Biomedical subjects

R Ylikahri

Publications and source records attributed to R Ylikahri.

At least 19 recordsLinked to original sources

PubMed1992

Alcohol and sauna bathing: effects on cardiac rhythm, blood pressure, and serum electrolyte and cortisol concentrations.

The effect of heavy drinking and sauna bathing on cardiac rhythm, blood pressure, and serum electrolyte and cortisol concentrations was studied in 10 healthy male volunteers. Sauna bathing induced a comparable, significant increase in heart rate with and without alcohol consumption. During sauna bathing without alcohol, systolic blood pressure remained at the baseline level, whereas sauna and alcohol together decreased systolic blood pressure markedly from 136 +/- 4 to 113 +/- 3 mmHg (P less than 0.01). Neither sauna alone, nor sauna combined with alcohol intake, increased the frequency of premature ventricular complexes. Serum potassium, calcium and cortisol concentrations changed slightly during sauna, but alcohol consumption did not contribute further to this. In conclusion, sauna bathing, even in combination with heavy drinking, does not appear to provoke cardiac arrhythmias in healthy young men. However, the risk of hypotension is increased when sauna bathing is combined with alcohol consumption.

Adult↗

PubMed1991

Transient hypoparathyroidism during acute alcohol intoxication.

BACKGROUND: Persons with chronic alcoholism frequently have hypocalcemia, hypomagnesemia, and osteoporosis. The short-term effects of alcohol ingestion on calcium and magnesium metabolism are poorly understood, however. METHODS: We measured serum calcium, magnesium, and phosphate concentrations in 17 normal men and 7 normal women before and at intervals up to 16 hours after the ingestion of 1.2 to 1.5 g of alcohol per kilogram of body weight over a 3-hour period (doses sufficient to cause acute intoxication). Urinary excretion of calcium, magnesium, and phosphate and serum calciotropic hormone levels were measured in 16 of these subjects. As a control, the same measurements were made after the ingestion of fruit juice instead of alcohol. RESULTS: The mean (+/- SE) peak blood alcohol level in the men was 37.5 +/- 1.6 mmol per liter, and in the women it was 38.0 +/- 3.2 mmol per liter. In the men the mean serum parathyroid hormone concentration decreased from 16.1 +/- 2.1 to 6.8 +/- 0.9 ng per liter at the end of the three-hour drinking period. The value at this time was 30 percent of that at the end of the three-hour session during which the men drank fruit juice (P = 0.004). The serum concentration of ionized calcium reached a nadir eight hours after the beginning of alcohol administration (decreasing from 1.18 +/- 0.01 to 1.15 +/- 0.01 mmol per liter; P less than 0.001 as compared with values during the fruit-juice study), and urinary excretion of calcium increased from 0.34 +/- 0.08 to 0.36 +/- 0.08 mmol per hour (P less than 0.01 as compared with values during the fruit-juice study). Serum parathyroid hormone levels exceeded base-line values during the last 4 hours of the 16-hour study period; this increase was accompanied by a decrease in the urinary excretion of calcium. Both serum levels of magnesium (in the first 6 hours) and urinary levels (in the first 12 hours) increased after the ingestion of alcohol. In the women, serum parathyroid hormone levels decreased from 29.2 +/- 2.8 to 17.3 +/- 2.6 ng per liter two hours after the administration of alcohol was begun (P less than 0.001) and increased above base-line values during the last four hours of the study period. The serum concentration of ionized calcium decreased from 1.20 +/- 0.01 to 1.16 +/- 0.01 mmol per liter, reaching a nadir 8 to 12 hours after alcohol administration was begun (P less than 0.001). CONCLUSIONS: Short-term alcohol administration causes transitory hypoparathyroidism. This decline in the secretion of parathyroid hormone accounts at least in part for the transient hypocalcemia, hypercalciuria, and hypermagnesuria that follow alcohol ingestion.

Adult↗

PubMed1991

Effects of selenium supplementation on blood and urine selenium levels and liver function in patients with primary biliary cirrhosis.

