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Biomedical subjects

G Arturson

Publications and source records attributed to G Arturson.

At least 19 recordsLinked to original sources

Purification and characterization of porcine C3. Studies of the biologically active protein and its split products.

Separation techniques for obtaining pure and biologically active swine C3 have been improved in this study. Using these procedures and through the further characterization of porcine C3, the possibilities for developing more specific techniques for the analysis of the complement system in swine have been improved. Plasma was initially treated with protease inhibitors, polyethylene glycol (PEG)-fractionation, plasminogen-depletion and a rapid chromatographic desalting step. The essential fractionation was carried out by DEAE-Sephacel chromatography. Contaminants were removed by size-exclusion (Sepharose CL-6B)- and hydroxylapatite-chromatography. The final recovery reached 56% with 73% retaining specific hemolytic activity. The amino acid composition (98.33%), the functional compatibility and the secondary structure of fragments and intact protein indicate a high degree of homology with human C3. In contrast with the findings of earlier studies was the considerable immunologic cross-reactivity observed with human C3, and the size difference between the human and the swine C3-beta subunit, which was found to be 10 kDa lighter than the human analogue. The finding that the swine C3b/iC3b/C3c fragments do not separate from C3 by agarose electrophoresis, unlike the human analogues, demonstrated that this commonly used simple parameter for the detection of complement activation cannot be used in the porcine model.

Amino Acids

Angiographic findings and need for amputation in high tension electrical injuries.

Because it is difficult to estimate the extent of deep tissue injury clinically, angiography was carried out in 28 patients with signs of damage from current flow through the body. Eight of the arteriograms showed normal extremities, 6 showed changes of small arteries, and 38 showed injury to the main arteries. In the latter group there were 24 total arterial occlusions, narrow irregular lumens in 10, and 4 had occlusion and distal refilling. Changes in the main arteries were most often seen near major joints where the internal body resistance as well as the density of the current are higher. Injury to the main arteries resulted in severe neuromuscular damage or amputation of the limb, whereas injury to small arteries resulted in little functional deficit. Of the 25 amputations 19 were at the level of the arterial occlusion. Spasmolytic drugs did not increase filling. We conclude that early angiography is valuable for the detection of deep injury and often indicates the level of adequate amputation or the need for immediate exploration. In some patients it indicates the necessity for arterial reconstruction.

Adolescent

Exchange of 3-methylhistidine in the splanchnic region in human infection.

This investigation was undertaken to determine the splanchnic exchange of 3-methylhistidine (3MH) in infection. Hepatic vein, femoral vein, and radial artery catheterizations were performed in 12 febrile patients with infections of varying severity. Differences in arteriovenous 3MH, analyzed by high-performance liquid chromatography, were multiplied by the plasma flows, determined by a dye dilution technique. The mean splanchnic efflux was 0.062 +/- 0.180 mumol/min (mean +/- SD) with uptake occurring in five patients. The splanchnic uptake was significantly (p less than 0.001) correlated with the urinary 3MH excretion and the peripheral release from the leg. It is concluded that in human infection, splanchnic 3MH release is low and in patients with high rates of myofibrillar catabolism there may even be an uptake. The urinary 3MH excretion is still a marker of myofibrillar protein breakdown because it correlates well with the release from the leg, regardless of whether the patient has a splanchnic uptake or a release.

Chromatography, High Pressure Liquid

Computer simulation of fluid resuscitation in thermal injury. A. B. Wallace memorial lecture 1987.

