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Biomedical subjects

M E Hillbom

Publications and source records attributed to M E Hillbom.

At least 19 recordsLinked to original sources
PubMed1992

Outcome in subjects with alcohol-provoked seizures.

The outcome in 165 subjects with either an unknown (n = 93) or an alcohol-related (n = 72) seizure etiology, admitted to the emergency room of a general hospital in 1977-1978, was assessed after 10 years on the basis of subsequent hospital records and death-certificate-based mortality data. Alcohol and/or drug poisoning was the most frequent cause of death in the group with alcohol-related seizures. Sixty-four percent of the deaths in this group were directly related to alcohol abuse. The crude mortality was 45.8 (expected 8.6)/100 persons/10 years in the group with alcohol-related seizures and 15.1 (expected 6.0)/100 persons/10 years in the other group, the odds ratio between the groups being 4.8. Twenty percent of those with an unknown seizure etiology were found to show alcohol-related seizures, while the seizure etiology remained unknown in 59%, and a specific etiology other than alcohol abuse was revealed in 21% during the follow-up period. We conclude that alcohol abuse is an important, though often undetected, seizure etiology carrying a poor prognosis. The difference in mortality between the groups was due more to alcoholism than to seizures. There was no difference in mortality between those with a first alcohol-related seizure and those with previous alcohol-related seizures.

Adolescent↗
PubMed1987

What supports the role of alcohol as a risk factor for stroke?

For more than 30 years, clinical observations to link alcohol abuse and stroke have accumulated in several countries. Studies of general populations have indicated that the risk for stroke increases with increasing alcohol consumption. Studies of young victims of stroke where the classical risk factors of stroke are uncommon, have demonstrated that even occasional heavy drinking carries an increased risk for stroke. In particular, the increased occurrence of strokes during weekends, the very time of heavy alcohol consumption in non-alcoholics, supports this notion. Alcoholics seem to get their strokes at an earlier age than non-alcoholics. Paradoxically, the published evidence has implicated drinking in both ischemic and hemorrhagic strokes, which suggests that there may be more than one mechanism by which alcohol can increase the risk. Strokes seem to be precipitated during the alcohol intoxication itself rather than the following withdrawal syndrome, but the contributing mechanisms, except for bleedings caused by external violence, are unknown. Alcohol can produce fluctuations in platelet reactivity and untoward interactions with certain drugs, but it remains to be demonstrated that such effects are temporally related to the onset of ischemic and hemorrhagic strokes.

Alcoholism↗
PubMed1984

Platelet aggregation and thromboxane B2 formation after ethanol abuse: is there a relationship to stroke?

Formation of thromboxane B2 (TXB2), a metabolite of the potent platelet-aggregating and vasoconstrictor agent thromboxane A2 (TXA2), during ADP-induced platelet aggregation was studied in 10 healthy men and in 10 male alcoholics during the 2-week period of detoxification. None of the alcoholics had anemia or thrombo-embolic disease. The platelets of the alcoholics were more sensitive for ADP and synthesized as much as triple the amount of TXB2 compared to those of the nonalcoholic donors. The effect was most striking during the rebound thrombocytosis and suggests that it could possible contribute to the increased incidence of various thrombotic diseases in the alcoholic.

Adult↗
PubMed1984

Should alcohol withdrawal seizures be treated with anti-epileptic drugs?

Seizures and delirium tremens were recorded among 292 randomly selected patients admitted to an in-patient alcoholism program. Despite the almost routine prophylactic use of anticonvulsant and sedative drugs the incidence of seizures and delirium tremens during detoxification in hospital was 3%. However, as most alcohol withdrawal seizures occurred immediately before admission, the overall seizure incidence was higher (10%). Those patients who developed seizures during detoxification admitted previous abuse of benzodiazepines or erratic use of phenytoin. The results suggest that prescribing of anticonvulsants to alcoholics may increase their seizure problems, because they are prone to erratic drug taking, and because of drug-alcohol interactions, increased drug metabolism and abuse of the sedative anticonvulsants.

Adult↗
PubMed1984

Diabetes and the alcohol consumption of AA and ANA rats.

Some earlier results have suggested a link between diabetes and voluntary ethanol consumption. Measurement of blood glucose levels now showed, however, that the AA line of rats developed for high alcohol intake is not diabetogenic. The alcohol-avoiding ANA line was somewhat more susceptible to streptozotocin-induced diabetes. Streptozotocin greatly increased blood glucose levels, water intake, and food consumption, but had no effect on the voluntary alcohol drinking of either AA or ANA rats. Normalization of blood glucose levels with insulin from osmotic minipump implants also failed to change their ethanol drinking. Thus, although the evidence from some other lines of rats and mice suggests that alcohol drinking is related to some forms of diabetes, the present results indicate that it is independent of the diabetes induced by streptozotocin and also of water and food intake regulation in this situation.