To study the mechanism of the reduced serum selenium concentration in patients with liver damage we administered 200 micrograms (2.53 mumol) selenium daily as selenium-rich yeast to 8 patients with primary biliary cirrhosis and 8 healthy controls over 16 weeks. Initially selenium concentrations in serum were 24% lower (P less than 0.001) in patients than controls. During supplementation serum selenium levels increased in both groups but the difference between them persisted. Throughout the study whole blood selenium levels and glutathione peroxidase activities were also somewhat lower (P = NS) in patients than controls. Selenium supplementation had no effect on whole blood glutathione peroxidase activities in either group. The basal 24 h urinary excretion of selenium was similar in both groups but was increased more by supplementation in patients than controls. Selenium administration did not influence the liver function of the patients. We conclude that impaired hepatic production of selenium-containing serum compounds is the most likely explanation for the reduced serum selenium concentration in patients with primary biliary cirrhosis.

Adult↗

PubMed1991

The effect of moderate alcohol intake on serum apolipoprotein A-I-containing lipoproteins and lipoprotein (a).

Two main types of lipoprotein particles are identified within high-density lipoprotein (HDL): those containing both apolipoprotein (apo) A-I and apo A-II (Lp A-I:A-II) and those containing only apo A-I (Lp A-I). To study the effects of prolonged moderate alcohol intake on apo A-I-containing lipoproteins in serum, 60 g/d of ethanol was administered to 10 healthy male volunteers (age, 27 to 45 years) during 3 weeks. The drinking period was preceded and followed by an abstinence period of 3 weeks. The HDL3 cholesterol level increased by 17% (P less than .01) and decreased by 22% (P less than .001) on and off alcohol, respectively. The HDL2 cholesterol increased by 17% (P = NS) during ethanol intake and decreased by 14% during the following abstention (P less than .01). The serum concentration of apo A-I increased by 17% (P less than .001) during drinking and came back to the starting level after 2 weeks of abstention. Ethanol intake caused an increase in the serum levels of both Lp A-I and Lp A-I:A-II, the former explaining one third of the total increase of apo A-I. The Lp (a) concentration decreased by 33% (P less than .05) during the first week of ethanol intake, but increased back to the starting level until the end of drinking. These data suggest that the increment of the antiatherogenic Lp A-I may be one beneficial effect provided by ethanol with respect to coronary heart disease.

Adult↗

PubMed1991

Effects of 3 weeks' moderate alcohol intake on bone and mineral metabolism in normal men.

To study the effects of prolonged moderate alcohol intake on bone and mineral metabolism, 60 g/day of ethanol was administered to 10 healthy male volunteers during 3 weeks. The drinking period was preceded and followed by an abstinence period of 3 weeks. The serum level of osteocalcin decreased by 30% towards the end of the alcohol period (P less than 0.01), recovering by 25% after the termination of drinking (P less than 0.01). The serum level of intact parathyroid hormone increased to the end of the drinking period (P less than 0.05). After stopping drinking it came back to baseline (P less than 0.05) within a week. The serum levels of 25(OH)D3, 1,25(OH)2D3, 24,25(OH)2D3, the serum and urinary levels of calcium, and the intestinal absorption of calcium measured by stable strontium remained practically unchanged throughout the whole observation period. We conclude that prolonged moderate alcohol intake impairs osteoblastic function, leading to lowered serum levels of osteocalcin, but it does not derange vitamin D metabolism.

Adult↗

PubMed1991

Physical exercise after alcohol intake: effect on plasma catecholamines and lymphocytic beta-adrenergic receptors.

The combined effects of alcohol intoxication and intense physical exercise on the adrenergic system were studied in eight healthy male volunteers. Ethanol (0.8 g/kg body weight) was administered perorally to bring about a mean serum concentration of 21 mmol/liter (0.1%); each subject also participated in an identical control session without alcohol. Acute alcohol intake alone did not change the concentrations of plasma adrenaline or noradrenaline or the density, affinity, and functioning (ability to mediate catecholamine-stimulated production of cAMP) of lymphocytic beta-adrenergic receptors. In contrast, acute ergometer exercise brought about an approximately 10-fold increase of plasma adrenaline and noradrenaline concentrations, a 2- to 3-fold increase of beta-adrenergic receptor density and an enhancement of isoproterenol-stimulated cAMP production. Alcohol intake immediately before the ergometer exercise did not modify these changes. In conclusion, acute physical exercise activates the human adrenergic system, with an increase of both plasma catecholamines and lymphocytic beta-adrenergic receptors. Moderate alcohol intoxication does not affect exercise-induced alterations of these parameters.