Following thermal injury many subsystems of the human body interact closely. The effects both of the pathological event in one subsystem and the subsequent therapy are masked or compensated by changes in other homeostatic subsystems. Not until the capacity of the homeostatic subsystems and/or the therapy is inadequate will the effects become obvious. The very complex postburn situation explains why there are so many different shock-preventing fluid therapy programmes and such crude and insecure monitoring of the therapy. In these situations when there are too many factors to be grasped by the unaided human mind, a computer-based 'patient-simulator' could be of value in diagnosis, monitoring and therapy of the severely ill patient with trauma. An extensive pathophysiological model has been designed to describe fluid shifts and haemodynamics in connection with fluid therapy of traumatic patients. The model makes it possible to calculate and predict clinically important state variables on the basis of fluid input and fluid losses. Sample runs are presented for illustrations in haemorrhage and fluid and salt loading. The model is also used to simulate treatment of a burn patient and the results are compared with measured physiological and biochemical variables. Furthermore, four different formulae for resuscitation of patients with thermal injuries according to Evans, Brooke, Parkland and a hypertonic fluid programme are simulated. The results illustrate the potential use of the 'patient-simulator' for designing fluid resuscitation programmes and attempt to optimize them with respect to infusion rate of the fluid administered.

Animals

The tragedy of San Juanico--the most severe LPG disaster in history.

During the early morning of Monday, 19 November 1984, one of the largest disasters in industrial history occurred in the Mexico City Area, causing the greatest rescue effort to assist population in an emergency ever undertaken. The tragic catastrophe started in a large LPG (Liquid Petroleum Gas) storage and distribution centre in San Juan Ixhuatepec, 20 km north of Mexico City. The facilities, owned by the Pemex State Oil Company, consisted of six spherical storage tanks (four with a volume of 1600 m3 and two with a volume of 2400 m3) and 48 horizontal cylindrical bullet tanks of different sizes. At the time of the disaster the storage tanks contained 11,000 m3 of a mixture of propane and butane. The inhabitants of San Juan Ixhuatepec numbered about 40,000, and a further 60,000 lived in the hills surrounding the village. The majority were poor country people living in one-story houses constructed of concrete pillars filled in with bricks and with roofs of iron sheets. The disaster started due to LPG leakage, probably a pipe leakage or rupture due to excess pressure. A vapour cloud built up and was slowly moved by the north-east wind towards the ground-placed flare pit located in the western part of the plant. The vapour cloud was ignited around 5:40 a.m. and was followed by an extensive fire at the plant area. The first explosion was registered on the seismograph at the University of Mexico at 05 h 44 min 52 s and was followed by a dozen explosions within the next hour, some of them of BLEVE type (Boiling Liquid Expanding Vapour Explosion) due to rupture of one or more storage tanks. Two of the explosions had an intensity of 0.5 on the Richter scale. Unburned and burning gas entered the houses south of the plant area and set fire to everything. Blast waves from the explosions not only destroyed a number of houses but also shifted several cylindrical tanks from their supports and added more gas to the fire. The smaller spheres and some of the cylinders exploded and fragments and even whole cylinders weighing around 30 tons, were scattered over distances ranging from a few to up to 1200 m.

Accidents, Occupational

Neutrophil granulocyte functions in severely burned patients.

Burns wound sepsis is not only the most common but also the most severe complication following extensive thermal injury. One conceivable explanation of this problem is a reduced capacity of the polymorphonuclear neutrophil leucocytes of these patients to combat the invading microbes. Fifty patients (42 male and 8 female) with deep dermal burns, covering 20-90 per cent of the total body surface area, were investigated from immediately after the injury until death or until healing of the wounds. The following functions of the neutrophil granulocytes were studied: chemotaxis and random migration utilizing a modified Boyden chamber technique, phagocytosis of Staph. aureus and IgG-coated latex particles, bactericidal capacity, e.g. killing of Staph. aureus and the neutrophil granulocyte content of: myeloperoxidase, lactoferrin, and chymotrypsin-like cationic protein. The presence of stimulators and inhibitors of the granulocyte functions was studied using gel filtration of the patient's serum on Sephacryl gel columns. Sera from all patients obtained within the first 1-3 days post-burn contained significantly increased amounts of heat-labile chemokinetic stimulating activity. Sera obtained between days 4 and 10 after injury contained significantly decreased amounts of heat-stable chemokinetic stimulating activity. Reduced chemokinetic activity was found during the third and fourth weeks following major burns (greater than or equal to 40 per cent) due to the presence of one or both heat-stable chemokinetic inhibitory activities. During the second week post-burn patients with burns larger than 40 per cent of the body surface area who showed an inhibition of chemotaxis, also had defects in phagocytosis, and often impaired bactericidal capacity concomitant with lower contents than normal of the granular enzymes. A hyaluronic acid preparation in low concentrations was found to counteract the migration inhibitory effect demonstrated in vitro in sera from patients with severe burns. Based upon these results a series of patients with severe burns and impaired functions of the neutrophil granulocytes have been treated with small amounts of this hyaluronic acid preparation subcutaneously. Very promising results have been noticed, similar to those found in vitro.

