scholarly journals Extracellular Diffusion Parameters in the Rat Somatosensory Cortex during Recovery from Transient Global Ischemia/Hypoxia

2008 ◽  
Vol 28 (10) ◽  
pp. 1665-1673 ◽  
Author(s):  
Norbert Zoremba ◽  
Aleš Homola ◽  
Karel Šlais ◽  
Ivan Voříšek ◽  
Rolf Rossaint ◽  
...  
Keyword(s):  
Somatosensory Cortex ◽  
Volume Fraction ◽  
Extracellular Volume ◽  
Extracellular Volume Fraction ◽  
Diffusion Parameters ◽  
Bilateral Common Carotid Artery ◽  
Apparent Diffusion ◽  
Weighted Magnetic Resonance Imaging ◽  
Postischemic Period ◽  
Rat Somatosensory Cortex

Changes in the extracellular space diffusion parameters during ischemia are well known, but information about changes during the postischemic period is lacking. Extracellular volume fraction (α) and tortuosity (Λ) were determined in the rat somatosensory cortex using the real-time iontophoretic method; diffusion-weighted magnetic resonance imaging was used to determine the apparent diffusion coefficient of water. Transient ischemia was induced by bilateral common carotid artery clamping for 10 or 15 mins and concomitant ventilation with 6% O2 in N2. In both ischemia groups, a negative DC shift accompanied by increased potassium levels occurred after 1 to 2 mins of ischemia and recovered to preischemic values within 3 to 5 mins of reperfusion. During ischemia of 10 mins duration, α typically decreased to 0.07 ± 0.01, whereas Λ increased to 1.80 ± 0.02. In this group, normal values of α = 0.20 ± 0.01 and Λ = 1.55 ± 0.01 were registered within 5 to 10 mins of reperfusion. After 15 mins of ischemia, α increased within 40 to 50 mins of reperfusion to 0.29 ± 0.03 and remained at this level. Tortuosity (Λ) increased to 1.81 ± 0.02 during ischemia, recovered within 5 to 10 mins of reperfusion, and was increased to 1.62 ± 0.01 at the end of the experiment. The observed changes can affect the diffusion of ions, neurotransmitters, metabolic substances, and drugs in the nervous system.

Transmural heterogeneity of diffusion anisotropy in the sheep myocardium characterized by MR diffusion tensor imaging

2007 ◽  
Vol 293 (4) ◽  
pp. H2377-H2384 ◽  
Author(s):  
Yi Jiang ◽  
Julius M. Guccione ◽  
Mark B. Ratcliffe ◽  
Edward W. Hsu
Keyword(s):  
Diffusion Tensor Imaging ◽  
Volume Fraction ◽  
Diffusion Tensor ◽  
Extracellular Volume ◽  
Extracellular Volume Fraction ◽  
Left Ventricular ◽  
Fiber Direction ◽  
Significant Difference ◽  
Mr Diffusion ◽  
Mr Diffusion Tensor Imaging

The orientation of MRI-measured diffusion tensor in the myocardium has been directly correlated to the tissue fiber direction and widely characterized. However, the scalar anisotropy indexes have mostly been assumed to be uniform throughout the myocardial wall. The present study examines the fractional anisotropy (FA) as a function of transmural depth and circumferential and longitudinal locations in the normal sheep cardiac left ventricle. Results indicate that FA remains relatively constant from the epicardium to the midwall and then decreases (25.7%) steadily toward the endocardium. The decrease of FA corresponds to 7.9% and 12.9% increases in the secondary and tertiary diffusion tensor diffusivities, respectively. The transmural location of the FA transition coincides with the location where myocardial fibers run exactly circumferentially. There is also a significant difference in the midwall-endocardium FA slope between the septum and the posterior or lateral left ventricular free wall. These findings are consistent with the cellular microstructure from histological studies of the myocardium and suggest a role for MR diffusion tensor imaging in characterization of not only fiber orientation but, also, other tissue parameters, such as the extracellular volume fraction.

Abstract 17263: Pre-Clinical Left Ventricular Myocardial Remodeling in Patients With Friedreich’s Ataxia: A Cardiac MRI Study

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_1) ◽  
Author(s):  
Karen A Takazaki1 ◽  
Thiago Quinaglia A. C. Silva ◽  
Alberto Martinez ◽  
Tomas Neilan ◽  
Ravi SHAH ◽  
...  
Keyword(s):  
Heart Failure ◽  
Volume Fraction ◽  
Extracellular Volume ◽  
Extracellular Volume Fraction ◽  
Friedreich’S Ataxia ◽  
Left Ventricular ◽  
Friedreich's Ataxia ◽  
Intracellular Water ◽  
Lv Mass ◽  
Burn Out

Background: Heart Failure (HF) is the most common cause of death in Friedreich’s ataxia (FRDA), an inherited mitochondrial disease. Myocardial fibrosis is a well-documented histopathological feature among FRDA patients with HF. Objectives: In this study we will investigate the myocardial extracellular volume fraction (ECV) and intracellular water lifetime (τ ic ), using T1-weighted CMR imaging, in a cohort of patients with FRDA without signs of heart failure. We will also investigate whether myocardial tissue phenotyping by CMR can highlight particular characteristics of LV remodeling in FRDA’s cardiomyopathy, beyond those currently assessed with imaging-based classification of disease severity. Methods: Twenty-six FRDA’s patients (age 26.6±9.3 years, 15 women) without signs of HF, and 10 healthy controls (32.6±7.3 years, 5 women) underwent cardiac magnetic resonance (CMR) studies for assessment of left ventricular (LV) function, myocardial T1, late gadolinium enhancement (LGE), extracellular volume fraction (ECV), and intracellular water-lifetime (τ ic ) as marker of cardiomyocyte size. Neurological decline was determined using the FRDA rating scale (FARS 3). Results: FRDA patients had normal LV ejection fraction (LVEF: 67.66±11.4 vs. 63.9±9.0, P=0.311), larger LV mass index (LVMASSi: 61.03±22.1 vs. 45±4.2g/m 2 , P<0.001), and decreased LV end-diastolic volume index (LVEDVi 53.42±12 vs. 75.7±16.1, P=0.002), compared with controls. ECV and τ ic , were increased in FRDA patients (ECV: 0.36±0.05 vs. 0.25±0.02, P<0.0001; τ ic : 0.13±0.07 vs. 0.06±0.03, P=0.001). ECV was positively associated with LV mass-to-volume ratio (r=0.628, P<0.001). FARS 3 correlated positively with disease duration (r=0.669, P<0.001), and negatively with τ ic , (r=0.478, P=0.039). LVMASSi and cardiomyocyte mass-index [(1–ECV)LVMASSi] declined with age, indicating that LV hypertrophy may transition to a “burn-out” phase with LV atrophy. Conclusions: LV hypertrophy in FRDA reflects an expansion of the myocardial interstitium and an increase in cardiomyocyte size. In contrast, the neurological decline was more likely with decreasing cardiomyocyte size, possibly an early sign of myocardial “burn-out” in FRDA.

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