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L Pekkanen

Publications and source records attributed to L Pekkanen.

14 recordsLinked to original sources

Tracheal sounds and airflow dynamics in surgically treated unilateral vocal fold paralysis.

The aim of this study was to investigate the changes in tracheal sounds and airflow dynamics in patients who underwent surgical medialization of a unilaterally paralysed vocal fold. Ten adults with unilateral vocal fold paralysis but no history of pulmonary diseases were included. Vocal fold medialization was performed by an injection of autologous fascia into the paralysed vocal fold. Recording of tracheal sounds, flow-volume spirometry and body plethysmography were carried out before and 4-14 months after the operation. The mean number of inspiratory wheezes per respiratory cycle increased from 0.02 (range 0-0.10) to 0.42 (range 0-0.86) and the mean number of expiratory wheezes per respiratory cycle from 0.03 (range 0-0.20) to 0.36 (range 0-0.89). The increment was statistically significant (P=0.03 and P=0.04, respectively). The mean expiratory sound amplitude, in terms of root mean square (RMS), increased from 31.5 dB (range 24.0-38.0) to 34.9 dB (range 25-42) (P=0.03) and the average peak inspiratory flow (PIF) decreased from 4.63 l s-1 (range 2.84-7.51) to 4.03 l s-1 (range 2.27-6.68) (P=0.01). The results indicate that when the paralysed vocal fold is brought into midline by a surgical procedure, the prevalence of inspiratory and expiratory wheezes increases and sound intensity rises. According to this preliminary data tracheal sound analysis gives additional information for the assessment of the subtle changes in the larynx.

Aged↗

Disturbances in airflow dynamics and tracheal sounds during forced and quiet breathing in subjects with unilateral vocal fold paralysis.

Variable extra thoracic obstruction has been found in spirometric studies in subjects with unilateral vocal fold paralysis. The aim of the study was to further evaluate airflow dynamics in these subjects with body plethysmography and tracheal sound analysis. Ten patients with unilateral vocal fold paralysis without a history of chronic pulmonary diseases and 10 healthy control subjects were studied. Flow-volume spirometry, body plethysmography and tracheal sound analysis were performed within 1 day. The study shows that peak inspiratory flow (PIF) and specific airway conductance (SG(aw)) expressed as percentage of Finnish reference values were significantly lower and airway resistance (R(aw)) was higher among the patients than among the controls (P=0.004, P=0.026 and P=0.004, respectively). The patients had higher sound amplitude of both inspiratory and expiratory tracheal sounds than the controls [root mean square (RMS) values of the power spectra were 31.5 and 25 dB, P=0.006 in inspiration and 31.5 and 26 dB, P=0.013 in expiration, respectively]. Quartile frequencies (F25 and F50) and RMS of expiratory tracheal sounds had significant negative correlation with PIF (P=0.02, P<0.001, P=0.02, respectively) and forced inspiratory volume in 1 s (FIV(1)) (P=0.01, P<0.001, P=0.01, respectively). There was also an association between F50 and peak expiratory flow (PEF) (P=0.02). According to the present study, both quiet breathing and forced inspiration are disturbed in subjects with unilateral vocal fold paralysis. A close relationship between tracheal sounds and respiratory function tests exists.

Aged↗

A new versatile PC-based lung sound analyzer with automatic crackle analysis (HeLSA); repeatability of spectral parameters and sound amplitude in healthy subjects.

A versatile PC-based lung sound analyzer has been developed for short-term recording and analysis of respiratory sounds in research and clinical applications. The system consists of two sound sensors, a flow sensor, a filtering signal amplifier and a PC with a data acquisition card and software for measurement and analysis of the sounds. The analyses include phonopneumography, time expanded waveform analysis, spectral analysis with time averaged Fast Fourier Transform, frequency analysis in time domain (sonogram), and automatic detection and waveform analysis of crackles. Short-term repeatability of spectral parameters of tracheal and lung sounds was studied in 10 healthy subjects. The coefficients of variation (CoV) of the averaged quartile frequencies (F25, F50 and F75) of lung sounds during flow-controlled tidal breathing were 3.7, 4.0 and 8.9% in expiration and 2.7, 3.5 and 4.5% in inspiration, respectively. CoVs of the averaged F25, F50 and F75 of expiratory tracheal sounds were 6.9, 3.0 and 2.4%, and those of inspiratory tracheal sounds 6.3, 2.6 and 3.3%, respectively. Examples of lung sound analysis of samples containing adventitious sounds such as crackles and wheezes are presented. The results indicate that the median frequency has the best repeatability of quartile frequencies of breath sounds and they suggest that the variations of those parameters are low enough for diagnostic purposes. The results also suggest that the analyzer can be a useful new tool for pulmonary research in the fields of physiological and clinical short-term studies of respiratory sounds.

