title: Evolution of cardiac and renal impairment detected by high-field cardiovascular magnetic resonance in mice with renal artery stenosis.
abstract: BACKGROUND
  Renal artery stenosis (RAS) promotes hypertension and cardiac dysfunction. The 2-kidney, 1-clip mouse model in many ways resembles RAS in humans and is amenable for genetic manipulation, but difficult to evaluate noninvasively. We hypothesized that cardiovascular magnetic resonance (CMR) is capable of detecting progressive cardiac and renal dysfunction in mice with RAS and monitoring the progression of the disease longitudinally.
  
  
  METHODS
  RAS was induced at baseline in eighteen mice by constricting the renal artery. Nine additional animals served as normal controls. CMR scans (16.4 T) were performed in all mice one week before and 2 and 4 weeks after baseline. Renal volumes and hemodynamics were assessed using 3D fast imaging with steady-state precession and arterial spin labelling, and cardiac function using CMR cine. Renal hypoxia was investigated using blood oxygen-level dependent (BOLD) MR.
  
  
  RESULTS
  Two weeks after surgery, mean arterial pressure was elevated in RAS mice. The stenotic kidney (STK) showed atrophy, while the contra-lateral kidney (CLK) showed hypertrophy. Renal blood flow (RBF) and cortical oxygenation level declined in the STK but remained unchanged in CLK. Moreover, cardiac end-diastolic and stroke volumes decreased and myocardial mass increased. At 4 weeks, STK RBF remained declined and the STK cortex and medulla showed development of hypoxia. Additionally, BOLD detected a mild hypoxia in CLK cortex. Cardiac end-diastolic and stroke volumes remained reduced and left ventricular hypertrophy worsened. Left ventricular filling velocities (E/A) indicated progression of cardiac dysfunction towards restrictive filling.
  
  
  CONCLUSIONS
  CMR detected longitudinal progression of cardiac and renal dysfunction in 2K, 1C mice. These observations support the use of high-field CMR to obtain useful information regarding chronic cardiac and renal dysfunction in small animals.
authors.forename: Behzad
authors.initials: B
authors.lastname: Ebrahimi
authors.forename: John A
authors.initials: JA
authors.lastname: Crane
authors.forename: Bruce E
authors.initials: BE
authors.lastname: Knudsen
authors.forename: Slobodan I
authors.initials: SI
authors.lastname: Macura
authors.forename: Joseph P
authors.initials: JP
authors.lastname: Grande
authors.affiliation: Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota, USA. Lerman.Lilach@mayo.edu.
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
mesh_terms: D000818:Animals; D062186:Arterial Pressure; D001284:Atrophy; D059347:Cardio-Renal Syndrome / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D004195:Disease Models, Animal; D018450:Disease Progression; D006339:Heart Rate; D006978:Hypertension, Renovascular / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D006984:Hypertrophy; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply* / Q000473:pathology; D019028:Magnetic Resonance Imaging, Cine; D008297:Male; D051379:Mice; D057507:Mice, 129 Strain; D011237:Predictive Value of Tests; D012078:Renal Artery Obstruction / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D012079:Renal Circulation; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D016277:Ventricular Function, Left