Alcohol Drinking↗
PubMed1983

Potentiation of ethanol toxicity by cyanamide in relation to acetaldehyde accumulation.

The possibility that acetaldehyde accumulation potentiates the acute toxicity of ethanol was studied by pretreating rats with cyanamide, an aldehyde dehydrogenase inhibitor. At 30 min after administration of ethanol (7 to 9 g/kg, po), the levels of acetaldehyde in femoral venous blood of cyanamide-treated rats were increased from 10 to 20 to 600 mumol/liter and at death the concentrations of acetaldehyde in heart blood and cerebrospinal fluid were still 7 to 9 and 4 to 9 times higher, respectively, than in rats given ethanol only. The cyanamide pretreatment (25 mg/kg) significantly increased the mortality of rats given 6.5 to 7.0 g/kg ethanol and decreased the LD50 of ethanol from 7.3 to 5.9 g/kg. Cyanamide increased the late mortality, possibly because of sustained acetaldehyde accumulation. Although administration of the alcohol dehydrogenase inhibitor, 4-methylpyrazole (4-MP, 10 mg/kg), prevented the accumulation of acetaldehyde, it only partly counteracted the effect of cyanamide on mortality. After coadministration of cyanamide and 4-MP, the LD50 of ethanol was 6.5 g/kg, and after 4-MP alone, 6.7 g/kg. 4-MP by itself seemed to increase the early mortality of rats to ethanol poisoning. The results suggest that the potentiating effect of cyanamide on ethanol toxicity can partly be explained by acetaldehyde accumulation and that 4-MP can be used to inhibit this accumulation providing its central depressant effect is taken into account.

Acetaldehyde↗
PubMed1983

Effect of ethanol on blood viscosity and erythrocyte flexibility in healthy men.

The effects of ethanol on blood rheology were studied in twelve healthy male volunteers each serving as his own control. They drank 1.5 g (33 mmol) of ethanol per kg body weight in fruit juice over 2.5 h under controlled laboratory conditions. Blood and plasma viscosity, packed cell volume and erythrocyte flexibility were measured before and 3, 12 and 16 h after ethanol ingestion began, and again during a second session equal volumes of fruit juice were consumed. Packed cell volume varied similarly after ingestion of juice with or without ethanol. Blood viscosity remained almost unchanged after ethanol, while drinking of juice caused an initial decrease followed by a significant (P less than 0.05) increase from 4.04 (SEM 0.06) to 4.32 (SEM 0.18) mPa.s. The juice also caused more significant fluctuations in erythrocyte rigidity (whole blood) than ethanol, which had parallel but insignificant effects. We conclude that a blood ethanol concentration of 28 mmol l-1 failed to induce any marked changes in blood rheology.

Adult↗
PubMed1981

Ethanol and acetaldehyde do not increase the blood-brain and blood-retinal barrier permeability to sodium fluorescein.

No extravasation of sodium fluorescein from capillaries of the cerebral cortex and retina could be demonstrated in rats during severe nonlethal ethanol and/or acetaldehyde poisoning. The results do not exclude the possibility that repeated intoxications may gradually open the blood-brain and blood-retinal barriers, but do indicate the absence of an effect during acute intoxication.

Acetaldehyde↗
PubMed1981

The calcium carbimide-ethanol interaction: lack of relation between electroencephalographic response and cerebrospinal fluid acetaldehyde.

Penetration of acetaldehyde into cerebrospinal fluid (CSF) was studied in healthy human volunteers during calcium carbimide-ethanol interaction. CSF was sampled via lumbar puncture and blood from a cubital vein. CSF and blood acetaldehyde concentrations varied from 1 to 41 and from 22 to 138 mumol/l, respectively. The results indicate that acetaldehyde penetrates the human blood-liquor barrier. Computer analysis of electroencephalograms (EEGs) recorded during the interaction showed reduction in alpha activity with a concomitant increase in delta activity. The changes were similar to those previously observed during 'normal' ethanol intoxication.

Acetaldehyde↗
PubMed1981

Acetaldehyde penetrates the blood-liquor barrier of goats.

