SUMMARY1. Oxygen consumption, mitochondrial content and composition, intracellular lipid stores and fibre size were studied in isolated cat muscles: predominantly glycolytic gracilis, purely oxidative soleus and gracilis transformed into an oxidative muscle by chronic low-frequency (10 Hz) electrical stimulation.2. Oxygen consumption in control gracilis at rest (0 303 + 0 050 ml 02 min-' 100 g-'; mean + S.E. of mean) was three to five times lower than in either stimulated gracilis (1-16+0-40) or soleus (1-57+0056); it was about two times lower during maximal contractions in control gracilis (5 15 + 0 24) than in either stimulated gracilis (11-6 +2'0) or soleus (9-34 + 0-78).3. The volume density of mitochondria in control gracilis (2-75 + 012 %) was half that of soleus (6-23 + 0 76) and only one-third that of stimulated gracilis (8-35 + 0-7 1). Subsarcolemmal mitochondria represented a significantly smaller fraction of the total mitochondrial volume in control gracilis than in either soleus or stimulated gracilis.4. The surface area of inner and outer mitochondrial membranes per unit volume of mitochondria ranged from 23-4 to 26'1 and from 14-0 to 16-5 m2 cm-3, respectively.Mean values of these variables were not significantly different among experimental groups. 5. The volume density of the intracellular lipid stores in control gracilis (0-232 + 0-041 %) was one-fourth of that in stimulated gracilis (0-860 +0-12) and one-fifth of that in soleus (1-17 + 0 27).6. The fibre cross-sectional area was 1670 + 260,m2 in control gracilis, 2250 + 280 in stimulated gracilis and 2390+110 in soleus. The difference was statistically significant only between control gracilis and soleus.7. There was a significant correlation between the volume density of mitochondria and maximal oxygen consumption for all three muscles combined.8. It was found that mitochondrial structure was similar in muscles with different oxidative capacities and that equal amounts of mitochondria consumed equal amounts of oxygen under limiting conditions of maximal in vivo respiration.

BACKGROUND AND PURPOSE:In acute hepatic encephalopathy, MR imaging abnormalities have been described in the PVWM, thalami, and corticospinal tracts. We sought to determine characteristic regions of involvement on FLAIR and DWI, to evaluate their reversibility, and to correlate MR imaging extent with clinical severity.

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The size of the capillary bed, assessed by capillary density (CD), capillary per muscle fibre ratio (C/F), total capillary length, surface area and volume was related to the oxidative capacity, assessed by the volume density of mitochondria and VO2max in cat muscles with a different composition of glycolytic and oxidative fibres: predominantly glycolytic gracilis, purely oxidative soleus and gracilis transformed towards oxidative by chronic low frequency (10 Hz) electrical stimulation. Maximal blood flow and lactate output were measured in the muscles during isometric contractions. When capillary supply was estimated by C/F ratio, there was a close correlation between various parameters only in stimulated gracilis. The combined data of all muscles showed a significant correlation between the total volume of mitochondria, VO2max and total capillary surface area. Capillary volume showed a tight correlation with maximal blood flow in both control and stimulated gracilis, but not in soleus. Maximal blood flow was correlated with VO2max in oxidative muscles (stimulated gracilis and soleus) but not in control glycolytic gracilis. Moreover normal gracilis did not show any relationship between the volume density of mitochondria and the size of the capillary bed. The latter was inversely correlated with the output of lactate which was greater in muscles with a lower C/P ratio. The data on gracilis indicates that the capillary bed can adapt to the increased demand for oxygen and a greater oxidative capacity induced by long-term activity imposed on a glycolytic muscle, while it may be more important for the removal of lactate in the glycolytic muscles under their normal activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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We read with great interest the description by U-King-Im et al 1 in the February issue of the American Journal of Neuroradiology (AJNR) of 4 patients with "acute hyperammonemic encephalopathy" on diffusion-weighted imaging (DWI). In the September 2010 issue of AJNR, we used a similar term of "acute hepatic encephalopathy" (most of the patients had hyperammonemia), and the terms could perhaps be considered interchangeable (notably, both would result in the acronym AHE). 2 We thank them for describing their findings, which are similar to the cases we described that, in our opinion, lie at the severe end of the spectrum of AHE. Of particular note is that 2 of their 4 patients died. In our study, 3 of 5 patients died; they had a similar distribution on DWI, which we termed "diffuse cortical involvement." U-King-Im et al 1 limited this description to the cingulate and insular gyri, but review of their available images demonstrates the abnormalities to be more extensive than those 2 regions. We do not point this out for the purpose of criticism; rather, we agree that these findings should alert the radiologist to the possibility of AHE. Thus, the combination of these 2 studies would indeed suggest (though preliminarily) that "diffuse cortical involvement" or alternatively "cingulate and insular involvement" may portend a poor outcome, though AHE is potentially reversible with therapy (such as lactulose).They also similarly noted thalamic brain stem involvement in 1 patient, which we noted in most of our 20 patients. Hence, it would be of interest to us whether subtle involvement of the thalami or dorsal brain stem existed on further review of fluid-attenuated inversion recovery (FLAIR) or DWI in these 4 patients or if they may have other patients who may have been eventually excluded from their study or not included due to stringent criteria, for example due to confounding diagnoses with preliminarily negative findings on MR imaging (we have noted that such situations uncommonly occur). Such confirmation of milder cases limited to the thalami, for example, would help solidify our findings that AHE occurs along a spectrum, with multifocal diffuse cortical findings being at the severe end.We proposed the terminology "acute hepatic encephalopathy" rather than "acute hyperammonemic encephalopathy" for several reasons: 1) Although some correlation likely exists, the degree of correlation between serum ammonia levels and AHE severity (the "ammonia hypothesis") is still controversial. 2) Ammonia levels may be mildly elevated in patients with chronic cirrhosis without symptoms of AHE. 3) Severely encephalopathic patients may have normal ammonia levels. 4) Serum ammonia has been shown to be a poor predictor as a single test for the presence of AHE.3,4 More recent evidence suggests rather that there is a synergistic effect between ammonia and various other inflammatory cytokines that results in excess glutamine within astrocytes, leading to osmotic swelling of the astrocytes and the subsequent brain edema as well as other neuro...