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Biomedical subjects

A Hauge

Publications and source records attributed to A Hauge.

At least 19 recordsLinked to original sources
PubMed2001

[Should iron preparations be available only by prescription?].

Many persons associate fatigue and lassitude with iron deficiency and take extra iron "to be on the safe side". This is an unfortunate practice, as the early symptoms of iron deficiency anaemia and of hereditary iron overload (homozygous primary haemochromatosis) are similar. Primary haemochromatosis is considerably more prevalent than earlier believed. As many as 5 per 1,000 of the Norwegian population may have two mutated genes for haemochromatosis, while up to 15% may be carriers of a single mutated gene, and for these an extra intake of iron may be hazardous. The condition is highly underdiagnosed. In Norway at present, iron preparations of 60-100 mg are sold over the counter in pharmacies without prescription and often by self-service. However, no one should use iron tablets until iron deficiency and its cause has been ascertained. To avoid uncritical use of iron, iron preparations should be available only by doctor's prescription. Prolonged abuse of iron tablets may result in secondary haemochromatosis.

Adult↗
PubMed2001

Reduced autonomic activity during stepwise exposure to high altitude.

Several studies have shown increased sympathetic activity during acute exposure to hypobaric hypoxia. In a recent field study we found reduced plasma catecholamines during the first days after a stepwise ascent to high altitude. In the present study 14 subjects were exposed to a simulated ascent in a hypobaric chamber to test the hypothesis of a temporary reduction in autonomic activity. The altitude was increased stepwise to 4500 m over 3 days. Heart rate variability (HRV) was assessed continuously in seven subjects. Baroreceptor reflex sensitivity (BRS) was determined in eight subjects with the 'Transfer Function' method at baseline, at 4500 m and after returning to baseline. Resting plasma catecholamines and cardiovascular- and plasma catecholamine- responses to cold pressor- (CPT) and mental stress-test (MST) were assessed daily in all and 12 subjects, respectively. Data are mean +/- SEM. Compared with baseline at 4500 m there were lower total power (TP) (35 457 +/- 26 302 vs. 15 001 +/- 11 176 ms2), low frequency (LF) power (3112 +/- 809 vs. 1741 +/- 604 ms2), high frequency (HF) power (1466 +/- 520 vs. 459 +/- 189 ms2) and HF normalized units (46 +/- 0.007 vs. 44 +/- 0.006%), P < or = 0.001. Baroreceptor reflex sensitivity decreased (15.6 +/- 2.1 vs. 9.5 +/- 2.6 ms mmHg(-1), P = 0.015). Resting noradrenaline (NA) decreased (522 +/- 98 vs. 357 +/- 60 pmol L(-1), P = 0.027). The increase in systolic blood pressure (SBP) and NA during mental stress was less pronounced (21 +/- 4 vs. 10 +/- 2% and 25 +/- 9 vs. -2 +/- 8%, respectively, P < 0.05). The increase in SBP during cold pressor test decreased (16 +/- 3 vs. 1 +/- 6%, P = 0.03). Diastolic blood pressure, HR and adrenaline displayed similar tendencies. We conclude that a transient reduction in parasympathetic and sympathetic activity was demonstrated during stepwise exposure to high altitude.

Adult↗
PubMed2000

[Thomas H.Huxley--the naval doctor who became Darwin's bulldog].

Thomas H. Huxley (1825-1895) was an English physician and biologist who had a deep impact on the Victorian age. More than any other at his time he introduced scientifically based values. As a member of London's school board he brought science into the curriculum, encouraging school-children to ask questions and to make their own observations. Huxley came from a lower middle class family with little money. By sheer determination and hard work he managed to get a medical education at Charing Cross Hospital Medical School. He then obtained a posting on H.M.S. Rattlesnake, which gave him a chance to explore the southern seas and to study marine species. The results were published by the Royal Society of which Huxley became a member at the age of 26, and later its president. After several years of uncertainty he secured a position at the Royal School of Mines, which he transformed into the Imperial College of Science. He was a prolific scientist with wide interests, doing valuable work in paleontology, taxonomy and ethnology. Huxley wrote numerous essays on philosophy and scientific subjects. He coined the word agnostic to explain his attitude to Christian dogma. His style was clear and direct, and his essays still read very well. However, Huxley is now mostly, perhaps unfairly, remembered for his defence of Darwin's theory of evolution. In his book Evidence as to man's place in nature, Huxley, in contrast to Darwin, deals with the evolution of humans, mainly based on comparative anatomy. Huxley advocated a firmly held belief that scientific truths will have a liberating effect on the minds of men. His lectures on scientific subjects attracted large audiences of people who had not had the benefit of a higher education.

Anatomy, Comparative↗
PubMed1997

[Dr Alexander M. Kellas and the first Mount Everest expedition].

