|Statement||by Oskar Klotz.|
|The Physical Object|
|Pagination||p. 707-725,  leaf of plates :|
|Number of Pages||725|
ISBN: OCLC Number: Notes: Cover title. "Reprinted from the Journal of experimental medicine, vol. XII, no. 6, ". We agree with Jores and others that not one but many factors may be at work leading to intimal hyperplasia. Among these factors may be mentioned infection, bacterial toxins, organic poisons, inflammation and increased arterial tension. The theory of Thoma that the connective tissue developed in the intima is compensatory cannot be sustained. CONCERNING COMPENSATORY HYPERPLASIA OF THE INTIMA. By Oskar Klotz. Abstract. From the evidence which we have at hand it is not possible to state that the proliferative changes in the intima are uniformly secondary to the weakening of the media. Common influences may act simultaneously upon the media and the : Oskar Klotz. 1. Author(s): Klotz,Oskar, Title(s): Concerning compensatory hyperplasia of the intima/ by Oskar Klotz. Country of Publication: United States Publisher.
CONCERNING COMPENSATORY HYPERPLASIA OF THE INTIMA - CORE. Kaiser et al. have shown that concentric intimal hyperplasia was associated with the accumulation of PDGF producing multinucleated giant cells and macrophages at the intima–media junction. Excessive production of MMPs by macrophages causes oxidative injury in the artery resulting in destruction of internal elastic lamina and aids in the. Intimal hyperplasia refers to a process in which the intima becomes thickened due to the presence of vascular smooth muscle cells and proteoglycan-rich extracellular matrix located between the endothelium and the internal elastic lamina (Figure ).This pathologic change is also referred to as neointimal hyperplasia and intimal thickening, in different settings. David L. Stocum, in Regenerative Biology and Medicine (Second Edition), 1 Compensatory Hyperplasia. Compensatory hyperplasia is the proliferation of cells while they maintain their differentiated structure and function. The classic example is liver regeneration (Michalopoulos and DeFrances, ; Trembly and Steer, ).After partial hepatectomy the hepatocytes of the liver, as .
Intimal hyperplasia is not a true disease, but a physiologic healing response to injury to the blood vessel wall.. It is the bane of endovascular intervention and vascular surgery. When the endothelium is injured, endothelial cells release inflammatory mediators that trigger platelet aggregation, fibrin deposition and recruitment of leukocytes to the area. Read Volume 12 Issue 6 of Journal of Experimental Medicine. Intimal Hyperplasia. The blood vessel intima is normally composed of just the thin endothelial cell lining of the vasculature. Intimal hyperplasia reflects additional biomass (cellular and matrix) within this layer. Mammals appear to have evolved intimal hyperplasic processes so that they become survival benefits. The earliest visualizable lesion of atherosclerosis is the fatty streak, which is an accumulation of lipid-laden macrophages in the vascular intima (FIGURE , FIGURE ). 4 Fatty streaks can be appreciated grossly as focal yellow areas of discoloration of intimal lipid-laden macrophages are often referred to as foam cells because of their foamy appearance.