Adult↗

PubMed1990

Serum lipids and lipoproteins in alcoholic women during pregnancy.

The concentrations of triglyceride, cholesterol, phospholipids, and proteins in the major lipoprotein fractions (very-low-density lipoprotein [VLDL], low-density lipoprotein [LDL], and high-density lipoproteins [HDL] HDL2 and HDL3) were monitored in 20 pregnant women who chronically abused alcohol and in 15 abstinent pregnant women. Five of the alcohol users gave birth to infants with fetal alcohol syndrome (FAS). Lipoproteins were fractionated by sequential flotation from samples taken at 16, 20, 24, 28, 32, 36, and 40 weeks of gestation and 6 to 8 weeks after delivery. In abstinent women, concentrations of VLDL and LDL triglyceride, cholesterol, phospholipids, and proteins increased in late gestation. Concentrations of HDL2-cholesterol, phospholipids, proteins, and total HDL2 were increased during the 16th to 28th weeks, but HDL3 remained unchanged. Alcohol abuse clearly reduced the normal increase in total and LDL-cholesterol, as well as in LDL phospholipids, proteins, and total LDL during the 24th to 40th weeks. LDL changes were most pronounced in alcoholic women who later produced FAS infants. Alcohol abuse also increased HDL3. Furthermore, in alcohol users, the normal increase in VLDL was accentuated, especially so in women with FAS infants, and that of HDL2 was reduced. The significance of the changes found remains obscure, but they may be related to impaired function of the fetoplacental unit.

Alcoholism↗

PubMed1990

Reduction of lymphocytic beta-adrenoceptor level in chronic alcoholics and rapid reversal after ethanol withdrawal.

Plasma catecholamine levels, lymphocytic beta-adrenoceptor densities and lymphocytic cAMP production were studied in 10 male subjects attending a withdrawal clinic after prolonged alcohol abuse. On admission the mean beta-adrenoceptor density was 29 +/- 9 fmol mg-1 protein (about 60% of the mean level of healthy control subjects, P less than 0.002). The following day a significant elevation of the beta-adrenoceptor level up to 46 +/- 19 fmol mg-1 protein (P less than 0.05) took place. This was accompanied by a parallel activation of the beta-adrenoceptor-mediated cAMP production of the lymphocytes. No major changes in beta-adrenoceptor levels or cAMP production took place during the next 7 days. Plasma catecholamine levels were elevated at arrival and decreased steadily during the withdrawal period. In conclusion, chronic alcoholism is associated with a reduction of lymphocytic beta-adrenoceptor density and functioning, which is followed by a rapid reversal during abrupt ethanol withdrawal. Thus an accelerated responsiveness to catecholamines may occur during the first ethanol-free day of chronic alcoholics.

Adult↗

PubMed1990

Pituitary-gonadal hormones and adrenal androgens in non-cirrhotic female alcoholics after cessation of alcohol intake.

To investigate the sex-hormone profiles associated with chronic alcoholism in women we examined 16 non-cirrhotic alcohol abusers (aged 18-46 years). They were admitted for the treatment of alcoholism (duration of 2-16 yrs) to a social hospital for 6 weeks. Their mean daily alcohol consumption was 170 g. Blood samples for serum LH, FSH, prolactin (PRL), oestrone (E1), oestradiol (E2), progesterone (P), 17-alpha-hydroxyprogesterone (17-OHP), androstenedione (A) and dehydroepiandrosterone (DHEA) were drawn three times a week during the hospital stay. Similar blood samples were taken from 10 control women during one menstrual cycle. The cycles were anovulatory in two patients and in none of controls. Serum LH and FSH levels were similar in alcoholic and control women but serum concentrations of PRL were increased 2-4-fold in alcoholic women. In the patients serum, concentrations of E1 and E2 tended to be lower during the follicular and midcycle phases, as did those of P and 17-OHP during the luteal phase. Compared with the controls, serum levels of A were increased 2-3-fold in the patients. A parallel difference between the two groups was seen in serum DHEA concentrations. We conclude that until liver injury, even heavy alcohol drinking has only minor effects on the secretion of gonadotrophins and ovarian steroids. Hypersecretion of PRL and adrenal androgens may well be an initiating mechanism for sexual dysfunction of female alcoholics.

