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R Myklebust

Publications and source records attributed to R Myklebust.

68 records · Page 4Linked to original sources

The membrane systems of the cardiac muscle cell of Cirolana borealis Lilljeborg (Crustacea, Isopoda).

The membrane systems of the cardiac muscle cell of the isopod Cirolana borealis Lilljeborg are described. The sarcolemma invaginates at the level of the Z band, forming transverse tubules. Narrow tubules branch off in a longitudinal direction from these transverse and radially arranged Tz-tubules forming a transverse collar at each A-I level, where dyadic and triadic junctions are formed with the sarcoplasmic reticulum. Two different orientations of the coupling discs have been detected in the supercontracted sarcomere, and this observation has been discussed. Adjacent myofibrils are separated by a double layer of sarcoplasmic reticulum.

Animals↗

Ultrastructure of muscle cells in Siboglinum fiordicum (Pogonophora).

Two different muscle types are found in the body of Siboglinum fiordicum: body wall muscle and blood vessel muscle. Both are of a myomesothelial type. The myofibrils of the body wall muscle are non-striated and consist of thick and thin myofilaments. Scattered dense bodies and attachment plaques are described. The sarcoplasmic reticulum forms a three-dimensional network in the myofibrils and only peripheral couplings are observed. The thick filaments are of a paramyosin type and have a diameter ranging from 400-1500 A. The blood vessels muscle is non-striated, but sometimes a sarcomere-like organization has been observed. Both thick and thin filaments are present. The thick filaments have a diameter of 250-400 A and lack transverse striations. Dense bodies and attachment of plaques are few. The sparse sarcoplasmic reticulum is restricted to the myofibril periphery where it makes peripheral couplings with sarcolemma. The luminal surface of the vessels is lined by a basal lamina with collagen-like inclusions. No endothelium is found. The body wall muscle and the blood vessel muscle are compared with other muscle types described in invertebrates.

Animals↗

Troponin bound calcium in electron micrographs of myocardial cells as demonstrated by the potassium-antimonate technique.

Following the K-antimonate reaction in atrial myocardial tissue, a pattern of evenly spaced cross striations of antimonate precipitates is demonstrated along the myofilaments. This spacing, found in both turtle and mouse atria, has a periodicity of about 400 A. In order to test the shifts of the antimonate reaction product in the tissue, a comparison is made between the localization of the antimonate precipitate as seen in viz. thin plastic sections and in cryo-ultra sections being dry-cut at -90 degree C from N2 frozen tissue. Preliminary results suggest only minor distributional differences in the sarcomeric pattern. On the basis of these tests, and, on the basis of previous studies by means of X-ray microanalysis, it is suggested that the periodic pattern of evenly spaced precipitates, reflects the localization of troponin bound calcium along the thin filaments during contraction.

Actins↗

The membrane systems of the cardiac muscle cell of Munida tenuimana G. O. Sars (Crustacea, Decapoda).

The membrane systems of the cardiac muscle cell of Munida tenuimana G. O. Sars are described. The sarcolemma invaginates at the Z level, forming tubules. Narrow tubules branch off in a longitudinal direction from these transverse and radially arranged tubules, forming a narrow transverse collar at the H level where dyadic and triadic junctions are formed with the sarcoplasmic reticulum.

Actins↗

A comparative study in the transmission electron microscope and scanning electron microscope of intracellular structures in sheep heart muscle cells.

The internal cellular structures of the sheep ventricular myocardium have been comparatively studied in the transmission electron microscope (TEM) and in the scanning electron microscope (SEM). For TEM studies the tissue was prepared according to standard methods. Thick sections (10 mum) of paraffin embedded material were, after they had been deparaffinized in toluene, critical point dried, coated with gold and examined in the SEM. The comparative TEM and SEM investigations revealed very good correspondence, and it is evident that the described preparation procedure for SEM has preserved the fine structures of myofibrils, mitochondria, T-Tubules and sarcoplasmic reticulum in an excellent life-like pattern. Of special interest was the three-dimensional demonstration of triads and circumferentially arranged T-tubules.

Animals↗

Identification of nerve fibres in the scanning electron microscope.

