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R Myklebust

Publications and source records attributed to R Myklebust.

At least 37 records · Page 2Linked to original sources
PubMed1994

Adenosine protects ultrastructure of isolated rat lungs against fat emulsion injury.

In isolated rat lungs subjected to fat emulsion damage, a model simulating adult respiratory distress syndrome, we have previously reported that adenosine (ADO) reduces pulmonary vascular resistance (PVR) and the fluid filtration rate (FFR). In the present study the aim was to examine morphologically this effect of ADO. Two groups of isolated rat lungs were subjected to the injury. Marked and significant differences were found between the groups; in lungs not given ADO, FFR and airway pressure were higher and, as evaluated by electron microscopy, the endothelial lining was thin and partly disrupted. The epithelial cells of the alveolar walls were also partly disrupted and the alveolar septa were split enclosing interstitial edema. In lungs receiving ADO from the onset of exposure to fat emulsion, FFR was lower and ultrastructure did not differ from non-injured non-treated controls perfused for the same length of time.

Adenosine↗
PubMed1993

[Tracheal compression treated with endoluminal stents].

Tracheobronchial stenoses can be caused by growth of endoluminal tumour or by external compression. Endoluminal tumours can be treated by means of endoscopically applied lasers, while tumours in the oesophagus, thyroid gland, or lymph nodes which compress the airways connor be reached by this type of treatment. We report four cases where life-threatening compression of airways by malignant tumours was successfully relieved by stenting the trachea with a silicone stent, Endoxane. The stent was inserted through a rigid bronchoscope, and the operative procedure was uneventful in all cases. Postoperatively, the patients did not experience severe discomfort from the stent, and neither dislocation of the stent nor retention of secretions was a problem. All the patients died of cancer-related causes, but none died from suffocation. It is concluded that tracheo-bronchial stenting is a valuable supplement to irradiation in palliative treatment of airway compression of airways caused by malignant tumours.

Adult↗
PubMed1991

[Tracheobronchial tumors treated with laser. 7-year experiences at Aker hospital].

The first Nd-YAG laser treatment for endoluminal airway obstruction in Norway was performed at Aker Hospital in November 1983. During the ensuing seven years 68 patients have been treated, involving altogether 172 procedures. During the early years a flexible bronchoscope was used to guide the flexible laser probe, in later years the usual practice has been to use the rigid bronchoscope, 54 patients were treated for malignant tumour, three for semi-malignant and 11 for benign tumour. In general, the best results were achieved with a proximal location of the tumour. Two patients died during the procedure from hypoxia, and one patient died from hemoptysis on the fifth day after operation. Based on retrospective studies of the clinical journal and the results from postmortem examination of 97 consecutive patients who died from pulmonary carcinoma, we anticipated that six of these patients would have benefited from laser treatment on at least one occasion during their disease. In Norway, with an incidence of approximately 400 cases of pulmonary carcinomas each year per million inhabitants, we estimate the need of lung laser procedures to be 25 per million each year.

Adolescent↗
PubMed1989

Functional impairment in isolated rat hearts induced by activated leukocytes: protective effect of oxygen free radical scavengers.

Ischemia-reperfusion activates polymorphonuclear leukocytes (PMN). Depletion of PMN has been shown to reduce the size of experimental myocardial infarction. We have studied whether PMN activated by phorbol myristate acetate (PMA) would depress function of the isolated rat heart, and if this effect was mediated by oxygen free radicals (OFR). Cells and/or drugs were added to the perfusate into the aortic cannula for 10 min, followed by a 30 min recovery period. Oxygen free radicals formation was verified by chemiluminescence (CL). PMA-activated PMN (n = 13) caused CL response of 27,493 +/- 5113 counts (mean +/- S.E.M.) and reduced left ventricular developed pressure (LVDP) to 30 +/- 9% and coronary flow (CF) to 49 +/- 7% of the baseline value at the end of the observation period. Addition of super-oxide dismutase (SOD) and catalase (CAT) (n = 11) reduced the CL response to 5623 +/- 806 counts, but did not influence either LVDP (36 +/- 15%) or CF (51 +/- 18%). Addition of thiourea (TU) to the activated cell suspension (n = 8) further reduced the CL response (3663 +/- 474 counts), and LVDP was 86 +/- 5% and CF was 87 +/- 3%. When TU + SOD + CAT was mixed with PMN + PMA (n = 11), the CL was almost abolished (117 +/- 21 counts) and LVDP was 73 +/- 8% and CF was 94 +/- 6%. When CF was reduced (n = 7) alike the CF reduction in the hearts receiving PMA + PMA, LVDP was not significantly changed at the end of the observation period (75 +/- 6%). Unactivated PMN (n = 8) caused minor response of LVDP and CF, similar to PMN + PMA + TU and PMN + PMA + SOD + CAT + TU. PMA alone (n = 8) was cardiotoxic and caused changes similar to PMN + PMA. This effect was not inhibited by scavengers (n = 6). The supernatant of the PMN + PMA suspension (n = 7) did not impair cardiac function, suggesting that no free PMA was available after mixing with PMN. We conclude that activated PMN in the coronary circulation depressed cardiac function and increased vascular resistance due to OFR production.