Adolescent↗

PubMed1990

Deranged vitamin D metabolism but normal bone mineral density in Finnish noncirrhotic male alcoholics.

To study the effect of prolonged ethanol consumption on calcium metabolism and on the prevalence of osteoporosis we examined 38 Finnish noncirrhotic male alcoholics (30-55 years of age) with dietary interviews and biochemical measurements and by measuring the bone mineral content of the forearm using single photon absorptiometry (SPA) and the bone mineral density of the spine, humerus and proximal femur using nonquantified computer tomography (CT) and dual-energy x-ray absorptiometry (DEXA). In comparison two groups of healthy controls were studied. The mean daily dietary intake of calcium was 1.3 g in the patients and 1.2 g in the controls. The dietary intake of vitamin D was equal in the study groups, too. The serum levels of calcium, phosphate and parathyroid hormone did not show any difference between the patients and controls but in the alcoholics the urinary excretion of calcium was reduced by 42% (p less than 0.0001) as compared to the controls. The serum levels of 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3, and 24,25-dihydroxyvitamin D3 were reduced in the alcoholics by 40% (p less than 0.0001), 23% (p less than 0.01), and 48% (p less than 0.0001), respectively, as compared to the controls. The alcoholic men had normal levels of serum testosterone and they did not have hypercortisolism. The bone mineral content of the dominant forearm measured by SPA was similar in the study groups as were the bone mineral densities (BMD) of the lumbar and humeral areas measured by CT. The BMD at the lumbar, femoral neck, Ward's triangle and trochanter sites measured by DEXA did not differ, either.(ABSTRACT TRUNCATED AT 250 WORDS)

24,25-Dihydroxyvitamin D 3↗

PubMed1990

The pulsatile secretion of gonadotropins and growth hormone, and the biological activity of luteinizing hormone in men acutely intoxicated with ethanol.

The effects of acute alcohol ingestion were studied on pulsatile secretion of immunoreactive luteinizing hormone (LH), follicle-stimulating hormone (FSH), and growth hormone (GH), and on serum bioactive LH, testosterone, cortisol, and prolactin. A dose of 1.5 g ethanol per kg of body weight was administered by mouth to eight healthy male volunteers (aged 20 to 26 years) during 3 hr from 1800 to 2100 hr. Blood samples were collected every 20 min for 20 hr until 1400 hr of the following day. Each subject served as his own control in an identical experiment without ethanol, carried out at least 1 month later. Ethanol ingestion decreased serum testosterone concentration on average by 23% (p less than 0.05) between 10 and 16 hr after starting the drinking. The mean levels of LH and FSH and the mean number and amplitude of LH and FSH pulses remained unchanged. Ethanol ingestion did not affect the biological activity of LH. In each subject alcohol administration reduced the nightly peak of GH secretion, and in addition, changed the timing of this peak in most subjects. Only marginal changes were found in the prolactin levels but ethanol ingestion increased the cortisol levels on average by 36% (p less than 0.05) between 11 and 14 hr after the start of drinking. We conclude that the decrement in serum testosterone evoked by ethanol is not attributable to impaired pulsatile secretion of gonadotropins nor to reduced biological activity of LH. In contrast, ethanol profoundly suppressed the pulsatile secretion of growth hormone.

Adult↗

PubMed1989

Maternal and paternal alcohol consumption and miscarriage.

To explore the role of parental alcohol consumption in miscarriage we interviewed 80 women who miscarried about their own and their partners' drinking habits. A control group of 81 gestational-age-matched women whose pregnancy ended in the delivery of a healthy infant at term were similarly questioned. The use of alcohol by women and men was equally frequent in both groups. Before pregnancy, the mean alcohol consumption per week had been about 1-2 drinks for the women and 4-5 drinks for the men. During the presumed day of conception, 13% of the women who miscarried and 11% of the women in the control group had drunk on average 3-4 drinks; the other women had been abstinent at this time. Of the partners, 13% and 15%, respectively, had taken a mean of 4-5 drinks. In both groups 58% of the subjects continued to consume alcohol during pregnancy. The mean consumption was about one drink a week by the women who miscarried and half a drink a week in the control group. Of women who miscarried, 36 had a blighted ovum and in this subgroup alcohol consumption in both women and men was similar to that in the other women who miscarried and their partners, suggesting that alcohol is not causally related to the development of a blighted ovum. These results suggest that moderate maternal or paternal alcohol consumption does not increase the risk of miscarriage.