Adolescent

Oedema measurements in a standard burn model.

A highly standardized, reproducible burn model on rat hind paw as well as a method to measure oedema volume non-invasively is described. Along with a review of the literature on earlier methods to measure post-burn oedema we present a statistical evaluation of the present model with notes on its applicability in various experimental settings.

Animals

The effect of prompt local cooling on oedema formation in scalded rat paws.

A standardized, reproducible burn model on rat paw was used and the effect of prompt local cooling on the oedema formation was measured using a newly developed non-invasive method. A transient reduction in oedema formation was observed lasting for a longer period of time with decreasing temperature down to 0 degrees C and increasing cooling time up to 120 min. The decrease in oedema formation was followed by an increase towards or above the amount of oedema in untreated scald injury. This post-cooling increase in oedema formation was related to the temperature and the exposure time of the cooling fluid. The immediate effects of cooling are most likely due to local restriction of the blood flow as a result of cold-induced vasoconstriction. The increase of the oedema formation after the cooling period may be due to reactive hyperaemia.

Animals

Early post-burn oedema in leucocyte-free rats.

A highly standardized, reproducible burn model on rat hind paws with objective measurement of oedema volume was used to study the post-burn oedema formation in leucocyte-free rats as compared to a matched group of normal rats. No difference in oedema volume could be detected during the first 4 h post-burn. Thus the mechanical effect of sticking leucocytes in the injured area or leucocyte derived substances do not seem to play any significant role in the early local oedema formation which we postulate is entirely mediated by local events.

Animals

Thermal balance during transurethral resection of the prostate. A comparison of general anaesthesia and epidural analgesia.

Heat loss during anaesthesia and surgery is a common problem. In patients with restricted cardio-pulmonary reserves this may endanger the postoperative outcome. In order to compare thermal balance we studied 25 men undergoing transurethral resection of the prostate (TURP), using either general anaesthesia (G.A.) or epidural analgesia (E.A.). Oxygen uptake, catecholamines, peripheral and central temperatures were followed in the per- and postoperative period. Heat production and total body heat were calculated from oxygen uptake and temperature measurements, respectively. Transurethral resection of the prostate resulted in a peroperative heat loss which was not influenced by the anaesthetic technique used and averaged 370 kJ during the first hour of surgery. G.A. reduced heat production while this was uninfluenced by E.A. After termination of general anaesthesia, oxygen uptake and plasma catecholamines increased, while no such changes could be detected using epidural analgesia. The ability to increase mean body temperature by increasing heat production was negatively correlated to age.

Age Factors

Transcapillary transport after thermal injury.

The pathophysiology of the burn wound is characterized by an inflammatory reaction leading to rapid edema formation due to (1) dilatation of resistance vessels with increased effective transcapillary filtration pressure, (2) increased extravascular osmotic activity created in damaged tissue, and (3) increased microvascular permeability to macromolecules. In extensive burns increased microvascular permeability was found also in tissues remote from the thermal injury. These reactions are due to direct heat effect on the microvasculature and to chemical mediators of inflammation. Important is the increased biosynthesis of prostaglandins at the site of tissue injury which may partly explain vasodilatation, increased microvascular permeability and accumulation of polymorphonuclear leucocytes observed following thermal injury. The morphological interpretations of the changes in the functional ultrastructure of the blood-lymph barrier following thermal injury seem to be a remarkable and persistant increase in the numbers of vacuoles and many open endothelial intercellular junctions. Further less explored changes of the interstitial tissue after severe burn trauma seem to be of great importance.

Animals