Biomedical subjects

O Mathieu-Costello

Publications and source records attributed to O Mathieu-Costello.

At least 91 records · Page 5Linked to original sources

PubMed1991

Stress failure in pulmonary capillaries.

In the mammalian lung, alveolar gas and blood are separated by an extremely thin membrane, despite the fact that mechanical failure could be catastrophic for gas exchange. We raised the pulmonary capillary pressure in anesthetized rabbits until stress failure occurred. At capillary transmural pressures greater than or equal to 40 mmHg, disruption of the capillary endothelium and alveolar epithelium was seen in some locations. The three principal forces acting on the capillary wall were analyzed. 1) Circumferential wall tension caused by the transmural pressure. This is approximately 25 dyn/cm (25 mN/m) at failure where the radius of curvature of the capillary is 5 microns. This tension is small, being comparable with the tension in the alveolar wall associated with lung elastic recoil. 2) Surface tension of the alveolar lining layer. This contributes support to the capillaries that bulge into the alveolar spaces at these high pressures. When protein leakage into the alveolar spaces occurs because of stress failure, the increase in surface tension caused by surfactant inhibition could be a powerful force preventing further failure. 3) Tension of the tissue elements in the alveolar wall associated with lung inflation. This may be negligible at normal lung volumes but considerable at high volumes. Whereas circumferential wall tension is low, capillary wall stress at failure is very high at approximately 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2) where the thickness is only 0.3 microns. This is approximately the same as the wall stress of the normal aorta, which is predominantly composed of collagen and elastin. The strength of the thin part of the capillary wall is probably attributable to the collagen IV of the basement membranes. The safety factor is apparently small when the capillary pressure is raised during heavy exercise. Stress failure causes increased permeability with protein leakage, or frank hemorrhage, and probably has a role in several types of lung disease.

Animals↗

PubMed1991

Ultrastructural appearances of pulmonary capillaries at high transmural pressures.

Electronmicroscopic appearances of pulmonary capillaries were studied in rabbit lungs perfused in situ when the capillary transmural pressure (Ptm) was systematically raised from 12.5 to 72.5 +/- 2.5 cmH2O. The animals were anesthetized and exsanguinated, and after the chest was opened, the pulmonary artery and left atrium were cannulated and attached to reservoirs. The lungs were perfused with autologous blood for 1 min, and this was followed by saline-dextran and then buffered glutaraldehyde to fix the lungs for electron microscopy. Normal appearances were seen at 12.5 cmH2O Ptm. At 52.5 and 72.5 cmH2O Ptm, striking discontinuities of the capillary endothelium and alveolar epithelium were seen. A few disruptions were seen at 32.5 cmH2O Ptm (mostly in one animal), but the number of breaks per millimeter cell lining increased markedly up to 72.5 cmH20 Ptm, where the mean frequency was 27.8 +/- 8.6 and 13.6 +/- 1.4 (SE) breaks/mm for endothelium and epithelium, respectively. In some instances, all layers of the blood-gas barrier were disrupted and erythrocytes could be seen moving into the alveolar spaces. In about half the endothelial and epithelial breaks, the basement membranes remained intact. The average break lengths for both endothelium and epithelium did not change significantly with pressure. The width of the blood-gas barrier increased at 52.5 and 72.5 cmH2O Ptm as a result of widening of the interstitium caused by edema. The cause of the disruptions is believed to be stress failure of the capillary wall. The results show that high capillary hydrostatic pressures cause major changes in the ultrastructure of the walls of the capillaries, leading to a high-permeability form of edema.

Animals↗

PubMed1990

Effect of sarcomere length on total capillary length in skeletal muscle: in vivo evidence for longitudinal stretching of capillaries.

It is generally assumed that when a muscle is shortened or extended the total length of capillaries does not change, implying that capillaries are nondistensible, longitudinally. On the basis of stereological estimates of capillary anisotropy versus sarcomere length, we propose that as long as capillaries are in a tortuous configuration muscle extension will merely decrease the tortuosity, leaving vessel length unaltered. Once capillaries have been pulled into a straight configuration, further extension of the muscle will cause the vessels to stretch. By means of intravital videomicroscopy we have demonstrated that stretching of individual capillaries does indeed occur over a sarcomere length range of 2.1 to 2.9 microns in rat extensor digitorum longus muscle. In vivo measurements of the lengths of six capillaries together with the sarcomere lengths of adjacent fibers were made in muscles positioned at various degrees of extension. Normalized data indicated that four capillaries stretched to the same degree as the muscle, one stretched more and another less. This may reflect differences in distensibility or tortuosity of capillaries in series with one another. The elastic stretching of capillaries during muscle activity may have important consequences in terms of shifts in permeability and increases in capillary surface area.

