title: [Effects of chronic hypoxia on left and right ventricular function and the expression of cardiac TRPC channels in rats].
abstract: OBJECTIVE
  To explore the effects of chronic hypoxia on left and right ventricular function and the expression of cardiac transient receptor potential canonical (TRPC) channels in rats.
  
  
  METHODS
  Forty eight SD male rats were randomly divided into control group (CON) and chronic hypoxic pulmonary hypertension model group (CH) (n = 24). In CH group, rats were exposed in chronic hypoxia environment (10% +/- 0.2% O2) to induce myocardial hypertrophy. After 3 weeks, mean systemic arterial pressure (mSAP), right ventricular systolic pressure (RVSP), left ventricular systolic pressure (LVSP), left or right ventricular pressure maximum rate of rise (LV/RV + dp/dt(max)), left or right ventricular pressure maximum rate of descent (LV/RV-dp/dt(max)), right ventricular hypertrophy index (RVMI) and left ventricular hypertrophy index (LVMI) were measured. Left and right ventricular myocardium tissue sections were stained by HE and observed under light microscope. Real-time polymerase chain reaction (real-time-PCR) and Western blot were performed to detect the expression of TRPC subfamily.
  
  
  RESULTS
  RVSP, RVMI, RV + dp/dt(max) and RV-dp/dt(max) were markedly elevated in CH group (P < 0.01) in comparison to CON group. LVMI was markedly reduced in CH group in comparison to CON group (P < 0.01). LVSP, LV + dp/dt(max) and LV- dp/dt(max) had no significant changes in CH group in comparison to CON group. Right ventricular myocardial cells of CH group became thick, the nuclei stained deeply, the shape of nuclei became not regularity. Left ventricular myocardial fibers did not change significantly. There was significant difference in the levels of mRNA and protein of TRPC1 between CON and CH groups.
  
  
  CONCLUSIONS
  For three weeks exposed to chronic hypoxia induced right ventricular hypertrophy specifically, raised the mRNA and protein expression of TRPC1 on right ventricular myocardial cells . TRPC1 might be involved in the development of cardiac hypertrophy.
authors.forename: Hui-Qin
authors.initials: HQ
authors.lastname: Chen
authors.forename: Mo-Jun
authors.initials: MJ
authors.lastname: Lin
authors.forename: Xiao-Ru
authors.initials: XR
authors.lastname: Liu
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006976:Hypertension, Pulmonary / Q000378:metabolism / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D050051:Transient Receptor Potential Channels / Q000378:metabolism*; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology
chemical_list: D050051:Transient Receptor Potential Channels