The use of silver as a "stain" for nerve fibres in scanning electron microscopy (SEM) preparations has been investigated. Samples of cardiac tissues were treated according to the Bielschovsky silver impregnation method. Following embedding in paraffin, successive sections were selected for light microscopy and for SEM studies, respectively. The silver impregnated fibres, when examined in SEM preparations, appeared nearly white against a greyish background of cardiac tissue. They were therefore easy to localize even at a low magnification. These nerve fibres were identified in the same tissue, but different blocks by means of transmission electron microscopy (TEM) studies and by fluorescence microscopy.

Animals↗

Ultrastructural changes in the myocardial myocytic mitochondria: crucial step in the development of oxygen radical-induced damage in isolated rat hearts?

The present study focuses on the sequential development of myocardial ultrastructural changes produced by oxygen radicals. Isolated rat hearts were perfused with oxygen radicals, generated by hypoxanthine and xanthine oxidase, for 5 and 10 min followed by a 35-min recovery period. The frequency of, and the association between, ultrastructural changes were examined by semiquantitative morphometry using the micrograph as unit. In each micrograph sarcolemmal, myocytic mitochondrial and myofilamental alterations were observed and graded as slight, moderate or severe. The myocytic nucleus and the endothelial cells were scored as normal or altered. Five min group: Among the cellular organelles examined, the myocytic mitochondria showed the highest frequency of alteration (in 15.3% of the micrographs). Among the grades of myocytic mitochondrial ultrastructural changes, slight alterations predominated (12.5%). Slight myocytic mitochondrial alterations were not significantly associated with the occurrence of ultrastructural changes of other cellular organelles. Endothelial ultrastructural alterations were sparse (1.5%). Ten min group: The frequency of altered organelles was greater when compared to the 5 min group. The myocytic mitochondria were still the most frequently altered component (61.7%), and myocytic mitochondrial ultrastructural alterations of all grades were strongly associated with the occurrence of other myocytic ultrastructural changes. In conclusion, the present study showed that myocytic mitochondrial changes predominated after both 5 and 10 min of oxygen radical exposure followed by recovery. In the 5 min group slight myocytic mitochondrial changes appeared independent of other myocardial changes, but in the 10 min group, however, myocytic mitochondrial changes were strongly associated with other myocardial ultrastructural changes. These results indicate that myocytic mitochondria are especially vulnerable to oxygen radicals, and further that myocytic mitochondrial ultrastructural changes may be a crucial step in the development of oxygen radical-induced myocardial damage.

Animals↗

Proliferation, differentiation and apoptosis in villous trophoblast at 13-41 weeks of gestation (including observations on annulate lamellae and nuclear pore complexes).

Ultrastructural, immunochemical, fluorescence and stereological studies were undertaken on human villous trophoblast from 13 weeks of gestation to term. The aim was to describe and quantify morphological changes during proliferation, differentiation and apoptosis in cytotrophoblast and syncytial regions of non-aggregated and aggregated nuclei. Numbers of trophoblast nuclei increased continuously from 13 weeks. In term placentae, intrasyncytial differentiation was characterized ultrastructurally by gradual decreases in nuclear size and packing density accompanied by nucleolar regression, and increasing heterochromatinization, envelope convolution and packing density of nuclear pore complexes. In densely packed areas, nuclear profiles resembled interlocking jigsaw pieces. Occasionally, these 'pre-apoptotic' nuclei were associated with annulate lamellae. Rarely, nuclear changes terminated in apoptosis with a characteristic pattern of condensed peripheral chromatin, a central island of euchromatin, no nucleoli and no discernible nuclear pores. Apoptotic nuclei were seen singly and within dense nuclear aggregations. Similar spatial patterns of nuclei and chromatin were seen in propidium iodide-stained sections at 13-41 weeks. Whilst the relative incidence of intensely fluorescent nuclei remained constant, absolute numbers increased linearly during gestation and correlated positively with the volume of syncytial knots. Nuclei labelled for DNA fragmentation occurred very infrequently and were also found in nuclear clusters as well as singly. We suggest that nuclear differentiation in syncytium has two phases: on entering syncytium, nuclei become committed to a long programmed pre-apoptotic phase which leads to a short apoptotic execution phase. We propose further that clustered nuclei (pre-apoptotic and apoptotic) in syncytial knots probably represent the extrusion component of normal continuous epithelial turnover.

Apoptosis↗

The initial phase of myocardial reperfusion is not associated with aggravation of ischemic-induced ultrastructural alterations in isolated rat hearts exposed to prolonged global ischemia.

