[Research in Danish departments of anesthesiology at the turn of the century. A bibliometric analysis]. / Forskning ved danske anaestesiologiske afdelinger ved årtusindeskiftet. En bibliometrisk analyse.

INTRODUCTION: This investigation was based on the surmise that the scientific activity in the specialty of anaesthesiology and intensive care medicine in Denmark is declining. MATERIAL AND METHODS: A quantitative and qualitative analysis of the development in Danish anaesthesiological research during the seven-year period of 1992-1998 was performed with bibliometrical methods and a count of the PhD and doctoral theses produced by Danish anaesthesiologists during that period. RESULTS: In the period investigated, a total of 906 scientific articles were published, of which 749 (83%) originated from university hospitals. Total production decreased by 15% between the two-year periods of 1992-1993 and 1997-1998, whereas the output from university hospitals alone decreased by 10%. The number of scientific publications per anaesthesiologist decreased by 34%, corresponding to 6.7% per year. The quality of the research published, as examined by the cumulative and average impact, showed a slight increase. The number of PhD and doctoral theses per year showed no change. DISCUSSION: Research activity in Danish anaesthesiology is declining, and the specialty seems to be losing scientific ground, both nationally and internationally.

[Treatment of hepatic encephalopathy with flumazenil]. / Flumazenil til behandling af hepatisk encefalopati.

Hepatic encephalopathy (HE) is the neuropsychiatric syndrome that occurs as a complication to liver failure in patients with acute or chronic liver disease. Mental status in this syndrome can range from subtle deficits to coma, with respiratory insufficiency and aspiration to the lungs. The mortality is high. The pathogenesis of HE is not clearly understood. One theory is that it reflects a metabolic disorder of the brain, developed from neuroactive nitrogenous metabolites in the gut that accumulate in plasma when there is an impaired hepatocellular extraction or porto-systemic shunting. Transient improvement of the condition is seen in a subgroup of patients after administration of flumazenil, a specific benzodiazepine antagonist. The group of patients with a positive response to flumazenil therapy may have a better prognosis. Flumazenil may be used in patients in the pretransplantation phase.

Gastrointestinal osmoreceptors and renal sodium excretion in humans.

The hypothesis that natriuresis can be induced by stimulation of gastrointestinal osmoreceptors was tested in eight supine subjects on constant sodium intake (150 mmol NaCl/day). A sodium load equivalent to the amount contained in 10% of measured extracellular volume was administered by a nasogastric tube as isotonic or hypertonic saline (850 mM). In additional experiments, salt loading was replaced by oral water loading (3.5% of total body water). Plasma sodium concentration increased after hypertonic saline (+3.1 +/- 0.7 mM), decreased after water loading (-3.8 +/- 0.8 mM), and remained unchanged after isotonic saline. Oncotic pressure decreased by 9.4 +/- 1.2, 3.7 +/- 1.2, and 10.7 +/- 1.3%, respectively. Isotonic saline induced an increase in renal sodium excretion (104 +/- 15 to 406 +/- 39 micromol/min) that was larger than seen with hypertonic saline (85 +/- 15 to 325 +/- 39 micromol/min) and water loading (88 +/- 11 to 304 +/- 28 micromol/min). Plasma ANG II decreased to 22 +/- 6, 35 +/- 6, and 47 +/- 5% of baseline after isotonic saline, hypertonic saline, and water loading, respectively. Plasma atrial natriuretic peptide (ANP) concentrations and urinary excretion rates of endothelin-1 were unchanged. In conclusion, stimulation of osmoreceptors by intragastric infusion of hypertonic saline is not an important natriuretic stimulus in sodium-replete subjects. The natriuresis after intragastric salt loading was independent of ANP but can be explained by inhibition of the renin-angiotensin system.

Isotonic and hypertonic sodium loading in supine humans.

The hypothesis that hypertonic saline infusion induces a greater natriuresis than infusion of the same amount of sodium as isotonic saline was tested in 8 supine subjects on fixed sodium intake of 150 mmol NaCl day(-1). Sodium loads equivalent to the amount of sodium contained in 10% of measured extracellular volume were administered intravenously over 90 min either as isotonic saline or as hypertonic saline (850 mmol L(-1)). A third series without saline infusion served as time control. Experiments lasted 8 h. Water balance and sodium loads were maintained by replacing the excreted amounts every hour. Plasma sodium concentrations only increased following hypertonic saline infusion (by 2.7 +/- 0.3 mmol L(-1)). Oncotic pressure decreased significantly more with isotonic saline (4.1 +/- 0.3 mmHg) than with hypertonic saline (3.2 +/- 0.2 mmHg), indicating that isotonic saline induced a stronger volumetric stimulus. Renal sodium excretion increased more than a factor of four with isotonic and hypertonic saline but also increased during time control (factor of three). Cumulated sodium excretions following isotonic (131 +/- 13 mmol) and hypertonic saline (123 +/- 10 mmol) were statistically identical exceeding that of time control (81 +/- 9 mmol). Plasma angiotensin II decreased in all series but plasma ANP concentrations and urinary excretion rates of endothelin-1 remained unchanged. In conclusion, hypertonic saline did not produce excess natriuresis. However, as the two loading procedures induced similar natriureses during different volumetric stimuli, part of the natriuresis elicited by hypertonic saline could be mediated by stimulation of osmoreceptors involved in renal sodium excretion. The supine position does not provide stable time control conditions with regard to renal excretory function.

Contribution of abdomen and legs to central blood volume expansion in humans during immersion.

The hypothesis was tested that the abdominal area constitutes an important reservoir for central blood volume expansion (CBVE) during water immersion in humans. Six men underwent 1) water immersion for 30 min (WI), 2) water immersion for 30 min with thigh cuff inflation (250 mmHg) during initial 15 min to exclude legs from contributing to CBVE (WI+Occl), and 3) a seated nonimmersed control with 15 min of thigh cuff inflation (Occl). Plasma protein concentration and hematocrit decreased from 68 +/- 1 to 64 +/- 1 g/l and from 46.7 +/- 0.3 to 45.5 +/- 0.4% (P < 0.05), respectively, during WI but were unchanged during WI+Occl. Left atrial diameter increased from 27 +/- 2 to 36 +/- 1 mm (P < 0.05) during WI and increased similarly during WI+Occl from 27 +/- 2 to 35 +/- 1 mm (P < 0.05). Central venous pressure increased from -3.7 +/- 1.0 to 10.4 +/- 0.8 mmHg during WI (P < 0.05) but only increased to 7.0 +/- 0.8 mmHg during WI+Occl (P < 0.05). In conclusion, the dilution of blood induced by WI to the neck is caused by fluid from the legs, whereas the CBVE is caused mainly by blood from the abdomen.