Animals↗

PubMed1990

Microvascular response to ischemia, and tissue structure, in normal and atrophied skeletal muscle.

The objective of this study was to explain why the normally observed reactive hyperemia in frog sartorius muscle following ischemia is absent when this muscle atrophies. Two possibilities were addressed: (1) absence is due to lowered O2 consumption, making the muscle more tolerant to ischemia, and (2) absence is linked to impaired vascular function in atrophy. We used 10 frogs after 2-3 months and 8 frogs after 7-14 months of laboratory captivity. Animals in the latter group had a significantly lower sartorius muscle weight, i.e., 85 +/- 33 vs 24 +/- 11 SD mg. Using intravital video microscopy, we measured red cell velocity in capillaries at the muscle surface, and densities of capillaries with moving (NCPER) and stationary red cells (NCSTAT) before and after 30 min ischemia. Ischemia induced a significant temporary increase in overall velocity (from 0.10 to 0.27 mm/sec) in normal muscles, but no increase in atrophied muscles. It resulted in no difference in NCPER between the two groups (preischemic levels in both groups: 15.0 cap/mm of test line), but in a significant difference in NCSTAT (3.8 vs 11.5 cap/mm in atrophy). Using light and electron microscopy, we also measured structural and ultrastructural parameters in both groups. In atrophied muscles the mean fiber cross-sectional area was lower (568 vs 1935 microns 2) and anatomical capillary density higher (892 vs 282 cap/mm2) than in normal muscles. Mitochondrial volume density was not statistically different from the 1.5% level in the normal muscle, while the lipid droplet volume density was larger (2.33 vs 0.58%). The percentage of capillaries with damaged endothelium was larger (33.5 vs 12.6%). Using histology, the white cell volume density per capillary volume was also found to be larger in atrophy (1.96 vs 0.83%). From the discrepancy between the lack of intergroup difference in preischemic NCPER and the 3.2-fold difference in anatomical capillary density we estimate that about 60% of capillaries were perfused with red cells in atrophied muscles. Although the preischemic rate of perfusion in these capillaries was comparable between the two groups, the postischemic response was not: reactive hyperemia was absent in atrophy. Our mitochondrial and lipid volume density data do not support the possibility that this absence was due to lowered O2 consumption, as these densities did not decrease with atrophy.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

Effects of hypoxia on capillary orientation in anterior tibialis muscle of highly active mice.

The plasticity of capillary orientation in response to combined hypoxic hypoxia and high activity levels was investigated in anterior tibialis muscle of Japanese waltzing mice (Mus wagneri rotans). Following 2 weeks of normobaric, normothermic hypoxia (PIO2 congruent to 87 Torr), muscles were perfusion-fixed in situ with glutaraldehyde and analyzed morphometrically. Muscles from hypoxic waltzers, HW, were compared with those from normoxic waltzers, NW, and normoxic control mice, N. At sarcomere lengths from 2.84 to 1.69 microns, tortuosity and branching increased capillary length 3 to 38%. When capillary orientation was related to sarcomere length, muscles from HW were not different from NW or N. At group-averaged sarcomere lengths of 2.22 microns (HW), 2.33 microns (NW) and 2.35 microns (N), tortuosity and branching contributed 16,20 and 18% respectively, to capillary length. We conclude that high activity levels under normoxic or hypoxic conditions in Japanese waltzing mice do not augment muscle capillary length by means of increased capillary tortuosity and/or branching.

Animals↗

PubMed1990

Analysis of capillary geometry in rat subepicardium and subendocardium.

