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Biomedical subjects

U Bagge

Publications and source records attributed to U Bagge.

At least 73 records · Page 4Linked to original sources
PubMed1981

Effects of graded compression on intraneural blood blow. An in vivo study on rabbit tibial nerve.

Compression applied to a peripheral nerve may easily interfere with intraneural blood flow. In the present experimental study, a vital microscopic technique was used to observe changes in intraneural microcirculation (intrafascicularly and extrafascicularly) when graded compression was applied to a rabbit's tibial nerve by a specially designed minicompression device. Interference with venular flow was observed already at a pressure of 20 to 30 mm Hg while arteriolar and intrafascicular capillary flow was impaired at about 40 to 50 mm Hg. At 60 to 80 mm Hg no blood flow could be observed in the nerve. Nerves observed 3 or 7 days after 2 hours of compression at 400 mm Hg showed no or very slow stagnant blood flow within the previously compressed segment. It is concluded that acute compression of nerve may cause persistent impairment of intraneural microcirculation due to mechanical injury to blood vessels.

Acute Disease↗
PubMed1981

Joint inflammation in rabbits induced by preformed immune complexes.

The rabbit knee joint was used to evaluate the inflammatory properties of immune complexes with different contents of antigen. Immune complexes made in vitro with antiserum from hyperimmunized rabbits and bovine serum albumin as antigen were injected into the joints. The reactivity of the individual animal was established by injection of normal rabbit serum into the contralateral joint. The number of leukocytes washed out from the joints at fixed intervals was used as a measure of the inflammatory properties of the immune complexes. With immune complexes formed at antigen excess the highest numbers of leukocytes, with a predominance of granulocytes, were found after 6 h of exposure. However, these complexes gave only weak complement activation in vitro, measured with a hemolysis assay. Complexes formed at optimal precipitation proportions gave high complement activation in vitro but only a small number of leukocytes in the joints at 6 h exposure. This finding may be explained by a rapid phagocytosis of the latter complexes while complexes formed at antigen excess are not readily phagocytized. This hypothesis is supported by the observation that higher leukocyte counts were found after shorter exposure times to complexes formed at optimal precipitation proportions than after exposure to complexes with antigen excess.

Animals↗
PubMed1981

Red cell shapes in capillaries.

The deformation of red blood cells (RBCs) has been studied in narrow glass capillaries using two microscopes mounted at right angles to allow three-dimensional analyses. It is found that the RBCs deform primarily by a folding of the disc about the longitudinal axis of the capillary.

Blood Flow Velocity↗
PubMed1981

Determination of wound strength for quantitation of skin damage after pressure ischemia. An experimental study in rabbits.

Rabbits skin folds were placed in plexiglass chambers enabling control of the skin fold temperature during cuff compression (200 mmHg) for 4 hours. In 10 animals the skin folds were kept at 36 degrees C - in another 10 animals the skin fold temperature was lowered to 10 degrees C. To quantitate the skin injury caused by the pressure ischemia a standardized wound was made, and immediately closed, after release of pressure. Control wounds were made in normal skin. Seven days later the mechanical strength of the wounds was tested by determination of breaking load. There was no significant difference in breaking load between the wounds made in normal skin and in the skin folds kept at 10 degrees C, whereas the breaking loads was significantly decreased in the wounds made in skin folds kept at 36 degrees C, i.e. normal skin temperature, compared with the controls. Thus, the results show that cooling may preserve the reparative capacity in skin subjected to pressure ischemia. It is assumed that this effect is related to a lowered cell metabolism during the ischemia. It may also be concluded that the pressure (mechanical) injury, being the same in both temperature groups, is less important than the ischemic injury.

Animals↗
PubMed1981

Vital microscopy of epidermal melanocytes.

Vital microscopy has been used to study melanocytes in the mouse. The morphology of the living epidermal melanocyte is described, including dendritic movements, cell division and melanosome transport.

Animals↗
PubMed1980

Control of tissue environment during vital microscopy of the microcirculation in the m. tenuissimus in cat.

The physiological preservation of the tenuissimus muscle preparation in cat during vital microscopy of the microcirculation is assessed, comparing the originally described technique with a modified approach. Differences in the compared techniques include modes of dissection and transillumination, room-air exposure and moisturizing procedures. The original technique involves extensive dissection, inadequate temperature control and irrigation in open air. The modified technique involves less surgery due to a new illumination system, controlled heating and a Mylar foil cover on the preparation to minimize room-air influences. Temperature measurements and analyses of energy metabolism (ATP, CP, glucose, G6-P and lactate) are used as objective criteria of tissue normalcy. The microcirculation and metabolism are evaluated during anesthesia (alpha-chloralose) at rest as well as in hemorrhagic shock. In the resting state, muscle temperature drops to 28 degrees C with the irrigation technique, whereas the Mylar technique keeps the temperature at 34--35 degrees C. Neither technique causes deviations in normal metabolism. In shock, however, the temperature in the irrigated tenuissimus muscle fall 8--9 degrees C below deep muscle temperature and there is a significantly attenuated metabolic response to ischemia, while the Mylar preparation follows the changes of unexposed muscle, both in temperature and metabolism.