In 1921 the government of Tibet gave permission for a British party to attempt Mount Everest from the northern Tibetan side. Little was known about the physiological and medical problems associated with ascents to extreme altitudes. The person who knew most about these topics was Dr. Alexander Kellas, lecturer in medical chemistry at the Middlesex Hospital Medical School. He had made a number of expeditions to the Sikkim Himal and the Tibetan border before the first world war, and had become increasingly interested in the problems caused by altitude. He was invited to join the Everest expedition but died on the approach march at Kampa Dzong on the Tibetan plateau, within sight of the mountain. Before he went on the expedition Kellas wrote an article entitled A consideration of the possibility of ascending Mt. Everest. This paper was never published, but the manuscript exists in the archives of the Royal Geographical Society and the Alpine Club in London. As Kellas saw it, the main issue was whether sufficient adaptation could occur to allow a climber to ascend from a camp at about 7,700 m to the summit (8,848 m) in one day without supplementary oxygen. His conclusion was that this was possible and, in fact, the first such ascent by Habeler and Messner in 1978 started from a camp at 7,900 m. Kellas calculated the pressure on the summit to be 251 mmHg, a more accurate figure than estimates based on the "Standard Atmosphere" Kellas estimated maximum oxygen uptake at the summit to be 970 ml/min, and the current value is thought to be about 1,070 ml/min. His estimates of the climbing rate near the summit closely parallels the rate of Habeler and Messner. Kellas had a talent for asking the right questions. He applied his considerable knowledge of physiology to the topic of high altitude, and his suggestions and recommendations were of consistently high quality. He deserves to be better known, both for his geographical surveys and for his pioneer work on high altitude medicine and acclimatisation. The 1921 expedition, after many failed attempts, discovered a possible route to the top of Mount Everest, which was used on all the summit attempts between the two world wars. The route went from Kharta, over the pass Lhakpa La, across East Rongbuk glacier and up via the north col.

Expeditions↗
PubMed1995

Acid-base regulation during hypothermia. a brief review.

Acid-base physiology has mainly focused on mechanisms that maintain normal, extracellular pH at a constant temperature. Usually it is the arterial blood which is considered. As reliable pH meters became generally available in the 1950s it was observed that an arterial pH of about 7.39-7.42 was maintained remarkably constant in normal man and in mammals in general. This moderate degree of blood alkalosis is maintained by chemical buffering, by appropriate adjustment of the lung ventilation and by the kidneys. To measure pH intracellularly was more difficult, but not impossible, and over some time it became apparent that intracellular fluid was close to neutrality. pH values around 6.8 was found. This is a favorable state for retention of metabolites inside the cells. From an analysis by Davis (1) of the ionization constants of several hundred watersoluble biosynthetic intermediates one may argue that the ideal intracellular pH would occur near the neutrality of water where most of these compounds are ionized and thus captured within the cells, with little tendency to escape across the cell membrane. Apparently, if cells are to defend their neutrality and also to eliminate their acid metabolites and CO2, there must be a considerable transmembrane H+ gradient: The hydrogen ion concentration at neutrality is 160 nmol/L (pH 6.8) and that of blood 40 nmol/l (pH 7.4).

Acid-Base Equilibrium↗
PubMed1993

[Chaos and fractals. Are these of interest to medical science?].

Biological systems are governed by nonlinear dynamics and often appear to be random, because the available information, though accurate, is usually incomplete. It is important to be aware of the fact that nonlinear deterministic systems can behave unpredictably in the long term. Traditional reductionism is unable to provide an adequate understanding of such systems. A more global description and explanation of forms, features and functions is required. Chaos theory and fractal geometry are of value in this respect. This article is an introduction to this relatively new field of science and mathematics.

Fractals↗
PubMed1993

Endothelin-1-induced increases in microvascular permeability in isolated, perfused rat lungs requires leukocytes and plasma.

Effect of endothelin-1 (ET-1) (10(-8) M) on pulmonary microvascular permeability was examined in isolated rat lungs perfused with blood or various blood components. Microvascular permeability was assessed by measuring fluid filtration rate (FFR) in lungs pretreated with papaverine in order to prevent changes in vascular smooth muscle tone. ET-1 significantly increased FFR (131.0 +/- 10.1 mg/min, P < 0.01) after perfusion with blood for 60 min. In lungs perfused with leukocytes resuspended in plasma, ET-1 increased FFR significantly both 30 min (40.4 +/- 11.4 mg/min, P < 0.01) and 60 min (97.4 +/- 14.5 mg/min, P < 0.01) after it was added to the perfusate. Heat inactivation (56 degrees C; 1 hr) of plasma did not attenuate this effect of ET-1 (94.4 +/- 25.1 mg/min, P < 0.01). When lungs were perfused with leukocytes resuspended in Krebs Ringer albumin instead of plasma, or with plasma only, ET-1 did not cause any change in FFR. In conclusion, ET-1 increases microvascular permeability in isolated blood-perfused rat lungs. The effect is critically dependent on the presence of leukocytes and plasma components other than complement.

Animals↗
PubMed1988

Effects of exercise and CO2 inhalation on the breathing pattern in man.

