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Biomedical subjects

F Olsen

Publications and source records attributed to F Olsen.

At least 19 recordsLinked to original sources
PubMed1999

The effect of thoracentesis on lung function and transthoracic electrical bioimpedance.

This study aimed to determine the relationship between improvement in lung function and changes in transthoracic electrical bioimpedance (TEB) after thoracentesis in patients with pleural effusions. Fifteen patients with pleural effusions due to either malignant (n = 8) or cardiac (n = 7) diseases were included. Pulmonary function was assessed before and after thoracentesis. During thoracentesis the patients were monitored with TEB. Using linear correlation analysis, the increases for each litre of aspirated thoracic fluid were: forced expiratory volume in 1 s (FEV1) 0.261; forced vital capacity (FVC) 0.331; total lung capacity (TLC) 0.58; and the lung diffusing capacity (DLCO); 2.4 ml min-1 mmHg-1. Baseline impedance increased by 2.3 Ohm l-1 aspirated thoracic fluid. The relative increase in baseline impedance was twice as high for patients with cancer as for patients with heart failure (P < 0.05). We found only minor changes in systolic blood pressure and mean arterial pressure. The improvements in diffusing capacity, airflow, and lung volumes after thoracentesis are correlated to an increase in baseline impedance, but changes are dependent on the primary disease.

Aged↗
PubMed1992

[Impedance cardiography--non-invasive measurement of central hemodynamic data].

The theory, method and apparatus behind a new computer technology for transthoracic electrical bioimpedance are described. Measurements and calculations of changes in the electrical conductivity of the thoracic segment during systolic upstroke provides the basis for non-invasive determination of stroke volume and cardiac output. Bioimpedance further offers a sensitive indicator of the content of thoracic fluid. Reports comparing measurements of cardiac output in various clinical conditions by bioimpedance versus invasive methods in general show good correlation. The field of applications and limitations of bioimpedance are described. Measurements are reproducible and the method can also be used in evaluating the cardiodynamic exercise response.

Cardiac Output↗
PubMed1991

Hypersensitivity of delayed type in hypertensive patients.

The agarose migration technique was used for demonstration of delayed-type hypersensitivity to arterial vessel wall antigens in patients suffering from chronic essential hypertension. By means of this technique, it was demonstrated that the migration indices from the hypertensive patients differed significantly from the normotensive control persons, P less than 0.005. The significant difference was abolished when anti-LIF was added to the migration tests. This means that a hypersensitivity of the delayed type had developed in the hypertensive patients and the results indicated that the hypersensitivity was an autoimmunity to arterial vessel wall antigens.

Adult↗
PubMed1989

Autoactivation of human recombinant coagulation factor VII.

Single-chain human recombinant factor VII produced by transfected baby hamster kidney cells was purified to homogeneity in the presence of benzamidine. The amidolytic activity of single-chain recombinant factor VII with a peptidylnitroanilide substrate, methoxycarbonyl-D-cyclohexanylglycyl-L-arginine-p-nitroanilide, was less than 1% of that obtained with factor VIIa. Purified single-chain recombinant factor VII spontaneously activated in the absence of inhibitor. The activation reaction was enhanced by at least 2 orders of magnitude in the presence of a positively charged surface, provided either as an anion-exchange matrix or as poly(D-lysine). The progress curve for factor VIIa generation was sigmoidal. Benzamidine inhibits recombinant factor VIIa activity and factor VII activation with identical inhibition constants (Ki) of 11 mM. In contrast, benzamidine inhibition of bovine factor Xa and bovine factor IIa was observed at Ki values equal to 0.3 and 0.5 mM, respectively. Bovine factors Xa and IIa are known activators of factor VII and the most likely contaminants of our recombinant factor VII preparations. Single-chain recombinant factor VII purified from cells cultured in the absence of bovine serum activated at the same rate as factor VII from cells cultured in the presence of bovine serum. This also excluded the possibility that the activation reaction was caused by contaminating bovine proteases. On the basis of these observations, we propose that factor VII is autoactivated in vitro in the presence of a positively charged surface.

Animals↗
PubMed1989

Aluminum concentrations in serum, dialysate, urine and bone among patients undergoing continuous ambulatory peritoneal dialysis (CAPD).

Aluminum (Al) concentration in serum, urine, and dialysate was estimated in 21 patients undergoing continuous ambulatory peritoneal dialysis (CAPD). In 12 of the patients bone Al concentration was measured as well. Mean serum Al level was 32.4 +/- 21.0 micrograms/l. The Al concentrations in the dialysate and urine were 9.1 +/- 4.1 micrograms/l and 52.5 +/- 47.3 micrograms/l, respectively. Bone Al concentration was 21.0 +/- 14.9 ppm and correlated significantly with concentrations of Al in serum (p less than 0.01) and dialysate (p less than 0.01). A mass transfer (MT) from the patients to the dialysate was observed in all patients (-44.0 +/- 28.8 micrograms/24 h). There was a highly significant correlation between peritoneal Al MT and serum Al (p less than 0.001), actual Al consumption (p less than 0.05) and bone Al concentration (p less than 0.005) supporting the existence of an overflow phenomenon. Despite very low Al levels in the dialysate, patients are at risk of elevated Al levels in the serum, dialysate, urine and bone because of consumption of Al-containing phosphate binders.

