scholarly journals Effects of atrial natriuretic peptide on ischemic brain edema in rats evaluated by proton magnetic resonance method.

Stroke ◽  
1991 ◽  
Vol 22 (1) ◽  
pp. 61-65 ◽  
Author(s):  
S Naruse ◽  
Y Aoki ◽  
R Takei ◽  
Y Horikawa ◽  
S Ueda
Keyword(s):  
Magnetic Resonance ◽  
Atrial Natriuretic Peptide ◽  
Brain Edema ◽  
Natriuretic Peptide ◽  
Proton Magnetic Resonance ◽  
Resonance Method ◽  
Ischemic Brain ◽  
Magnetic Resonance Method ◽  
Ischemic Brain Edema ◽  
Atrial Natriuretic

Effect of Atrial Natriuretic Peptide on Ischemic Brain Edema: Changes in Brain Water and Electrolytes

Neurosurgery ◽  
1990 ◽  
Vol 27 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Naoyuki Nakao ◽  
Toru Itakura ◽  
Hideyoshi Yokote ◽  
Kunio Nakai ◽  
Norihiko Komai
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Brain Edema ◽  
Natriuretic Peptide ◽  
Ischemic Brain ◽  
Ischemic Brain Edema ◽  
Brain Water ◽  
Atrial Natriuretic

Solvent effects in ultraviolet spectral studies of hydrogen bonding between phenol and N,N-dimethylacetamide

1967 ◽  
Vol 45 (18) ◽  
pp. 2033-2038 ◽  
Author(s):  
F. Takahashi ◽  
W. J. Karoly ◽  
J. B. Greenshields ◽  
N. C. Li
Keyword(s):  
Hydrogen Bonding ◽  
Magnetic Resonance ◽  
Complex Formation ◽  
Equilibrium Constant ◽  
Proton Magnetic Resonance ◽  
Mixed Solvent ◽  
Resonance Method ◽  
Spectral Studies ◽  
Magnetic Resonance Method ◽  
Hydrogen Bonded

Ultraviolet spectral studies of hydrogen bonding between phenol and N,N-dimethylacetamide (DMA) in several media are reported. The equilibrium constant for the formation of the phenol–DMA complex is strongly solvent dependent, varying from 295 1/mole in cyclohexane to 130 in CCl4 and 16 in CHCl3, all at 28°. The greatly reduced value in CHCl3 indicates that the measured equilibrium constant is only an apparent one which does not take into account the decrease in free DMA concentration resulting from hydrogen-bonded complex formation with the solvent acting as hydrogen donor. In CCl4/CHCl3 mixed solvent, in the range of [chloroform] = 0 to 1.227 M, the measured equilibrium constant, K′, varies linearly with K′ [chloroform]. The slope of the line corresponds to the equilibrium constant for the formation of the hydrogen-bonded complex between CHCl3 and DMA in CCl4. The value, 0.9 1/mole, agrees with that obtained from a proton magnetic resonance method. The agreement is particularly noteworthy when we consider that the concentrations of phenol used in the proton magnetic resonance and ultraviolet spectral methods differ by a factor of 200, which leads definitely to the conclusion that the hydrogen-bonded CHCl3–DMA complex formed is 1:1. In cyclohexane/CHCl3 mixed solvent, similar results are obtained.

A study of imidazole by the proton magnetic resonance method

1970 ◽  
Vol 6 (6) ◽  
pp. 750-753 ◽  
Author(s):  
Yu. A. Teterin ◽  
A. G. Kiselev ◽  
L. N. Nikolenko
Keyword(s):  
Magnetic Resonance ◽  
Proton Magnetic Resonance ◽  
Resonance Method ◽  
Magnetic Resonance Method

scholarly journals Experimental ischemic brain edema: morphological and magnetic resonance imaging findings

2007 ◽  
Vol 22 (5) ◽  
pp. 1-8 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Naoyuki Miyasaka ◽  
Zhao Fengyo ◽  
Ichiro Yamada ◽  
Makoto Nakane ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Mr Imaging ◽  
Brain Edema ◽  
Cerebrovascular Disorders ◽  
Ultrastructural Changes ◽  
Magnetization Transfer Ratio ◽  
Imaging Findings ◽  
Tissue Elasticity ◽  
Ischemic Brain ◽  
Ischemic Brain Edema

✓Magnetic resonance (MR) imaging is a powerful tool for detecting and characterizing ischemic edema, a serious complication of ischemic cerebrovascular disorders. In this article the authors investigate the relationships between MR imaging findings and structural/ultrastructural changes in ischemic brain edema by using various animal models of experimental cerebral ischemia. The authors observed the following: 1) Ischemic edema was detectable by diffusion weighted MR imaging as early as 15 minutes after the onset of vascular occlusion. A decrease in the apparent diffusion coefficient (ADC) corresponded to the early cellular/cytotoxic type of brain edema and the decrease was proportionate to the degree of intracellular water accumulation. 2) Postischemic transient normalization of the ADC after the initial decrease did not signify histological recovery but rather slowly progressing infarction. 3) Histological degradation of postischemic tissue correlated with the decrease in tissue elasticity and the magnetization transfer ratio. 4) Transient cytotoxic edema localized in the substantia nigra preceding neuronal death was detectable on MR images after ipsilateral striatal infarction. Thus, MR imaging is a powerful tool for detecting and characterizing brain edema associated with ischemic stroke.

scholarly journals Differential Effects of Atrial Natriuretic Peptide on the Brain Water and Sodium after Experimental Cortical Contusion in the Rat

2003 ◽  
Vol 23 (10) ◽  
pp. 1212-1218 ◽  
Author(s):  
Shinji Fukui ◽  
Giovanna Fazzina ◽  
Angela M Amorini ◽  
Jana G Dunbar ◽  
Anthony Marmarou
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Brain Edema ◽  
Natriuretic Peptide ◽  
The Body ◽  
Blue Dye ◽  
Dependent Manner ◽  
Cgmp Pathway ◽  
Cortical Contusion ◽  
Brain Water ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) plays an important role in the regulation of water and sodium in the body via cyclic GMP (cGMP) pathway. Although ANP has been shown to be protective in cerebral ischemia or intracerebral hemorrhage, its role in traumatic brain injury (TBI) has yet to be elucidated. We herein assessed ANP effects on brain water and sodium in TBI. Controlled cortical impact (3 mm depth, 6 m/sec) was used to induce an experimental cortical contusion in rats. Continuous administration of ANP 0.2 (n = 6) or 0.7 μg/kg/24 h (n = 6), cGMP analogue (8-Bromo-cGMP) 0.1 (n = 5) or 0.3 mg/kg/24 h (n = 5), or vehicle (n = 6) was begun 15 minutes after injury, using a mini-osmotic pump implanted into the peritoneal cavity. At 24 hours after injury, ANP significantly exacerbated brain edema in the injured hemisphere in a dose-dependent manner while it reduced brain sodium concentrations in both hemispheres. These ANP effects could be mimicked by a cGMP analogue. In the second series (n = 20), BBB integrity was assessed by evaluating the extravasation of Evans blue dye. ANP or cGMP analogue significantly worsened BBB disruption in the injured hemisphere at 24 hours after injury. These findings suggest that ANP administration exacerbates brain edema after the experimental cortical contusion in rats, possibly because of an increase in the BBB permeability via cGMP pathway, whereas it reduces brain sodium levels.

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