Biomedical subjects
A Skulberg
Publications and source records attributed to A Skulberg.
Letter: Occupational hazard of halothane.
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Resuscitation of cardiac arrest outside hospitals: experiences with a mobile intensive care unit in Oslo.
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Halothane induced liver damage.
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The protective effect of vasopressin during occlusion of the portal vein in pigs.
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Human liver transplantation without azathioprine.
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[Use of calcium in liver transplantation].
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Experiences with a doctor-manned ambulance service in Oslo.
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[A doctor-manned ambulance service in Oslo].
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Susceptibility of mink to Clostridium botulinum type E toxin.
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Phospholipase C-evoked glycerol release in energy depleted rat myocardial cells.
Preincubation of rat myocardial cells in hypoxic substrate-free Krebs-Ringer bicarbonate buffer (pH 7.4, 37 degrees C) resulted in a substantial decline in high energy phosphates (ATP and CP). Thus, 20 and 60 min preincubation produced a 18 and 72% decline in ATP content, whereas the parallel decline in CP content was 51 and 73%. This energy depletion was accompanied by a change in cell morphology from the initial rod-shaped form to rounded up (hyper-contracted) myocytes. In cells preincubated in substrate-free normoxic buffer, both normal morphology and energy homeostasis were maintained. When energy depleted myocytes later were incubated in the presence of phospholipase C (PLC), this resulted in a substantial release of glycerol, amounting to 92 and 137 nmol/10(6) cells.2 h in 20 and 60 min energy depleted myocytes, respectively. In addition, PLC caused an increased leakage of lactate dehydrogenase in energy depleted myocytes. Normal cells, on the other hand, were apparently not affected by PLC. These data suggest that PLC selectively attacks energy depleted and/or structurally damaged myocytes. This could well enhance the breakdown of the natural barrier between the extra- and intracellular compartments and thus augment the cellular damage during ischemia. Moreover, energy depleted myocytes appeared exceptionally sensitive to this enzyme, since the levels required to cause glycerol or lactate dehydrogenase release were several orders of magnitude lower than that required to cause membrane permeation in other cell types.
Effects of hypoxia on lipolysis in isolated rat myocardial cells.
The effect of hypoxia on myocardial lipolysis (glycerol release) was investigated in freshly isolated, calcium-tolerant rat ventricular myocytes. Hypoxia was produced by gassing the incubation medium (Joklik-minimum essential medium, supplemented with 1.2 mM MgSO4, 1 mM DL-carnitine, 1.5 mM CaCl2 and 0.6 mM palmitate bound to 0.15 mM fatty acid free bovine serum albumin) with 95% N2-5% CO2. Control (normoxic) incubations were carried out under air-5% CO2 atmosphere. Basal glycerol release increased from 46.6 +/- 3.0 nmol/10(6) cells.30 min in normoxia to 64.5 +/- 4.3 nmol/10(6) cells.30 min in hypoxia (p less than 0.05). Addition of isoprenaline (10 microM) resulted in a significant (p less than 0.05) stimulation of the glycerol release both in normoxia and in hypoxia, but the enhancement above basal rates was apparently lower in hypoxia (8.7 +/- 2.5 nmol/10(6) cells.30 min) than in normoxia (12.2 +/- 2.7 nmol/10(6) cells.30 min). Furthermore, whereas the isoprenaline-induced rise in lipolysis both in normoxia and hypoxia was prevented by inclusion of propranolol (10 microM), propranolol did not affect the hypoxia-induced increase in lipolysis. Thus, the above findings suggest that myocardial lipolysis may be stimulated by local non-adrenergic mechanisms during hypoxia.
Chest compression--an alternative to the Heimlich manoeuver?
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On the technique of external cardiac compression.
ECG, arterial flow and pressure were recorded during external cardiac compression (ECC) in a patient whose heart had ceased beating. The patient was a 68-year-old female who remained comatose for 2 weeks after an emergency laparotomy for perforated diverticulitis of the colon. She developed sepsis, renal failure, and cardiopulmonary failure. During ECC, the pressure on the sternum was maintained for about 0.5 sec (sustained pressure technique), flow and mean arterial pressure were improved by 32 and 20%, respectively, as compared with flow and pressure obtained with a quick and more jerky compression. During spontaneous heart activity with a low blood pressure, a superimposed ECC improved both flow and mean arterial pressure. Calcium chloride and adrenaline injected into the right atrium increased the tone and contractile power of the heart and greatly improved flow and pressure when the heart was subsequently compressed during asystole.
Placebo-controlled comparison of single intramuscular doses of ketorolac tromethamine and pethidine for post-operative analgesia.
The analgesic efficacy and safety of single doses of 10 mg and 30 mg ketorolac tromethamine and 100 mg pethidine were evaluated in a double-blind, parallel-group study. The drugs were administered intramuscularly to patients experiencing moderate, severe or very severe pain immediately following major abdominal surgery. A total of 129 patients were randomly assigned to receive either active drug (n = 32 for each treatment group) or placebo (n = 33), and the patients assessed pain intensity and pain relief on a visual analogue scale at regular intervals over the following 8 h. During the first 2 h, pethidine had a more rapid onset of action than ketorolac or placebo, and thereafter 100 mg pethidine and 30 mg ketorolac were equally effective. Ketorolac, at a dose of 10 or 30 mg, and 100 mg pethidine were clinically and statistically more effective than placebo, with 30 mg ketorolac having a similar efficacy to 100 mg pethidine over the 8-h study period and 10 mg ketorolac being slightly less effective than 30 mg ketorolac. No serious adverse events were reported.