Adult↗
PubMed1986

Organic solvents and presenile dementia (the painters' syndrome). A critical review of the Danish literature.

Since 1971 a series of Danish medical articles have been published which concludes that the occupational inhalation of organic solvents can induce a chronic cerebral disease manifesting itself in a presenile syndrome. As the articles have mainly dealt with the exposure of painters, the disease has also been called "the painters syndrome". The publications have brought about, by law, an almost exponential recognition of "the painters syndrome" as an occupational disease. It has therefore become necessary to undertake a critical scientific analysis of the Danish publications which appeared between 1972 and February 1983. The conclusion of this evaluation is, that the Danish articles do not prove that occupational exposure to organic solvents produces a presenile demens. The indications that it does are very slender. The importance of adhering strictly to present regulations of working conditions is emphasized.

Dementia↗
PubMed1986

Duration of delayed-type autoimmunity against arterial vessel-wall antigens following acute hypertensive damage to arterial vessels in rats.

Acute hypertensive damage to small arteries and arterioles in rats was induced by intravenous injections of Hypertensin. The in vitro immunological method of the agarose migration technique was used to demonstrate delayed-type autoimmunity against arterial vessel-wall antigens. By this technique the autoimmunity could be demonstrated for about 16 weeks after the acute hypertensive damage to the arterial vessels. The results of the autoimmunity were given as migration indices. These were lowest during the first 4-5 weeks after the damage to the vessels whereupon they showed higher and higher values, and finally the migration indices were identical with those of the control rats after about 16 weeks.

Angiotensin Amide↗
PubMed1985

Further evidence of the development of delayed-type autoimmunity against arterial vessel-wall antigens following acute hypertensive damage to arterial vessels in rats.

Acute hypertensive damage to arterial vessels was induced by intravenous injections of hypertension. The in vitro immunological method of the agarose migration technique was used for demonstration of delayed-type autoimmunity against arterial vessel-wall antigens following the damage of the arterial vessels. By means of this technique it was demonstrated that the migration indices from the rats with induced hypertension differed significantly from the control rats, P less than 0.005. This means that an autoimmunity of the delayed type had developed after the hypertensive damage to the arterial vessels. The autoimmunity was tissue specific.

Angiotensin Amide↗
PubMed1981

Induction of chronic arterial hypertension in rats by repeated transient hypertensive rises in blood pressure. Possible pathogenetic role of delayed hypersensitivity against arteries and arterioles.

Repeated transient rises in blood pressure to hypertensive levels were induced by intravenous injections of angiotensin once or twice weekly. This procedure induced chronic arterial hypertension in five of fourteen rats (36%) within 4-6 weeks of starting the injections. Intracutaneous tests using homogenized common carotid arteries and histological examination of the kidneys gave support to the hypothesis that the transient rises in blood pressure to hypertensive levels resulted in a delayed hypersensitivity (DHS) reaction against components in small arteries and arterioles. This DHS reaction seemed to be responsible for an increased permeability of arterial vessels to plasma components causing exudative thickening of the walls of small arteries and arterioles and thereby narrowing of their lumina. When the lumina of small arteries and arterioles are narrowed, peripheral resistance to blood flow increases, and arterial hypertension results.

Angiotensin II↗
PubMed1980

Transfer of arterial hypertension by splenic cells from DOCA-salt hypertensive and renal hypertensive rats to normotensive recipients.

Arterial hypertension was transferred from DOCA-salt hypertensive and renal hypertensive rats to normotensive rats by intravenous injection of splenic cells. Thirteen normotensive recipients were injected intravenously with splenic cells from the hypertensive donors. Eleven developed arterial hypertension (85%), that is, with a systolic blood pressure exceeding 140 mm Hg. Three of the recipients developed hypertensive levels up to 155-160 mm Hg, which was almost up to the levels in the donors. The increase of the blood pressure in the recipients was significant when compared to controls injected intravenously with splenic cells from normotensive donors (p less than 0.001). Skin tests, performed by intracutaneous injection of homogenized common carotid arteries in half of the recipients, showed positive reactions 24 hours after the injection. Microscopical examination of heart and kidney from the other half demonstrated mononuclear infiltration into arterial and arteriolar walls and exudative changes in these walls. Due to exudative thickening of the vessel walls the lumina were narrowed. The hypothesis is advanced that the recipient rats developed arterial hypertension as a result of a transferred delayed hypersensitivity directed against the arterial walls. This hypersensitivity reaction caused insudation of plasma components into the arterial walls, narrowing of their lumina and an increased peripheral resistance to the blood flow, so that arterial hypertension developed.

Animals↗