Conflicting opinions exist concerning the breathing pattern in man during resting and stimulated ventilation. Some but not all investigators have reported the existence of an abrupt change, a 'breakpoint', in the relation between mean tidal volume and mean inspiratory time. Different opinions exist as to whether the slope and the intercept for the relation between mean minute ventilation and mean tidal volume are identical regardless of the mode of stimulating the ventilation. We have studied 10 subjects, at rest and during graded stimulation of ventilation by CO2 inhalation and exercise. No breakpoint was observed in the relations between (1) mean tidal volume and mean inspiratory time and (2) mean tidal volume and mean expiratory time, even if a wide range of tidal volumes was achieved in our subjects. Carbon dioxide inhalation (normoxic or hyperoxic) and exercise gave different regression lines for the relation between mean minute ventilation and mean tidal volume in 8 out of 10 subjects with a larger slope during exercise. At exercise inspiratory time decreased with any increase in tidal volume, while during CO2 breathing no consistent change in inspiratory time was seen. Mean inspiratory flow was linearly related to exercise load and apparently also to arterial carbon dioxide pressure. We conclude that CO2 breathing gives a breathing pattern which is different from that obtained with exercise in the majority of normal subjects. Furthermore, we could not confirm the existence of breakpoints in relations describing the breathing pattern of normal man.

Adult↗
PubMed1987

Changes in human cerebral blood flow due to step changes in PAO2 and PACO2.

The effect of moderate hypoxia on cerebral blood flow (CBF) in man has not been well described, and little is known about the interaction of changes in arterial PO2 and PCO2 as regards CBF. Using a non-invasive doppler ultrasound method we have measured the instantaneous mean blood velocity (which is proportional to CBF as long as the cross-section of the vessel is constant) in the carotid artery in four healthy unanaesthetized subjects. We found in all subjects that a reduction in alveolar PO2 from about 13 to about 8.7 kPa with maintained constant alveolar PCO2 (PA, CO2) caused CBF to increase gradually over 10 min (half-time about 4 min) to about 125% of control. The CBF decreased quickly (half-time about 45 s) towards control when alveolar PO2 was reset to 13 kPa. As measured 5 min after a step-change in PA, O2, the change in CBF was independent of PA, CO2 within the range 3.3-6.7 kPa. An increase in PA, O2 to about 33 kPa reduced CBF only if PA, CO2 was in the hypercapnic range. Unexpectedly we found that the CBF response showed 'adaptation' during both maintained increase and decrease in PA, CO2. The CBF started to return towards control level within 10 min after induction of hypo- or hypercapnia. We conclude that also moderate hypoxia causes increased CBF in unanaesthetized man within a wide range of PA, CO2.

Adult↗
PubMed1987

CO2 sensitivity in humans breathing 1 or 2% CO2 in air.

Ventilation increases when the concentration of CO2 in the inspired gas is increased, thereby limiting the increase in alveolar and arterial PCO2. The extent of this compensation at low levels of inspired CO2 has been debated. In five healthy humans, we have measured arterial PCO2, arterial pH and ventilation during exposure to 1 and 2% CO2 in the inspired gas. Each exposure lasted at least 7 min and arterial blood was sampled over at least 30 s during the last minute of each period. The ventilation was measured in the sixth and seventh min. The protocol included the sequences: control-test-control and test-control-test with 'test' representing CO2 loading and 'control' 0% CO2, respectively. We found that arterial PCO2 increased and pH decreased at both levels of inspired CO2. The mean increase in arterial PCO2 was 0.09 and 0.25 kPa, at CO2 1 and 2%, respectively. Three subjects were exposed to 1% CO2 in the inspired gas for 28 min flanked by similar control periods. In each period arterial blood samples were taken at 2- or 3-min intervals. Arterial PCO2 remained elevated for at least 20 min during the CO2 loading. The sensitivity to CO2 (ratio of increase in ventilation to increase in arterial PCO2) was within the range described by others at higher levels of inspired CO2. Arterial PCO2 increased by about 10% of the imposed load. We conclude that the increase in ventilation provides only incomplete compensation for exposure to CO2: arterial CO2 is increased and arterial pH decreased also at very low levels of inspired CO2.

Adult↗
PubMed1987

Arterial P CO2 and lung ventilation in man exposed to 1-5% CO2 in the inspired gas.

Conflicting results have been published on the shape of the curve relating the change in lung ventilation to the change in alveolar or arterial PCO2 induced by increased inspired CO2 (the CO2 sensitivity). In this study eight human subjects with in-dwelling arterial cannulae were each exposed to five different levels of increased inspired CO2 (1-5%). Arterial PCO2 and ventilation were measured in the 7th minute of each period of CO2 exposure. Each CO2 exposure period was flanked by control periods in which similar measurements were carried out during air breathing. We found non-linear increases in both ventilation and arterial PCO2 with increasing levels of inspired CO2. When 5% CO2 in air was inspired the arterial PCO2 increased by about 15% of the inspired CO2 load. There was no significant non-linearity in the relation between change in alveolar ventilation (normalized to body surface) and change in arterial PCO2. The inter-individual variation in CO2 sensitivity was less when alveolar ventilation was normalized to the CO2 output rather than to body surface area. We conclude that the sensitivity to CO2 is close to constant within the range 0-5% CO2 in the inspired gas.

Adult↗