Animals↗
PubMed1980

White blood cell deformability and plugging of skeletal muscle capillaries in hemorrhagic shock.

The cause of maldistributed capillary perfusion in hemorrhagic shock was investigated in a combined in vivo and in vitro study. The cat tenuissimus muscle was observed by vital microscopy before and after withdrawal of 45% of the blood volume. The induced shock conditions reduced the number of perfused capillaries about 50%. Close examination of the scattered, nonperfused capillaries showed that they remained open and almost invariably contained one or several leukocytes. These cells were usually located at the bulgings of endothelial cell nuclei, and when occasionally dislodged, recirculation immediately occurred. Platelet or erythrocyte aggregates were not seen in the microvasculature in shock. To test whether the trapping of leukocytes reflected an impaired deformability of these cells in shock or was merely a pressure dependent phenomenon, deformability studies were performed on leukocytes in vitro. Central venous blood was drawn before and 2 h after bleeding and leukocytes were separated by sedimentation. The passage-time of single leukocytes through a glass capillary stenosis at constant driving pressures was used as an index of cell deformability. No qualitative changes in stiffness were found after shock. The distribution of cell passage-times indicated, however, that the stiffest portion of the leukocyte population was removed from the circulation in shock.

Animals↗
PubMed1980

Three-dimensional observations of red blood cell deformation in capillaries.

The shape changes of red blood cells (RBCs) flowing in narrow glass capillaries have been studied by the use of two microscopes viewing the cells simultaneously at right angles along a horizontal and a vertical optical axis. The observations show that the primary mode of deformation of RBCs in a narrow capillary is a folding or bending about the longitudinal axis of the capillary rather than a compression and extension of the cells in the plane of the original disk, which has been suggested previously [10].

Capillaries↗
PubMed1979

Cuff pressure and microvascular occlusion in the tracheal mucosa. An intravital microscopic study in the rabbit.

A method is described for the intravital microscopic observations of rabbit tracheal mucosa microcirculation during compression with a thin, transparent high volume cuff. The cuff pressure (CP) required to cause complete ischemia in the mucosa over the cartilages was measured and a correlation was found to the mean arterial blood pressure (MAP). Ischemia was not observed below CP-MAP ratios of 0.40 for untreated animals or below 0.44 for animals where the MAP had been elevated by adrenalin. However, marked reduction of the microvascular blood flow was present at lower CP-MAP ratios, 0.2-0.3, which at a MAP of 75 mmHg corresponds to cuff pressures of 15-20 mmHg. It is therefore advocated that endotracheal cuff pressures are kept below these values to avoid ischemic tissue injury.

Animals↗
PubMed1979

A technical and biomechanical comparison between two types of microvascular anastomoses. An experimental study in rats.

The microvascular sleeve anastomosis, where one vessel is inserted into the other, was compared with the conventional end to end anastomosis. In an experimental study in rat femoral arteries 42 anastomoses of each kind were examined. Operating time, patency rates, flow rates and strength of the anastomoses were recorded at various postoperative time intervals. It is concluded that the sleeve anastomosis is quicker to perform and that the two types of anastomoses in biomechanical respects are similar. Flow rates are slightly decreased immediately postoperatively in the sleeve anastomosis but this is of a temporary nature.

Animals↗
PubMed1978

Intravital microscopy of the microcirculation in man during and after experimentally controlled ischemia.

In man, using a skin tube chamber technique, microvascular reactions during and after complete experimental ischemia was studied by intravital microscopy. During 1 and 2 hour ischemia the trapped blood cells did not adhere to each other or to the vascular walls except for RBCs which formed rouleaux. Reflow after 1 and 2 hour ischemia was rapid with a hyperemic reaction and a transient increase in WBC stickiness. Thus, a mild and reversible inflammatory reaction was provoked by the short ischemic insult. During 6 hour ischemia most of the blood cells maintained their integrity. However, in a few vessels the RCSs formed homogeneous masses indicating hemolysis of some of the RBCs. There was also marked diapedesis of RBCs and increased WBC stickiness, but the platelets did not react to form thrombi. After the 6 hour ischemia reflow occurred in all vessels and the homogeneous masses seemed to cause only a temporary hindrance to reflow. The final outcome of the 6 hour ischemic insult was uncertain since in one of the two experiments there was a complete circulatory standstill 24 hours after the ischemia while in the other there was an almost normal blood flow.

Adult↗