Adult↗

Swift increase in alcohol metabolism (SIAM) in the mouse: comparison of the effect of short-term ethanol treatment on ethanol elimination in four inbred strains.

Ethanol metabolism increases 2 to 3 hr after the administration of ethanol. This phenomenon, called the swift increase in alcohol metabolism, has been compared in four inbred strains of mice (DBA/2J, C3H/HeJ, AKR/J and C57BL/6J). Basal rates of ethanol elimination were determined in individual mice after an i.p. injection of ethanol (2 g/kg). Little variability in this basal rate of ethanol elimination was observed within each strain. Mice were then exposed to ethanol vapor (20--22 mg/l) and rates of ethanol elimination were determined every 2 hr for 8 hr. By 2 to 3 hr, the rates of ethanol elimination initially increased 2- to 3-fold and then declined toward basal rates over the 8-hr interval in all strains studied. In another experiment, the dose of ethanol was varied to produce blood ethanol levels ranging from 50 to 250 mg/100 ml in both basal- and ethanol vapor-treated mice. Ethanol elimination increased greater than 1.5-fold in all four strains studied when basal rates were compared to rates observed after 4 hr of vapor treatment at the same blood ethanol level; however, the dose at which the maximal increase occurred differed among the strains. DBA/2J mice exhibited a maximal increase in the rate of ethanol elimination when ethanol concentrations were in the range of 30 to 50 mg/100 ml; the increase was smaller as the dose was increased. In contrast, AKR/J and C57BL/6J mice required 100 to 150 mg/100 ml of ethanol to activate the swift increase in alcohol metabolism effect. These data indicate clearly that the swift increase in alcohol metabolism effect is a common phenomenon and that dose and time relations differ in various inbred strains of mice.

Animals↗

The effects of dietary thiamin on voluntary ethanol drinking and ethanol metabolism in the rat.

1. The influence of a deficiency or surplus of thiamin in the diet on voluntary ethanol consumption, ethanol elimination rate and blood acetaldehyde concentration was studied in rats. 2. Both the high-thiamin diet containing 20 mg thiamin hydrochloride/kg and the thiamin deficient diet containing no measurable thiamin produced obvious functional effects on thiamin metabolism in rat tissues after 4 weeks as demonstrated by measurements of the blood transketolase (sedoheptulose-7-phosphate: D-glyceraldehyde-3-phosphate glycolaldehyde-transferase; EC 2.2.1.1) activity and the extent of thiamin pyrophosphate-stimulation of the enzyme. 3. During the first week on the test diets the prospective ethanol free-choice groups had 1.72 M-ethanol as their only drinking-fluid. Subsequently they had a choice between ethanol and tap water for three weeks. During the free-choice period the rats on the high-thiamin diet drank only one-fifth as much ethanol as the rats given the optimum diet with 4 mg thiamin hydrochloride/kg. 4. The thiamin-deficient rats showed a significant tendency to increase ethanol drinking, when intake was expressed relative to total energy intake, but their intake of ethanol on a g/kg body-weight basis was approximately the same as that of the group given the optimum-diet. 5. The observed differences in voluntary ethanol drinking associated with different levels of dietary thiamin cannot be explained by changes in the ethanol elimination rate or the acetaldehyde accumulation in blood during the oxidation of ethanol.

Acetaldehyde↗

The effects of dietary niacin and riboflavin on voluntary intake and metabolism of ethanol in rats.

The effects of dietary deficiency and excess of niacin and riboflavin on voluntary drinking of 10% (v/v) ethanol were studied in male rats. The effectiveness of dietary deficiency and excess of both niacin and riboflavin on tissue levels of these vitamins was demonstrated by measurements of urinary N1-methylnicotinamide and blood glutathione reductase (EC 1.6.4.2) activity. A high-niacin diet containing 75 mg niacin/kg food decreased ethanol intake by about 36% compared to the control diet containing 15 mgniacin/kg. Niacin or riboflavin deficiency and a high-riboflavin diet containing 40 mg rtary levels of niacin or riboflavin did not influence on ethanol elimination rate or levels of blood acetaldehyde during ethanol oxidation. Therefore, blood acetaldehyde was not responsible for the decreased ethanol intake of rats fed with a high-niacin diet. It was concluded that the increased ethanol intake caused by dietary deprivation of B-vitamin complex found in earlier studies is not a result of deficiency of niacin or riboflavin but niacin may be involved in the decrease in ethanol drinking, which follows dietary B-vitamin complex supplementation.