Goats received ethanol or acetaldehyde via carotid arterial infusions. Cerebrospinal fluid (CSF) was sampled for a lateral cerebral ventricle and blood from a jugular vein. Ethanol infusions produced only negligible levels of acetaldehyde in blood and CSF, but acetaldehyde infusions resulted in high levels. In contrast to ethanol, acetaldehyde was rapidly eliminated from both blood and CSF after discontinuing the infusion. The results indicate that even small amounts of acetaldehyde easily penetrate the blood-liquor barrier of goats.

Acetaldehyde↗
PubMed1980

Difficulties in measuring human blood acetaldehyde concentrations during ethanol intoxication.

The determination of human blood acetaldehyde (AcH) concentrations is complicated by two artefactual reactions, one resulting in the disappearance of AcH prior to deproteinization of the blood and the other resulting in the formation of AcH during deproteinization. The AcH formation increases with increasing ethanol concentration and decreases with increasing blood dilution, while the rapid AcH disappearance is initiated at the start of the blood collection. The magnitudes of these artefactual reactions are of such an order that a re-evaluation of previous reports on human blood AcH levels is needed. To circumvent these difficulties we suggest that blood should be deproteinized immediately (less than 5s) after arterial or venous puncture and corrections for AcH formation should be determined under the experimental conditions employed. The first data available on human blood AcH concentrations during ethanol intoxication, determined with such methods (20 to 40 micro M AcH after 1 g/kg ethanol), revealed no differences between the estimated in vivo arterial and venous AcH concentrations.

Acetaldehyde↗
PubMed1980

Occurrence of cerebral seizures provoked by alcohol abuse.

Alcohol intoxication was detected in the immediate history of 277 (49%) of the 560 consecutive seizure patients brought to the emergency room of Meilahti hospital in Helsinki during the course of a year, most of these patients being young men of working age. The alcohol-provoked seizures occurred mainly on Sunday and Monday, following the weekly pattern of alcohol consumption in Finland, and preceded delirium tremens in 21 patients (4%). Even short periods of intoxication (1-2 days) provoked seizures. The data indicate that among patients with a previous history of recurrent alcohol-withdrawal seizures, new treatable diseases of the CNS, especially acute brain injuries, are frequently encountered. Therefore, all seizure problems, not neglecting those of alcoholics, should be carefully examined.

Adolescent↗
PubMed1980

Does cellular tolerance develop to the lethal effect of ethanol in the rat?

Rats were kept intoxicated by forced intragastric administration of a liquid diet containing ethanol for 4 days or 3 weeks. Control animals were pair-fed with the same liquid diet containing starch instead of ethanol. After withdrawal the animals pretreated for 3 weeks showed tolerance to the lethal effect of ethanol as indicated by significantly prolonged survival and higher cerebrospinal fluid ethanol level at death after an oral test dose of 15 g/kg. The tolerance disappeared within a week. Metabolic tolerance, although present, did not prolong the survival of the animals, and the results suggest involvement of cellular tolerance in the central nervous system.

Animals↗
PubMed1978

Role of gastric emptying on ethanol poisoning in rats.

Intraperitoneal glucose was demonstrated to significantly inhibit the absorption of ethanol ( 2 g/kg) administered orally to rats. The effect was due to slowed emptying of the stomach, verified by analysis of the stomach contents and of blood enthanol levels. The observation agrees with previous findings, according to which the rate of stomach emptying is inversely related to the blood glucose level. However, when glucose was given intravenously 15 minutes after oral administration of a lethal dose of ethanol (12.5 g/kg) no significant inhibition of ethanol absorption could be observed. Intravenous propantheline, pyrithioxine and methylene blue were also unable to prolong the survival time or to influence the lethal blood ethanol concentration (about 170 mmol/l) of the enthanol-poisoned rats.

Administration, Oral↗
PubMed1978

Effect of ethanol on cardiac function in rats genetically selected for their ethanol preference.

The heart rate of male ANA (Alko, Non-alcohol) and AA (Alko, Alcohol) rats was significantly increased after peroral administration of 2.7 g ethanol/kg, but the tachycardia was of shorter duration in ANA rats, which avoid the drinking of ethanol solution. The PR intervals in the electrocardiograms of ANA rats became significantly longer than those of AA rats when 13.5 g ethanol/kg was given. The QT intervals were likewise longer in the electrocardiograms of ANA rats, but before as well as after the administration of ethanol. The results suggest that intracardiac conduction is more depressed by acute ethanol in the ANA than the AA strain of rats.

Alcohol Drinking↗