Biomedical subjects

O Mathieu-Costello

Publications and source records attributed to O Mathieu-Costello.

96 records · Page 6Linked to original sources

PubMed1985

Biochemical and ultrastructural changes of skeletal muscle mitochondria after chronic electrical stimulation in rabbits.

The purpose of the present investigation was to follow and correlate changes of structural and biochemical markers of energy metabolism during chronic electrical stimulation of tibialis anterior muscle in rabbits. In the superficial portion of the muscle, 5 to 6-fold increases occurred in enzyme activities of the citric acid cycle and of fatty acid oxidation after 28 days of stimulation. Enzyme activity changes in the deep, more oxidative part of the muscle were relatively smaller. Consequently, levels of the citric acid cycle enzymes became similar in superficial and deep parts of the muscle after the longest stimulation periods. With the exception of hexokinase, which increased in parallel with the citric acid cycle enzymes, glycolytic enzymes decreased 2 to 3-fold. Muscle mass and fibre size remained unchanged, while capillary density and capillary to fiber ratio increased 2-fold. The volume density of total mitochondria increased in a fashion similar to the changes of the enzymes of the citric acid cycle (7-fold in superficial and 3.5-fold in deep parts of the muscle) and, thus, approached values found in heart muscle. Disproportionate changes in enzyme activities of ketone body utilisation and of mitochondrial glycerolphosphate oxidase indicated qualitative changes within the mitochondrial population. However, the proportion of subsarcolemmal to interfibrillar mitochondria, as well as the area of inner mitochondrial membrane per unit volume of mitochondrion remained unchanged. Similarly, intracellular lipid deposits remained unchanged with stimulation. It is concluded that there is an excellent agreement between morphometric and biochemical measurements of tissue oxidative capacity.

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PubMed1985

Morphometry of the amount of smooth muscle cells in the media of various rabbit arteries.

Our objective in this study was to evaluate the relative amount of smooth muscle cells in the medial layer of various rabbit arteries. The fixation of smooth muscle cells in the arterial wall is difficult and the differential effect of glutaraldehyde (GA) and fixative vehicle on cell ultrastructure in different tissues is controversial. We compared the effect of various concentrations of the vehicle and glutaraldehyde (osmolarity ranges for total fixative, 350-1030 mOsm) on the arterial wall ultrastructure. We found that a 600 mOsm GA solution (isotonic vehicle; 2.5% GA) adequately preserves arterial wall structures. The relative amount of smooth muscle cells in the media differed in various segments along the arterial tree. It ranged from 35% (thoracic aorta) to 74% (tibial artery). The importance of weighting the contractile response of different arteries in vitro to their relative smooth muscle cell content is discussed.

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PubMed1984

Density of newly synthesized plasma membrane proteins in intracellular membranes. I. Stereological studies.

As the spike proteins of Semliki Forest virus (SFV) pass from their site of synthesis in the endoplasmic reticulum (ER) to the cell surface, they must be concentrated and freed from endogenous proteins. To determine the magnitude of this sorting process we have measured the density of spike proteins in membranes of the intracellular transport pathway. In this first paper, using stereological procedures, we have estimated the surface areas of the ER, Golgi complex, and plasma membrane of infected and mock-infected baby hamster kidney cells. First, we estimated the mean cell volume in absolute units. This was done using a novel in situ method which is described in detail. Infection by SFV was found to have no effect on any of the parameters measured. In the accompanying paper ( Quinn , P., G. Griffiths, and G. Warren, 1984, J. Cell Biol., 2142-2147) these stereological estimates were combined with biochemical estimates of the amount of spike proteins in ER, Golgi complex, and plasma membrane to determine the density in the membranes of these compartments.

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PubMedDate not supplied

Strength of the pulmonary blood-gas barrier.

The mammalian pulmonary blood-gas barrier is well known to be extremely thin. For example, in the human lung, half of the area of the barrier (the 'bulging' part) has a thickness of only 0.2-0.4 micron. We show here that the barrier is also immensely strong. This is an essential requirement because the capillary wall stresses during heavy exercise become very large (about 7 x 10(4) N/m2 = 70 kPa) when capillary pressure increases to 30 mmHg. Stress failure of the pulmonary capillary wall consistently occurs in experimental rabbit preparations at abnormally high pressures exceeding 40 mmHg and may be the cause of bleeding into the lung in galloping racehorses. The great strength of the thin side of the blood-gas barrier can be attributed to the extracellular matrix, especially the type IV collagen which is predominantly located in the very thin lamina densa. The alveolar wall is therefore particularly vulnerable to injurious agents which attack type IV collagen such as autoantibodies in Goodpasture's Syndrome and perhaps neutrophil elastase in emphysema. The combination of extreme thinness and great strength of the blood-gas barrier poses a unique design requirement.

Animals↗

PubMedDate not supplied

Capillary ultrastructure and functional capillary density.

We briefly summarize our findings on alterations in capillary structure in skeletal muscle and heart in response to up to 30 min of ischemia. In frog sartorius muscle, reactive hyperemia was absent in atrophy. Increased spatial heterogeneity of red cell velocity in individual capillaries was observed, as were increases in the percentage of capillaries with damaged endothelium and white cell volume density in capillaries. Examination of the effect of aging on the response of the vascular bed to 30 min ischemia in extensor digitorum longus muscle of Fisher 344 rats suggested that the lack of postischemic hyperemia and structural alterations in frog muscle were related to disuse rather than aging per se. However, the specific study of disuse in rat extensor digitorum longus muscle after chronic application of tetrodotoxin revealed both capillary damage and a postischemic hyperemic response. It suggested an effect of the degree of tissue deterioration on the hyperemic response after short-term disuse in rat muscle, compared to longer-term atrophy in frog. Morphometric data in isolated rabbit heart suggested a link between microvascular compression as a result of tissue edema and decreased perfusion after 30 min total ischemia.

Aging↗

PubMedDate not supplied

Stress-induced injury of pulmonary capillaries.

The lung is particularly vulnerable to injury because the blood-gas barrier is so extremely thin. Furthermore, the mechanical stresses in the barrier become very high when capillary pressure is raised, or when the lung is inflated to a high volume. The strength of the blood-gas barrier on the thin side can be attributed to the type IV collagen in the basement membranes. Abnormally high stresses in the walls of the pulmonary capillaries result in ultrastructural changes including disruptions of both the alveolar epithelial and capillary endothelial layers. All Thoroughbred racehorses break their pulmonary capillaries when they gallop. Also, elite human athletes develop changes in the permeability of the blood-gas barrier at high levels of exercise. Pathological conditions resulting in stress failure include: 1) high-altitude pulmonary edema; 2) neurogenic pulmonary edema; 3) severe left ventricular failure; 4) mitral stenosis; and 5) overinflation of the lung. There is a spectrum of low permeability to high permeability edema as the capillary pressure is raised. Remodeling of pulmonary capillaries apparently occurs at high capillary pressures. It is likely that the extracellular matrix of the capillaries is continuously regulated in response to capillary wall stress.

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