Animals↗
PubMed1988

The selenium-deficient rat heart with special reference to tolerance against enzymatically generated oxygen radicals.

The tolerance against two different levels of enzymatically generated oxygen radicals was studied in isolated Langendorff-perfused hearts from selenium (Se)-deficient and control rats. The glutathione peroxidase activity of the Se-deficient hearts was less than 5% of that of the controls. Examination of the ultrastructure was made after random sampling using morphometric methods. Selenium-deficient hearts demonstrated some areas with myocytes with intracellular oedema. Oxygen radicals (hydrogen peroxide and superoxide) were generated by adding xanthine oxidase for 12 min (high dose: 25 U/l; low dose: 12.5 U/l) and hypoxanthine to the buffer of isolated Langendorff-perfused rat hearts. Left ventricle-developed pressure (LVDP) and high-energy phosphates (ATP and CP) were measured. After the low dose of oxygen radicals, LVDP was reduced to 32.7 +/- 6.5% (mean +/- SEM) of initial values in the Se-deficient group, but only to 58.3 +/- 8.4% in the control group (p less than 0.05). After the high dose, LVDP decreased abruptly to zero in both groups. However, ATP content was significantly (p less than 0.05) lower in Se-deficient than in control hearts. Perfusion with oxygen radicals (low dose) resulted in the appearance of mitochondrial damage in both groups, but intracellular oedema was still present only in the Se-deficient hearts. It is concluded that protection against oxygen radicals was reduced in Se-deficient hearts. This was probably due to loss of myocardial glutathione peroxidase activity.

Adenosine Triphosphate↗
PubMed1987

Changes in guinea pig muscle histology in response to reduced mobility.

Dorsiflexion of one hind foot has been prevented in guinea pigs by means of a light prosthesis. The gastrocnemius and soleus muscles of both hind legs have been removed after a period of 2 weeks, and the fiber cross-sectional areas of type 1 and 2 fibers in both muscles have been measured. Comparison of the values in normal and affected muscles shows that the limited reduction in free movement of the foot led to a significant atrophy in types 1 and 2 fibers in both muscles. The use of this simple prosthesis appears to have no effect on any other function of the leg except for the restriction of the lengthening of gastrocnemius and soleus muscles, and the results show that some of the hypotheses about the muscle atrophy seen in fully immobilized limbs cannot account for the changes observed in the present experiments and seem to be of limited validity.

Animals↗
PubMed1987

Ultrastructural changes induced in the isolated rat heart by enzymatically generated oxygen radicals.