The sustained high-energy turnover of cardiac muscle presents a formidable challenge to the O2 delivery systems. One major determinant of blood-tissue gas exchange potential is capillary surface area per volume of muscle fiber, Sv(c,f). Estimation of Sv(c,f) necessitates quantification of capillary orientation. Capillary geometry was analyzed systematically in subepi- (epi) and subendocardium (endo) of glutaraldehyde perfusion-fixed rat heart (n = 4). On 1-micron sections cut rigorously transverse and longitudinal to the muscle fiber axis we determined capillary number per fiber square millimeter on transverse, QA(0), and longitudinal, QA(pi/2), sections, capillary diameter, d(c), fiber cross-sectional area, a(f), and sarcomere length, l. Sv(c,f) was computed as pi.d(c).Jv(c,f), where Jv(c,f) is capillary length per fiber volume determined on the basis of a directional distribution model of capillary segments (Fisher axial). Analysis of capillary density, QA(alpha), in sections taken at angles alpha [from 0 to 90 degrees (pi/2) to fiber axis] showed that the Fisher axial distribution provides a good fit to capillary segment orientation in cardiac muscle. No systematic difference was found in fiber size (epi = 269.7 +/- 28.9, endo = 283.8 +/- 16.3 microns 2), capillary diameter (epi = 4.9 +/- 0.3; endo = 4.5 +/- 0.2 microns), Jv(c,f) (epi = 6,302 +/- 558; endo = 5,957 +/- 492 mm-2), or capillary surface per volume of muscle fiber (epi = 968.1 +/- 76.5; endo = 838.2 +/- 93.0 cm-1) between epi and endo. Contribution of capillary tortuosity and branching to Jv(c,f) ranged from 6-27% (epi) and 8-21% (endo) over the small ranges of l considered (epi = 2.09-2.23; endo = 2.04-2.17 microns).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Muscle fiber size and chronic exposure to hypoxia.

Sarcomere length is practically never considered when fiber size and dependent variables are compared between muscles or experimental conditions. Because of the direct dependence of fiber cross-sectional area on muscle shortening, it is imperative to normalize measurements of fiber size, and related variables (e.g. capillary number/mm2 of fiber) to sarcomere length. We examined the relationship between fiber cross-sectional area and sarcomere length in muscles of animals chronically exposed to high altitude (deer mice, Peromyscus maniculatus, native to 3800 m, and rats, Sprague-Dawley, kept at the same altitude for 5 months) compared to sea-level controls. We found no difference in fiber cross-sectional area, normalized to sarcomere length, between high altitude and control animals in either species. It has been demonstrated that sarcomere length can vary by as much as 30-44% and 43-76% in biopsy and perfusion-fixed muscles, respectively. Therefore, identifying relatively small changes in fiber size in response to a given experimental condition in such material without normalizing for sarcomere length is difficult if not impossible. Furthermore, if the conditions of the investigation induce differences in sarcomere length between experimental and control animals, artifactual changes in fiber cross-sectional area will be produced.

Altitude↗

PubMed1989

Skeletal muscle capillary geometry: adaptation to chronic hypoxia.

The potential for gas and metabolite exchange across the capillary bed is determined largely by the capillary length and surface area available for blood-tissue transfer. It has been suggested that chronic exposure to hypoxia increases capillary tortuosity; however, the degree of orientation of capillaries in muscles of sea level animals chronically exposed to hypoxia has never been quantified rigorously. An augmented capillary tortuosity would increase capillary length per volume of muscle fiber, Jv(c,f), irrespective of whether new capillaries are formed. To resolve this issue, female rats (278 +/- 5 g) were maintained for 5 months in a temperate environment at 3800 m (PIO2 = 91 Torr). Capillary tortuosity and Jv(c,f) were estimated from transverse and longitudinal sections in perfusion-fixed M. Soleus and M. Gastrocnemius. Values were compared with weight-matched controls (274 +/- 7 g). Neither capillary density (normalized to sarcomere length 2.1 microns, hypoxic = 1292 +/- 79, control = 1282 +/- 43 mm-2) nor capillary-to-fiber ratio (hypoxic = 2.50 +/- 0.15, control = 2.57 +/- 0.05) were changed after altitude exposure. Capillary tortuosity was a function of sarcomere length in all animals and this relationship was not changed by hypoxia. Capillary length per volume of muscle fiber was unchanged (hypoxic = 1541 +/- 72, control = 1531 +/- 44 mm-2) as was mean capillary diameter. We conclude that chronic exposure to 3800 m does not change capillary tortuosity or surface area in rat M. Soleus or M. Gastrocnemius.

Adaptation, Physiological↗

PubMed1989

Muscle capillary tortuosity in high altitude mice depends on sarcomere length.

At given capillary-to-fiber ratio and sarcomere length, capillary tortuosity determines capillary length and the geometry of blood-tissue exchange in muscles. It is therefore an important determinant of the potential efficiency of O2 supply to the muscle fibers. Reports have indicated that capillary tortuosity increases with adaptation to hypoxia. Unfortunately, sarcomere length was not taken into account. Because capillary tortuosity increases substantially as the muscle shortens, it is important to measure sarcomere length when comparing capillary configuration among muscles. We addressed the question of whether or not capillary tortuosity is greater in skeletal muscles of high altitude mice compared to sea-level, when account is taken of sarcomere length. Calf and thigh muscles of high altitude (3800 m; inspired PO2, 91 mm Hg) and sea-level deer mice, Peromyscus maniculatus, were perfusion-fixed in situ at sarcomere lengths ranging from 1.9 to 2.4 microns. Capillary-to-fiber ratio, capillary length per volume of fiber, and the degree of orientation (anisotropy) of capillaries were estimated by morphometry. In both sea-level and high altitude mice, capillaries were relatively straight in extended muscles, and substantially more tortuous in muscles fixed at shorter sarcomere length. There was no systematic difference in the degree of tortuosity of capillaries in the high altitude compared to sea-level mice, when account was taken of sarcomere length. Capillary length per volume of muscle fiber and capillary-to-fiber ratio were not significantly different between the two groups.

