta, all clamps were removed, and bleeding points were brought under control using black silk stitches. The vasa vasorum of the aortic wall thus became blocked by newly produced emboli. The obstruction of the vasa vasorum was confirmed by injecting Berlin blue solution or by taking microangiograms4'5. In control experiments, physiological saline was injected instead of the thrombin mixture.
Dogs were killed at intervals after the operation, and specimens from the abdominal aorta were studied histopathologically.
Fig. 1. Transverse section of abdominal aorta 2 weeks after operation. Thickening of the intima and destruction of the media are seen. (Elastica Van Gieson, x 30.)
Fig. 2. Microangiogram of transverse section 1 mm thick in the region shown in Fig. 1. In the outer part of the media and the adventitia (at bottom), only a few vasa vasorum without anastomoses can be seen. (x c. 25.)
Three days after the operation, the intima showed a slight thickening. After 1-4 weeks, the intima showed a marked thickening with proliferation of muscle cells, production of elastic and collagen fibres, and an increase in the amount of substance stained by metachrome. Muscle cells and elastic fibres in the media were destroyed. After 6-8 weeks there was marked fibrosis of the vessel walls and deposition of lipid in the hypertrophied intima.
Thus, obstruction of the vasa vasorum alone in the abdominal aorta of the dog produced arteriosclerotic vascular lesions such as marked thickening of the intima, destruction of the media, and fibrosis of the vessel wall. It seems reasonable to assume that these vascular damages were produced by a disturbance of nutrition and flow of tissue fluid in the aortic wall after obstruction of the vasa vasorum.
These observations tend to confirm that disfunction of the vasa vasorum plays an important part in the patho-genesis of vascular lesions.Schlichter, , J. G., Katz, , J. G., and Meyer, , J., Amer. J. Med. Sci., 218, 603 (1949).PubMedISIChemPortSchlichter, , J. G., Arch. Pathol., 42, 182 (1946).ISIHoffmann, , E., Langenbecks Arch. Klin. Chir., 305, 257 (1964).ArticleChemPortSmetana, , H., Virchows Arch., 274, 170 (1930).Clarke, , J. A., Z. Zellforsch. Mikros. Anat., 66, 212 (1965).ISIChemPort