Abortion, Spontaneous↗

PubMed1989

Effect of acute ethanol intake and hangover on the levels of plasma and urinary catecholamines and lymphocytic beta-adrenergic receptors.

To determine whether acute ethanol administration affects the function of the adrenergic system the concentrations of plasma catecholamines and cyclic AMP (cAMP), the level of lymphocytic beta-receptors, the concentration of basal and isoproterenol-stimulated lymphocytic cAMP and the excretion of urinary catecholamine metabolites were studied in six healthy men. These parameters were also measured during the hangover, both under resting condition and during an anaerobic ergometer exercise. Acute intake of ethanol (1.5 g/kg body weight) had no statistically significant effect either on plasma adrenaline and noradrenaline concentrations or beta-adrenergic receptor levels. Ethanol consumption did neither change the urinary excretion of catecholamine metabolites (homovanillic acid, normetanephrine, metanephrine, and 3-methoxyhydroxymandelic acid). Exercise was associated with a 6-10-fold elevation in plasma adrenaline and noradrenaline concentrations and with a two- to threefold elevation on beta-adrenergic receptor levels. This effect of exercise was not modified by preceding alcohol intake and resulting hangover. These preliminary findings suggest that acute alcohol intake does not significantly alter the concentration and functioning of human beta-adrenergic receptors.

Adult↗

PubMed1989

Methanol as a marker of alcohol abuse.

Serum methanol levels were studied in 16 skid-row alcoholics, 16 alcoholics entering a detoxification unit, 193 drunken drivers, and 50 social drinkers, all of whom had a blood-ethanol concentration exceeding 5 mmol/liter at the time of sampling. Highest mean serum methanol level was found in alcoholics entering detoxification (636 +/- 68 mumol/liter, p less than 0.001 as compared to social drinkers), followed by skid-row alcoholics (567 +/- 105 mumol/liter, p less than 0.001), drunken drivers (231 +/- 11 mumol/liter, p less than 0.001) and social drinkers (127 +/- 10 mumol/liter). During 2 days heavy drinking mean serum methanol concentration in 10 nonalcoholic volunteers increased from 177 +/- 15 mumol/liter 1 h after the beginning of drinking to 322 +/- 29 mumol/liter 42 h after the beginning of drinking (p less than 0.001). In 70 of the drunken drivers urinary methanol concentration was determined as well and a fairly good correlation (r = +0.56, p less than 0.001) between serum and urinary methanol levels were found. Our results suggest that methanol determined either from serum or urine can be used as a biological marker of alcohol abuse.

Adult↗

PubMed1989

Effect of alcohol on blood dolichol concentration.

Serum dolichol levels were studied in 95 active alcoholics and 16 abstinent alcoholics (at the time of blood sampling) and compared to those of 41 social drinkers. Active alcoholics had a significantly higher mean serum dolichol concentration (182.7 +/- 5.1 ng/ml, p less than 0.001 than either abstinent alcoholics (138.7 +/- 5.4 ng/ml) or social drinkers (142.1 +/- 4.1 ng/ml). During weekend (48 hr) heavy drinking (5.5 g of alcohol per kg b.w.) no significant changes were seen in mean serum dolichol concentrations in 10 healthy, nonalcoholic volunteers. Neither did moderate drinking for 10 days (60 g of alcohol daily)--preceded and followed by a period of abstinence--produce any significant changes in serum dolichol levels in 10 nonalcoholic subjects. During detoxification treatment of 12 alcoholics, mean serum dolichol concentration stayed constant for the first 7 days; on entering treatment it was 227.7 +/- 15.0 ng/ml, on the 3rd day 238.5 +/- 15.9 ng/ml, and on the 7th day of treatment 222.6 +/- 18.6 ng/ml. Our results show that as well as increasing urinary dolichol excretion, chronic alcohol abuse also produces increased serum dolichol concentrations. However, contrary to urinary dolichols, serum dolichol levels do not react significantly to heavy drinking lasting for 48 hr in nonalcoholic volunteers. Furthermore in alcoholics increased serum dolichol concentrations do not decrease as rapidly during abstinence as urinary dolichol concentrations do.

