Marfan syndrome, affecting approximately one out of every 5,000 people, is
characterized by abnormal bone growth, ectopia lentis, and often-fatal aortic dilation and
dissection. The root cause is a faulty extracellular matrix protein, fibrillin-1, which
associates with elastin in many tissues. Common carotids from wild-type controls and
mice heterozygous for the mgR mutation, the most commonly used mouse model of
Marfan syndrome, were studied in a biaxial testing device. Mechanical data in the form
of pressure-diameter and force-stretch tests in both the active and passive states were
collected, as well data on the functional responses to phenylephrine, carbamylcholine
chloride, and sodium nitroprusside. Although little significant difference was found
between the heterozygous and wild-type groups in general, the in vivo stretch for both
groups was significantly different from previously studied mouse vessels. Although the
two groups do not exhibit significant differences, this study comprises a control group
for future work with mice homozygous for mgR, which do exhibit Marfan-like
symptoms. As treatment of Marfan syndrome improves, more Marfan patients will
survive and age, increasing the likelihood that they will develop many of the vascular complications affecting the normal population, including hypertension and
atherosclerosis. Therefore, it is imperative to gather biomechanical data from the Marfan
vasculature so that clinicians may predict the effects of vascular complications in Marfan
patients and develop appropriate methods of treatment.
| Identifer | oai:union.ndltd.org:tamu.edu/oai:repository.tamu.edu:1969.1/ETD-TAMU-1048 |
| Date | 15 May 2009 |
| Creators | Taucer, Anne Irene |
| Contributors | Humphrey, Jay D., Wilson, Emily |
| Source Sets | Texas A and M University |
| Language | en_US |
| Detected Language | English |
| Type | Book, Thesis, Electronic Thesis, text |
| Format | electronic, application/pdf, born digital |
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