Adaptation, Physiological↗

PubMed1989

Capillary tortuosity in rat soleus muscle is not affected by endurance training.

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Capillary tortuosity in skeletal muscles of mammals depends on muscle contraction.

Capillary orientation (anisotropy) was compared in hindlimb muscles of mammals of different size and/or different aerobic capacity (dog, goat, pony, and calf). All muscles were fixed by vascular perfusion at sarcomere lengths ranging from 1.5 to 2.7 micron. The ratios of capillary counts per fiber cross-sectional area on two sets of sections (0 and 90 degrees) to the muscle fiber axis were used to estimate capillary anisotropy and the coefficient c(K,0) relating 1) capillary counts on transverse sections (a commonly used parameter to assess muscle capillarity) and 2) capillary length per volume of fiber (i.e., capillary length density). Capillary orientation parallel to the muscle fiber axis decreased substantially with muscle fiber shortening. In muscles fixed at sarcomere lengths of 2.69 microns (dog vastus intermedius) and 1.52 microns (dog gastrocnemius), capillary tortuosity and branching added 7 and 64%, respectively, to capillary length density. The data obtained in this study are highly consistent with the previously demonstrated relationship between capillary anisotropy and sarcomere length in extended vs. contracted rat muscles, by use of the same method. Capillary anisotropy in mammalian locomotory muscles is curvilinearly related to sarcomere length. No systematic difference was found in capillary tortuosity with either body size, athletic ability, or aerobic capacity. Capillary tortuosity is a consequence of fiber shortening rather than an indicator of the O2 requirements of the tissue.

Animals↗

PubMed1989

Protection against pulmonary O2 toxicity by N-acetylcysteine.

N-acetylcysteine (NAC) is a known antioxidant. We therefore investigated NAC as an agent protective against O2 toxicity in the lung. Twelve dogs were anaesthetized with sodium pentobarbital and ventilated with 100% O2 for 54 h. Five were given diluent and 7 intravenous NAC (loading dose prior to 100% O2 ventilation of 150 mg.kg-1 and maintenance dose of 20 mg.kg-1.h-1). Every 6 h, physiological evaluation of the pulmonary circulation, mechanical properties, and gas exchange was performed. Post-mortem evaluation consisted of gross examination and weighing followed by light and electron microscopy. By both functional and structural criteria, NAC protected against the effects of 100% O2. The NAC group developed significantly less increase in pulmonary vascular resistance, arterial carbon dioxide tension (PaCO2) and lung wet weight, while dynamic compliance was greater. NAC also delayed the development of abnormal ventilation-perfusion relationships and was associated with reduced pulmonary white cell accumulation, with less evidence of alveolar and interstitial oedema. NAC may well be worthy of evaluation as a therapeutic agent in human diseases characterized by oxidant damage.

Acetylcysteine↗

PubMed1988

Capillary configuration in contracted muscles: comparative aspects.

We compared the degree of orientation (anisotropy) of capillaries in skeletal muscles of animals with large differences in oxygen needs and/or tolerance to hypoxia (mammals of different size; reptiles; birds; mammals native to high altitude; diving mammals). In terrestrial mammals, we found a substantial increase in capillary tortuosity with fiber shortening, in muscles with large differences in capillary density (capillary counts/fiber mm2 in transverse sections ranging 450-4350). There was no systematic difference in muscle capillary tortuosity with body size (mouse to pony), or with adaptation to high altitude (deer mice) or to prolonged periods of anoxia (Harbor seals), when account was taken of sarcomere length. A substantial increase in capillary tortuosity was also found in contracted skeletal muscles of the alligator with remarkably low capillary density (capillary counts/fiber mm2 in transverse sections, 120-280). On the contrary, we found that in pigeon pectoralis, a highly aerobic muscle with large capillary density and a large number of capillary anastomoses running perpendicular to the muscle fiber axis, the decrease in capillary anisotropy with decreasing sarcomere length was smaller than in other muscles. Our results indicate that 1) sarcomere length at which samples are fixed needs to be taken into account when capillary counts in transverse sections are compared between muscles and/or after different experimental conditions, and 2) muscle capillary tortuosity is a consequence of fiber shortening, rather than an indicator of the O2 requirements of the tissue.