Acetaldehyde↗

Pyrithiamin shortens ethanol-induced narcosis and increases voluntary ethanol drinking in rats.

To investigate the role of thiamin deficiency in increasing voluntary ethanol intake in rats the effect of ethanol on the central nervous system was studied by measuring the duration of ethanol narcosis in pyrithiamin-treated rats. The duration of ethanol-induced narcosis was significantly shorter and blood ethanol concentration at the moment of righting reflex recovery was higher in pyrithiamin-treated rats than in controls. Thus, the shorter ethanol narcosis of pyrithiamin-treated rats was not a result of a change in ethanol metabolism but rather suggests changes in the central effects of ethanol. Treatment with thiamin increased the duration of ethanol narcosis to the initial level in rats pretreated with pyrithiamin. During the same pyrithiamin treatment as used for the narcosis test voluntary ethanol intake of rats was higher than during optimal treatment by thiamin. The results suggest that there might be a decrease in central sensitivity to ethanol in pyrithiamin treated rats, which may have a role in increasing their voluntary ethanol drinking.

Alcohol Drinking↗

Dietarily-induced changes in voluntary ethanol consumption and ethanol metabolism in the rat.

1. The voluntary ethanol consumption, ethanol elimination rate and blood acetaldehyde level after intraperiotoneal injection of ethanol were studied in rats receiving diets with highly imbalanced proportions of dietary protein, carbohydrate and fat. 2. The rats, which received the low-protein diet containing 0.05 of the total energy as protein, 0.80 as carbohydrate and o.15 as fat, drank only approximately half as much ethanol as did the control group, which received 0.30 of its total food energy from protein, 0.55 from carbohydrate and 0.15 from fat. Ethanol elimination rate in the low-protein group was decreased and the blood acetaldehyde level after ethanol injection was markedly increased. 3. On the high-fat diet, which contained 0.30 of the total energy from protein, 0.05 from carbohydrate and 0.65 from fat, the rats drank significantly more ethanol than did the rats on the control diet; their ethanol elimination rate was decreased but their blood acetaldehyde level was not affected. 4. In conclusion, the strong decrease in voluntary ethanol drinking by the low-protein group may have been caused by the increased acetaldehyde accumulation in the blood, but a particularly low blood acetaldehyde level was not one of the factors inducing excessive ethanol drinking in the high-fat group.

Acetaldehyde↗

An inborn alcohol tolerance in alcohol-preferring rats. The lack of relationship between tolerance to ethanol and the brain microsomal (Na+K+) ATPase activity.

Alcohol tolerance, measured as performance on the tilting plane after ethanol injection (2.5 g/kg body weight i.p.), was examined in the AA strain of rats which voluntarily drink large amounts of alcohol, in the ANA strain which drink very little alcohol, and in ordinary albino rats which consume intermediary amounts of alcohol. The AAs showed the highest innate ethanol tolerance; the ANAs had the lowest innate tolerance. After chronic alcohol administration, both AA and ANA strains increased their tolerance, but the AAs remained superior to the ANAs. The chronic ethanol treatment did not significantly change the (Na+K+) ATPase activity of the crude microsomal fraction of the brains of the strains.

Adenosine Triphosphatases↗

Effect of a low-protein diet on acetaldehyde metabolism in rats.

The effect of dietary changes on liver alcohol and aldehyde dehydrogenase activities as related to effects on ethanol and acetaldehyde metabolism was investigated. Feeding rats for 8 weeks on diets rich in carbohydrate or fat, but with normal protein content, induced minor changes relative to giving a balanced diet. A low-protein, high-carbohydrate diet (5 per cent and 80 per cent of calory content, respectively) caused a significant reduction of both alcohol and aldehyde dehydrogenase activities in the liver. The activity of the high-Km aldehyde dehydrogenase in the microsomal and soluble fractions appeared to be more reduced than that of the low-Km enzyme in the mitochondrial fraction. The tail blood acetaldehyde was significantly higher in rats on the protein deficient diet in spite of their reduced ethanol elimination rates. The results suggest that protein deficiency deranges acetaldehyde metabolism and may thus increase the possible contribution of acetaldehyde to the effects caused by ethanol metabolism.

Acetaldehyde↗