[The regression of medial smooth muscle in host arteries supplying human cancers and its functional significance].
The hemodynamics prevailing in cancer tissue are known to be quite abnormal, at least in some cases, in that the tumor vessels are inert to vasoactive stimuli, a feature that has been exploited in the development of pharmacoangiography or induced hypertension chemotherapy. However, not only has this feature yet to be correlated with the structural changes occurring in the vascular wall, but also the remarkable differences existing among cancer patients in its manifestation await future elucidation. In a series of human cancers, we have been aware of peculiar degenerative changes differently involving the medial smooth muscle of tumor-supplying host arteries, which we have assumed act together with the muscular, newly formed "tumor vessels" in creating the abnormal reactivity of cancer blood flow, at the same time accounting for its wide variability. From this viewpoint, cancer-supplying host arteries were submitted to morphometry of their medial smooth muscle in 30 surgical specimens of carcinoma of the stomach or colon, and in 30 autopsied livers with hepatocellular carcinoma. In GI cancers it was disclosed that the percentage volume of smooth muscular cells in the medial layer, as high as 80% in segments of unaffected artery located at a distance from a cancer, rapidly fell to 30% or less as it reached and penetrated into a tumor, and that at the tumor center, a host artery was often transformed into a dilated sac with a purely collagenous wall. Morphometry of hepatocellular carcinoma also demonstrated unambiguous atrophy of the medial muscular layer of host hepatic arteries, which was shown to be significantly thinner than in control specimens even at a distance from the cancer. This too, was interpreted to be a contributory factor in the cancer circulation typically devoid of regulatory activity. We stress that the functional significance of these features of tumor-supplying host arteries should be taken into consideration when studying the behavior of individual cancers in arteriography, pharmacoangiography or induced hypertension chemotherapy.
D001158:Arteries / Q000473:pathology; D006528:Carcinoma, Hepatocellular / Q000098:blood supply; D003110:Colonic Neoplasms / Q000098:blood supply; D006439:Hemodynamics; D006801:Humans; D008113:Liver Neoplasms / Q000098:blood supply; D009131:Muscle, Smooth, Vascular / Q000473:pathology*; D009369:Neoplasms / Q000098:blood supply* / Q000473:pathology; D013274:Stomach Neoplasms / Q000098:blood supply