Alligators and Crocodiles↗

PubMed1988

Capillary configuration and fiber shortening in muscles of the rat hindlimb: correlation between corrosion casts and stereological measurements.

It has been a matter of discussion whether the dramatic increase in capillary tortuosity visualized in shortened muscles by vascular cast represents in vivo situations. In this study, we combined vascular cast and stereological methods in the same samples, in order to obtain (1) measurements of sarcomere length in the same muscles from which corrosion casts were prepared, and (2) scanning electron micrographs of the three-dimensional arrangement of capillaries in the same muscles where capillary anisotrophy was estimated by morphometry. Various rat skeletal muscles (soleus, gastrocnemius, and gracilis) were examined at lengths ranging from full shortening to full extension. We found a very good correlation between capillary geometry in material prepared for vascular casts and in muscles perfusion-fixed in situ. All muscles, cast and noncast, showed the same progressive curvilinear decrease in capillary anisotropy with decreasing sarcomere length. Capillary tortuosity visualized by corrosion casts in shortened muscles is a consequence of fiber shortening, within physiological sarcomere lengths; it does not represent an artifact related to the casting procedure.

Animals↗

PubMed1987

Capillary tortuosity and degree of contraction or extension of skeletal muscles.

The effect of muscle contraction, and extension, on capillary anisotropy was investigated in rat m. soleus fixed by vascular perfusion at sarcomere lengths ranging from 1.62 micron (tetanizing stimulation of sciatic nerve) to 2.85 micron (ankle joint maximally flexed. Capillary length density and tortuosity were estimated by morphometry using two sets of sections (0 and 90 degrees to the fiber axis). Capillary orientation distribution was evaluated from a series of sections taken at 0 to 90 degrees (by steps of 5-10 degrees) to the fiber axis in six preparations (sarcomere length range, 1.62-2.85 micron; capillary length density, 900-2000 mm-2). The Fisher axial distribution provided a good fit for modeling capillary orientation distribution in each case. For a comparable capillary length density per volume of muscle fiber (approximately equal to 2000 mm-2), the degree of orientation of capillary segments parallel to the fiber axis was two and four times larger in extended m. soleus than in the muscles fixed at 1.98- and 1.62-micron sarcomere lengths, respectively. In preparations fixed at 2.85, 1.98, and 1.62 micron, capillary length density per volume of muscle fiber was, respectively, 14, 44, and 65% larger than revealed by capillary counts per sectional area of muscle fiber on transverse section only, an often used parameter to compare capillarity in different muscles.

Animals↗

PubMed1987

Effects of left circumflex Ameroid constrictor placement on adrenergic innervation of myocardium.

We evaluated the adrenergic innervation of the swine and canine myocardium after placement of an Ameroid constrictor around the left circumflex coronary artery (LCX). Fluorescent histochemistry was used to identify adrenergic nerve terminals in the myocardium and coronary vasculature. Ameroid occlusion of the proximal LCX in 10 pigs for 3 wk resulted in 6 +/- 1% infarction as well as myocardial ischemia in the left circumflex region of pigs studied during exercise. However, placement of the Ameroid constrictor did not significantly alter the surface density of the nerve terminals in the LCX region of myocardium when compared with innervation of control hearts. Histological examination of the coronary arterial adrenergic innervation in Ameroid-occluded pigs revealed that coronary vessels in the circumflex region of the heart were innervated. Similarly, in seven LCX Ameroid-occluded dogs, no significant decrease in adrenergic innervation of the LCX region of myocardium was observed when compared with control dogs. In contrast LCX Ameroid-occluded pigs demonstrated significant (P less than 0.01) denervation of the left anterior descending (LAD) region of myocardium when compared with control animals. The close proximity of adrenergic nerve bundles in the proximal LAD region indicates that denervation of the myocardium supplied by the LAD may result from the dissection and/or fibrosis associated with placement of the Ameroid constrictor on the proximal LCX. Our results suggest that placement of an Ameroid constrictor on the proximal LCX does not significantly alter the adrenergic innervation of the LCX-perfused myocardium or its associated coronary vasculature. However, denervation of LAD-perfused myocardium and its vasculature may result.

Adrenergic Fibers↗

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.

Animals↗

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.

Animals↗