This study describes the effect of oxygen radicals on the ultrastructure of the isolated Langendorff-perfused rat heart. Oxygen radicals were enzymatically generated by xanthine oxidase (0.025 U/ml) and hypoxanthine (0.96 mM). Hearts were perfusion-fixed for electron microscopy and stereological technique was performed to obtain estimates of volume fractions (Vv) of different tissue components. Perfusion with oxygen radicals resulted in areas with severely damaged myocardial cells. These changes included swelling and cristolysis of mitochondria, disruption of filaments, development of intracellular edema and focal disruption of the sarcolemma. Stereological examination revealed few alterations after 5 min perfusion with oxygen radicals. After 10 min perfusion with oxygen radicals, however, the Vv (myocyte/myocardium) increased from 0.542 +/- 0.042 (mean +/- S.D.) to 0.663 +/- 0.144, and this paralleled the development of Vv (cellular edema/myocyte) being 0.047 +/- 0.028. Vv (capillary wall/capillary) increased from 0.215 +/- 0.046 to 0.411 +/- 0.123 indicating endothelial swelling. Although the mitochondria appeared swollen, Vv (mitochondria/myocyte) remained constant. The effect of a 35 min recovery period on the ultrastructure was minor. The application of SOD and catalase together with xanthine oxidase and hypoxanthine reduced the observed changes significantly, thus proving the participation of oxygen radicals. This study confirms that oxygen radicals can induce major alterations in myocardial ultrastructure.

Animals↗
PubMed1987

Protection by superoxide dismutase and catalase in the isolated rat heart reperfused after prolonged cardioplegia: a combined study of metabolic, functional, and morphometric ultrastructural variables.

To determine the protective effect during ischaemia and reperfusion of removing oxygen radicals two groups of isolated Langendorff perfused rat hearts were arrested with cardioplegic solution at 4 degrees C and kept ischaemic at 15 degrees C for 210 min before being reperfused for 60 min at 37 degrees C. To remove oxygen radicals superoxide dismutase and catalase were added to the cardioplegic solution and to the buffer during the first 30 min of reperfusion in one group, the other group serving as control. At the end of reperfusion the first derivative of left ventricular developed pressure (dP/dt), coronary flow, high energy phosphate concentrations, and ultrastructure were determined. The ultrastructure was examined using a stereological method based on point counting and the results presented as volume fractions (Vv). DP/dt after 60 min of reperfusion was 61.6(5.6)% (mean (SEM)) of the initial values in the control group and 77.6(3.4)% in the superoxide dismutase and catalase supplemented group (p less than 0.05). In the supplemented group coronary flow was significantly higher than in the control group but only in the first part of reperfusion. The concentrations of adenosine triphosphate and creatine phosphate in the control group were 9.9(1.0) and 19.6(1.8) mumol.g-1 dry weight respectively; corresponding values in the supplemented group were 14.4(2.1) and 29.4(3.6) mumol.g-1 dry weight. The morphometric examination of the ultrastructure showed no significant difference in interstitial fluid accumulation evaluated by Vv(myocyte/myocardium) measurements and there was no difference in mitochondrial alteration between the two groups. There was, however, a significant reduction in the volume of cellular oedema (Vv(cell oedema/myocyte)) in the supplemented group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Impact of experimental endogenous gram-negative peritonitis on the pancreas of the rat as evaluated by cationic trypsin-like immunoreactivity in peritoneal fluid and serum and by electron microscopy of pancreatic tissue.

Endogenous gram-negative peritonitis leading to septic shock was induced in rats by a defined perforation of the coecum. Cationic trypsin-like immunoreactivity (CTLI) was measured in peritoneal fluid and serum by a radioimmunoassay method. Five, 10, and 15 h after the coecal perforation, CTLI in peritoneal fluid was significantly higher than before the coecal perforation and also higher than in the corresponding control rats. Moreover, CTLI in serum was under the same conditions significantly higher 10 and 15 h after the induction of peritonitis. Gel chromatography of peritoneal fluid and serum during peritonitis showed free CTLI and CTLI bound to both alpha-1-antitrypsin and alpha-2-macroglobulin, whereas only free CTLI could be detected in serum from control rats. These findings were accompanied by local ultrastructural changes in the acinar cells as evaluated by electron microscopy. The pathophysiologic implications of the findings are discussed.

Animals↗
PubMed1986

Influence of oxygen radicals generated by xanthine oxidase in the isolated perfused rat heart.

To investigate the cardiac effects of enzymatically generated oxygen radicals isolated Langendorff rat heart preparations were perfused with hypoxanthine (0.96 mmol X litre-1) plus xanthine oxidase (0.025 U X ml-1). Oxygen radicals produced an immediate increase in coronary flow. After 10 min a pronounced reduction in contractile performance, as well as in concentrations of high energy phosphates, was seen. Electron microscopical examination showed damage with cellular oedema as a prominent finding. These effects were all effectively reversed by the specific enzymes, superoxide dismutase and catalase, proving that they were due to oxygen radicals.

