Pathophysiological Study on Thoracic Ascending Aorta of Mice with Myh11^R247C Heterozygous Mutation in Norepinephrine-induced Hypertension Model

  Objevtive  To explore the thoracic ascending aortic （TAA） pathophysiological characteristics of heterozygous mutant Myh11^R247C/+ mice under the norepinephrine-induced hypertension mode.

  Methods  Female heterozygous mutant Myh11^R247C/+ and wild type Myh11^+/+ mice were selected as experimental group (HET group) and control group (WT group), respectively. The hypertensive model was induced by intraperitoneal injection of norepinephrine (NE), and TAA diameter and invasive blood pressure (Bp) data were collected dynamically in real time using high-frequency ultrasound imaging and invasive arterial blood pressure monitoring technique, so as to indirectly analyze TAA compliance of two groups of mice. At the same time, the incidences of hemothorax and TAA rupture were further analyzed by autopsy and histology.

  Results  After injection of NE, heterozygous mice did not show a higher Bp increase percentage in systole or diastole comparing with wildtype mice. However, heterozygous mice exhibited 17% and 32% higher TAA diameter dilation percentage than wildtype ones in systole and diastole respectively. Two heterozygous mice had TAA dissection and rupture, and the incidence of hemothorax in heterozygous mice (3/5) was higher than that in wildtype (0/5).

  Conclusion  It was very likely that the altered TAA wall compliance of mutant Myh11^R247C/+ mice had led to a higher TAA dilation degree than that in wildtype, and even could be the potential reason of TAA dissection and rupture.