Adult↗

PubMed1989

Significant increases in urinary dolichol levels in bacterial infections, malignancies and pregnancy but not in other clinical conditions.

The effect of different clinical conditions on urinary dolichols was studied in 219 hospital patients and in 24 pregnant women. Significantly increased urinary dolichol levels were found in patients with severe bacterial infections (mean +/- SEM, 37.5 +/- 8.0 micrograms/mmol creatinine, P less than 0.001), in patients with haematological or metastatic (23.3. +/- 5.1, P less than 0.05) as well as localised (15.4 +/- 1.8, P less than 0.01) malignancies and in pregnant women (22.2 +/- 1.8, P less than 0.001) as compared to healthy controls (6.6 +/- 0.4). These results show that urinary excretion of dolichols may be increased, not only in alcoholics and patients with some rare neurodegenerative storage diseases, but also in patients suffering from various other diseases.

Adult↗

PubMed1988

Comparison of the effects of two different doses of alcohol on serum lipoproteins, HDL-subfractions and apolipoproteins A-I and A-II: a controlled study.

Our earlier studies have shown that heavy alcohol intake increases the serum concentration of HDL2. The present study aimed to test which HDL subfraction is affected by moderate alcohol intake, and to examine the time- and dose-dependency of alcohol-induced changes in serum lipoproteins. Therefore, 30 or 60 g day-1 of alcohol were given to 10 healthy male volunteers during two 3-week periods separated by an abstinence period of 3 weeks. Lipoproteins were fractioned by sequential flotation. On both doses the total HDL3 concentrations rose progressively, the maximum increases being 10 and 25% at the end of respective drinking periods. In contrast, the HDL2 increased slightly only on the dose of 60 g day-1. The serum concentrations of apoprotein A-I and A-II increased on both doses but significantly only on the dose of 60 g day-1; the increments being 22 and 35%, respectively. On the basis of these and our earlier findings we conclude that (i) the effects of heavy and moderate alcohol intake on serum HDL-subfractions are different: the former preferentially increases the HDL2 whereas the latter augments the HDL3; (ii) alcohol-induced changes in serum lipoproteins are both time- and dose-dependent.

Adult↗

PubMed1988

Acute cardiovascular and metabolic effects of acetate in men.

We studied the potential contribution of acetate to the cardiovascular effects of ethanol in 12 healthy male volunteers. Sodium acetate, or sodium chloride in control experiments, was infused i.v. at the rate of 0.033 mEq/kg/min for 60 min. Left ventricular function was examined by M-mode echocardiography and systolic time intervals during infusion and for 60 min thereafter. Blood acetate rose during infusion from 0.19 +/- 0.02 (mean +/- SEM) to a maximum of 0.99 +/- 0.08 mmol/liter. Changes in serum free fatty acids, glycerol, and ketone bodies indicate that acetate inhibited peripheral lipolysis. The volume of urine excreted during the acetate experiment (305 +/- 37 ml) was significantly larger (p less than 0.01) than during the chloride experiment (181 +/- 21 ml). Left ventricular function did not differ between the experiments during the infusions even though at 45 min heart rate was increased by acetate (7%; p less than 0.01, between infusions). After the infusion period, at 75 min the treatment by acetate increased cardiac output from the baseline by 17% (p less than 0.05, between infusions), and decreased peripheral arterial resistance (19%, p less than 0.05), and diastolic blood pressure (10%, p less than 0.01). Circumferential fiber shortening velocity was increased during the acetate experiment maximally by 7% (p less than 0.01) from the baseline at 120 min. These data indicate that acetate is an arterial vasodilator and a mild diuretic and may slightly improve myocardial performance in the concentrations encountered during ethanol metabolism in men.

Acetates↗