Animals↗
PubMed1986

Reversible and irreversible changes in the dog heart during acute left ventricular failure due to experimental multifocal ischaemia.

Acute left ventricular (LV) failure was induced in closed-chest pentobarbital anaesthetized dogs (n = 15), by injection of 50 micron plastic microspheres into the main left coronary artery. There were marked reductions of cardiac output and peak LV dp/dt after the embolization, while LV end-diastolic pressure (LVEDP) increased markedly. Biopsies were taken 1, 2, 3, 4, 6, 8, 10, 36, 48 hours, 7 and 14 days after injection of microspheres. Histological examination of the left ventricle revealed multiple ischaemic lesions distributed throughout the are supplied by the left main coronary artery. Oilred O staining revealed deposition of fine lipid droplets in the ischaemic cardiac muscle cells bordering on the necrotic areas. Ultrastructurally the lipid-containing cells showed numerous vacuoles localized in association with the mitochondria. The vacuoles could be observed already 1 hour after embolization and increased in number up to 48 hours. At the end of the observation period at two weeks, the number of lipid droplets was markedly reduced and the heart regained its functional activity. It is concluded that the myocardial lesions induced by coronary embolization of plastic microspheres were associated with acute left ventricular pump failure and consist of multiple foci of damaged myocardium with a central core of necrotic tissue. In the periphery of these lesions there were myocytes with lipids and other signs of light and moderate ischaemic injury. Our suggestion is that these cells represent a region of intermediate injury of "border zone" cells that are a potentially salvageable myocardium.

Animals↗
PubMed1985

Critical evaluation of methods for electron microscopy of cervical mucus.

The ultrastructure of cervical mucus has been studied by scanning (SEM) and transmission (TEM) electron microscopy. The images differ according to the methods used for preparation; different patterns were found in the same sample when the freeze-drying and critical point-drying methods were used for SEM. When using TEM, the specimen appeared more homogeneous, with fine fibrils and granules. This accords with the theory that the cervical mucus consists of a randomly entangled fibrillar network. Electron microscopy of cervical mucus requires preparation procedures which involve considerable risk of creating artefacts. In our experience the TEM technique produces fewer artefacts and therefore gives pictures more true to the in vivo situation.

Cervix Mucus↗
PubMed1983

An ultrastructural study of cryofractured myocardial cells with special attention to the relationship between mitochondria and sarcoplasmic reticulum.

A comparative study of various cryofracturing techniques has been conducted on the mammalian myocardial cell. Quench freezing of fresh or fixed tissue in melting Freon 22 resulted in severe cellular damage due to ice crystallization. Fixation with Karnovsky's fixative prior to quenching had no modifying effect on the size and distribution of the ice crystals. The crystals were orientated primarily in the direction of the long axis of the myofibrils, manifested as empty tube-like structures in the scanning electron microscope (SEM). Regular cross-bridging often seen at the Z-band levels indicated that ice crystals, at least in some portions of the cells, were confined within the sarcomere. Within the same cell the size of the ice crystals could vary considerably. Treatment of the tissue with polyvinylpyrrolidone (PVP) prior to rapid freezing had no noticeable cryoprotective effect. The surface of the thin layer of PVP surrounding the freeze dried tissue appeared amorphous in the SEM. However, the first evidence of ice crystallization was found a few micrometers under the surface. The freezing artefacts were completely circumvented if the cryofracturing was carried out on ethanol-impregnated or on critical point dried material. While the first method resulted in a smooth fracture plane passing through the cell structures, the intracellular fracture plane of the critical point dried material followed the surface of the cell organelles. Separation of the cell organelles caused by freezing or by critical point drying revealed thread-like structures extending from the mitochondrial surface. Re-examination of SEM-processed material in the transmission electron microscope (TEM) revealed that these structures were part of the sarcoplasmic reticulum (SR), and that a close contact between the SR and the outer mitochondrial membrane existed. TEM of conventional prepared material revealed that strands of electron-dense material, here named 'mito-reticular junctional fibres', bridged the narrow gap between the mitochondrial surface and the SR. It is suggested that these fibres have a specific anchoring function.