The present study focuses on the qualitative and sequential development of myocardial ultrastructural changes during the first 10 min of reperfusion in isolated rat hearts exposed to 60 min of global ischemia. The frequency of and the association between ultrastructural changes were examined by semiquantitative morphometry using the micrograph as unit. In each micrograph the subcellular components of the myocytes (sarcolemma, mitochondria, myofilaments and nucleus) and the endothelial cells were evaluated and graded as slightly, moderately, or severely altered. Ischemia alone induced moderate to severe ultrastructural alterations. The myocytes revealed sarcolemmal disattachment or rupture. The myocytic mitochondria had a clear matrix with abundant broken cristae and amorphous matrix densities. The myofilamental pattern was irregular or even disrupted, and most nuclei had reduced density and showed margination of chromatin. The endothelium showed vacuolization, rupture of the plasma membrane, and extracellular accumulation of cellular debris. During the first 2 min of reperfusion severe ultrastructural alterations were partly reversed. After 10 min of reperfusion both the frequency and grade of myocardial ultrastructural alternations were similar to that observed after ischemia. Cristal adhesions occurred predominately during reperfusion and were associated with moderately and severely altered myocytic mitochondrial alterations. In conclusion, the results showed that ischemic-induced ultrastructural alterations were transiently improved upon reperfusion. With exception of the development of cristal adhesions, the acute phase of reperfusion was not associated with additional ultrastructural changes in isolated buffer-perfused rat hearts exposed to prolonged ischemia.

Animals↗

Ultrastructure of reperfused skeletal muscle: the effect of oxygen radical scavenger enzymes.

The aim of the present study was (1) to examine changes in ultrastructure and subcellular volume fractions in reperfused skeletal muscle and (2) to examine the effect of pre- plus postischaemic treatment with oxygen radical scavenger enzymes. Experiments were performed in 8 pentobarbital anesthetized dogs. The gracilis muscle was denervated and vascularly isolated on both lower limbs, except for the main artery and vein. A catheter was advanced through the distal end of the femoral artery for supply of superoxide dismutase (SOD) and catalase (each enzyme 12,000 U/10 min prior to ischaemia and 36,000 U/30 min at reperfusion) through the muscle artery to the muscle on one side. A catheter in the muscle vein secured the collection of venous blood to avoid a supply of SOD and catalase to the other muscle. Ischaemia was induced on both sides by clamping the branch of the femoral artery supplying the muscle for 4 h, and the muscle was thereafter reperfused for 1 h. Ultrastructural examination (morphometric by point counting and semiquantification) of the reperfused tissue revealed mitochondrial damage, margination of nuclear chromatin, lipid droplets, filamental disruption, as well as oedema in both endothelial and myofibrillar cells. In addition some influence of treatment with SOD and catalase could be seen, mainly in reduction of the number of micrographs with cellular oedema and especially oedema in endothelial cells.

Animals↗

Reversible ultrastructural alterations in the myocytic mitochondria of isolated rat hearts induced by oxygen radicals.

The present study focuses on reversible mitochondrial ultrastructural alterations in myocardial myocytes that correspond or accompany reversible metabolic depression observed after oxygen radical exposure. The myocytic mitochondrial membranes and matrix of isolated Langendorff-perfused rat hearts were examined by semiquantitative morphometry using the electron micrograph as unit. The hearts were exposed to either standard perfusion (group A), 10 min of oxygen radicals together with superoxide dismutase and catalase followed by 35 min of recovery (group B), 10 min of oxygen radicals alone (group C), or 10 min of oxygen radicals followed by 35 min of recovery (group D). Mitochondrial ultrastructural alterations were detected in only a few micrographs in groups A and B. The frequency of micrographs with mitochondrial ultrastructural alterations was 69% in group C and 62% in group D. In the group exposed to 10 min of oxygen radicals without recovery (group C) condensed pentalaminar membranous profiles arranged in parallel, interpreted to be closely adhering cristae, were detected in the intracristal compartment of myocytic mitochondria in 50% of the micrographs. The cristal adhesions were associated with other mitochondrial ultrastructural changes. Cristal adhesions were not present in group A or B, and were rarely found in the group exposed to 10 min of oxygen radicals followed by 35 min of recovery (group D). Thus, the cristal adhesions appear to be reversible alterations caused by exposure to oxygen radicals.

Animals↗