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      Modulation of Arterial Growth of the Rabbit Carotid Artery Associated with Experimental Elevation of Blood Flow

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          We examined the growth of the right common carotid artery of young rabbits after ligating the left common carotid artery at 3 weeks of age, a procedure that approximately doubled right carotid blood flows. Flow increased from 0.065 ± 0.003 to 0.096 ± 0.009 ml/s within 1 h and, at 15 weeks of age, carotid blood flows in experimental animals (0.747 ± 0.102 ml/s) were more than double of those of sham-operated control animals (0.334 ± 0.053 ml/s). Contralateral carotid ligation resulted in more rapid increases in diameter of the artery with growth in the experimental animals. At 15 weeks of age, the vessel was 15% larger than that of sham-operated controls (2.70 ± 0.09 vs. 2.34 ± 0.05 mm). This more rapid growth of diameter resulted in shear stresses that were not different from controls despite the higher blood flow rates. Interestingly, however, shear stresses in control arteries fell from 17.4 ± 3.4 to 9.19 ± 1.16 dyn/cm<sup>2</sup> over the experimental period (p < 0.05). Elastin accumulation in the experimental artery was much more rapid than in controls and elastin contents were 49% more than in controls at 15 weeks of age. DNA and collagen contents were not significantly affected by contralateral carotid ligation. Previously, we found that experimental manipulations that decreased flow in the same artery of weanling rabbits substantially affected elastin and DNA accumulation, but had no effect on collagen contents. We conclude that increased blood flow is associated with arterial growth and specifically with accumulation of elastin, a wall constituent that bears much of the wall tension at resting blood pressure, and therefore is a primary determinant of resting vessel dimensions.

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          Linkage of Marfan syndrome and a phenotypically related disorder to two different fibrillin genes.

          Marfan syndrome (MFS), one of the most common genetic disorders of connective tissue, is characterized by skeletal, cardiovascular and ocular abnormalities. The incidence of the disease is about 1 in 20,000, with life expectancy severely reduced because of cardiovascular complications. As the underlying defect is unknown, MFS diagnosis is based solely on clinical criteria. Certain phenotypic features of MFS are also shared by other conditions, which may be genetically distinct entities although part of a clinical continuum. Immunohistochemical studies have implicated fibrillin, a major component of elastin-associated microfibrils, in MFS aetiology. Genetic linkage analysis with random probes has independently localized the MFS locus to chromosome 15. Here we report that these two experimental approaches converge with the cloning and mapping of the fibrillin gene to chromosome 15q15-21, and with the establishment of linkage to MFS. We also isolated a second fibrillin gene and mapped it to chromosome 5q23-31. We linked this novel gene to a condition, congenital contractural arachnodactyly, that shares some of the features of MFS. Thus, the cosegregation of two related genes with two related syndromes implies that fibrillin mutations are likely to be responsible for different MFS phenotypes.
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            Developmental Regulation of Aortic Elastin Gene Expression Involves Disruption of an IGF-I Sensitive Repressor Complex


              Author and article information

              J Vasc Res
              Journal of Vascular Research
              S. Karger AG
              February 1998
              06 February 1998
              : 35
              : 1
              : 1-7
              Toronto Hospital Research Institute andDepartment of Pathology, University of Toronto, Canada
              25559 J Vasc Res 1998;35:1–7
              © 1998 S. Karger AG, Basel

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              Page count
              Figures: 8, References: 33, Pages: 7
              Research Paper


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