Animals↗
PubMed1983

Morphologic changes in atrial myocardial cells after cold cardioplegic standstill and during reperfusion in coronary bypass surgery.

Changes in the morphology of myocardial cells during reperfusion after long cardiac ischemia were studied as a sensitive indicator of myocardial damage. Observations were made by light and electron microscopy on specimens of atrial myocardium from 20 patients undergoing uneventful coronary bypass surgery with global hypothermic (less than 18 degrees C) cardioplegic protection. The findings in biopsy specimens taken before and immediately after cardiac arrest and following 20 and 60 min of reperfusion were arbitrarily graded in a semiquantitative scoring system. More than 60 min of cold cardioplegic arrest resulted in foci of altered myocardial structure, as seen in biopsies prior to reperfusion. After 20 min of reflow, intracellular and interstitial edema was found and no regression of the subcellular changes had taken place. (Worsening was observed in 7 cases.) After 60 min of reperfusion the myocardial ultrastructure had normalized in all the patients who had had ischemic cardiac arrest for less than two hours. In two hearts with longer ischemia (120 and 140 min), scattered areas of myocytes undergoing progressive changes were seen, although the postoperative myocardial performance was normal. Provided that the observed atrial changes were representative of left and right ventricle, the study indicates that reperfusion per se may enhance edema and cellular derangement, and that reperfusion for more than 20 min is usually necessary for normalization of the myocardium after more than one hour of ischemia.

Adult↗
PubMed1980

On the origin of Z-band material and myofilaments in myoblasts from the human atrial wall.

The origin of cardiac myofibrils in cells from the atrial wall in human embryos was studied, Z-band substance appears throughout the cytoplasm as irregular electron dense patches in a network of thin filaments. The thin and thick filaments are synthesized as separate units in the sarcoplasm and are later aggregated into myofibrils. Complexes of Z substance and thin filaments occur numerously at different stages of myofibrillar organisation. Thick filaments are formed in close proximity to free ribosomes and are later incorporated in an hexagonal pattern into the Z-band/thin filament complex.

Cytoplasm↗
PubMed1980

A correlative transmission and scanning electron microscopic study of the pigeon myocardial cell.

A comparative study of the pigeon ventricular myocardial cell has been performed by transmission electron microscopy (TEM) and by scanning electron microscopy (SEM). Three-dimensional access to the cell interior was obtained by cryo-fracturing paraffin-embedded tissue immersed in liquid nitrogen. The TEM studies revealed parallelly arranged myofibils separated by rows of mitochondria. The sarcoplasmic reticulum is represented by a well-developed network of tubules which, at the Z- and H-band level of the sarcomere, expands to form belt-like cisternae. The cisternae at the Z-band level lie in close proximity to both myofilaments and mitochondria. Transverse tubules are absent and thus only peripheral couplings are present. SEM observations of the fractured tissue revealed the spatial relationship between the different cell organelles, the most important of these being the parallel myofibrils and the mitochondria. The conspicuous ridges transversing the myofibril at the Z-band level consist mainly of expanded Z-bands, but overlying SR-tubules also contribute to these ridges. Traces of the SR can sometimes be seen covering the myofibrils. The close proximity between the SR and the mitochondria was also confirmed in the SEM. Preparation and examination of SEM prepared tissue in the TEM confirmed that no essential damage or reorganization of cell organelles had taken place during tHE SEM procedure. On the other hand some shrinkage of the tissue, which was probably caused by critical point drying, was noticed.

Animals↗
PubMed1980

Development of specific granules in embryonic cardiac myocytes of the human auricular wall.

Atrial specific granules first appear in the human auricle by about 7 weeks of fetal development. They are rapidly formed between the 7 and 8 week stages. Granules are fairly evenly spread at the onset of their appearance. As they increase in number they soon aggregate in the juxtanuclear and subsarcolemmal positions. The electron dense matrix of granules of young cardiomyoblasts is condensed and/or synthesized within the Golgi cisternae. Large and electron dense cisternae are sometimes observed in close connection with mature specific granules. Bristle coated vesicles develop by a "budding off" process from the lateral margins of the Golgi cisternae. A fusion between bristle coated vesicles and specific granules is indicated.

Golgi Apparatus↗