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Biomedical subjects

O Strubelt

Publications and source records attributed to O Strubelt.

At least 73 records · Page 4Linked to original sources
PubMed1982

Fasting accelerates the in vivo metabolism of carbon tetrachloride in rats.

Exposure of fed and fasted rats to CC1(4) vapor (114 ppm) for 6 h in a closed system increased serum enzyme activities (GOT, GPT, SDH) only in fasted animals. The in vivo metabolism of CC1(4), studied in the same system, was accelerated by fasting; the half-life of the elimination phase being reduced by approx. 33%. The enhanced susceptibility to CC1(4) induced by fasting seemed to be due to the accelerated bioactivation of CC1(4) to the toxic trichloromethyl free radical.

Alanine Transaminase↗
PubMed1982

[Experimental studies on therapeutic modification of sparteine poisoning].

We investigated the influence of an intoxication with sparteine (10 mg/kg X min i.v.) on heart rate, arterial blood pressure, cardiac output, stroke volume and total peripheral resistance in anesthetized rats. The leading feature of the cardiovascular activity of sparteine in rats was a strong bradycardia whereas blood pressure, cardiac output and peripheral resistance only slightly decreased and stroke volume even increased. The death of the rats occurred with a sudden stop of the QRS complexes in the ECG and an abrupt fall of blood pressure. Isoprenaline, orciprenaline, dopamine and prenalterol were compared with respect to their efficacy in reversing sparteine-induced toxicity in rats. Prenalterol proved to be the best antidote on account of its specific action on adrenergic beta 1-receptors. This result was affirmed in two experiments in pigs. Isoprenaline may also be used as an antidote for sparteine but decreases the blood pressure. Vasoconstrictors like dopamine should only be used in sparteine intoxication when a severe fall of blood pressure occurs which can not be overcome by prenalterol or isoprenaline.

Anesthesia↗
PubMed1981

Influence of 2,4-dinitrophenol on the susceptibility of rats to hepatotoxic injury.

Treatment of rats with 2,4-dinitrophenol (DNP) markedly enhanced the release of enzymes into serum induced by carbon tetrachloride (CCl4). DNP also aggravated the hepatotoxic response to paracetamol but not that to allyl alcohol, bromobenzene and thioacetamide. DNP-induced hypoxia resulting in an accelerated metabolic activation of CCl4 presumably accounts for the interaction between DNP and CCl4.

2,4-Dinitrophenol↗
PubMed1980

Anti-inflammatory effect of ethanol and other alcohols on rat paw edema and pleurisy.

The rat paw edema due to carrageenan, yeast, and dextran was dose-dependently antagonized by oral administration of ethanol. Carrageenan-induced paw edema was also inhibited by methanol, 1-propanol, and 1-butanol. The rat carrageenan pleurisy was reduced by oral pretreatment with methanol, ethanol, 1-propanol, 1-butanol, and dimethyl sulfoxide. Central depression, altered adrenal functions, increased osmolality, and hypothermia were no important factors for these actions of solvents. It is concluded that the inhibitory effect of ethanol on inflammatory responses increases the susceptibility of alcoholics to infection.

1-Propanol↗
PubMed1980

Influence of hypoxia on the hepatotoxic effects of carbon tetrachloride, paracetamol, allyl alcohol, bromobenzene and thioacetamide.

Exposure of rats to a reduced oxygen tension (6% O2, 94% N2) for 6 h increased the serum enzyme and the histological lesions induced by carbon tetrachloride (CCl4). Hypoxia did not enhance the hepatotoxic response to paracetamol, allyl alcohol, bromobenzene or thioacetamide. No correlation was found between the changes in hepatotoxicity induced by hypoxia and those after treatment with ethanol. Hepatic hypoxia therefore was not the pathogenetic mechanism responsible for ethanol-induced enhancement of hepatotoxicity.

Acetaminophen↗
PubMed1980

The influence of silybin on the hepatotoxic and hypoglycemic effects of praseodymium and other lanthanides.

In rats, i.v. administration of praseodymium, cerium and lanthanum (3 to 14 mg/kg) produced a dose-dependent increase in the serum activities of GOT, GPT and SDH. These dose-response curves of serum enzyme activities were shifted to the right by simultaneous treatment with silybin (75 mg/kg i.p.). Silybin also attenuated the increase of bromosulphthaleine retention and prevented the accumulation of liver triglycerides induced by praseodymium (7 mg/kg i.v.). Furthermore, silybin reduced the mortality rate of rats treated with high doses of the lanthanides. Rats treated with praseodymium (7 mg/kg i.v.) developed a pronounced hypoglycemia. On the 3rd day after praseodymium injection liver glycogen decreased to 4%, liver glutathione (GSH) to 82%, hepatic microsomal cytochrome P-450 content to 53%, aniline hydroxylase activity to 58% and aminophenazone demethylase activity to 40% of the control values. Silybin prevented praseodymium-induced hypoglycemia completely and the changes in the biochemical parameters of liver function partially but did not influence the decrease of liver GSH.

Animals↗
PubMed1980

Antifibrillatory, cardiovascular and toxic effects of sparteine, butylsparteine and pentylsparteine.

The negative bathmo- ino and chronotropic effects of sparteine, butylsparteine and pentylsparteine were quantitatively determined in isolated rat atria. The antifibrillatory potency was studied in rats (aconitine arrhythmia), guinea pigs (digoxin arrhythmia) and in cats (spontaneous arrhythmia). In order to appraise the cardiovascular compatibility of these drugs, additional circulatory effects were studied in rats and cats. Acute toxicity following intravenous, intraperitoneal and oral administration was assessed in male and female mice. Pentylsparteine was more potent than sparteine and had a better therapeutic index.

Animals↗
PubMed1980

Hemodynamic failure induced by narcotic and toxic doses of 12 CNS depressants in intact and pithed rats.

UNLABELLED: Heart rate (HR), cardiac output (CO), stroke volume (SV), arterial blood pressure (BP), and peripheral resistance (PR) were assessed in awake rats and in rats anesthetized with hexobarbital, pentobarbital, secobarbital, secbutabarbital, methaqualone, chloral hydrate, urethane, ethanol, guaiphenesine, meprobamate, diazepam and chlorpromazine (respired artificially). Anesthesia mostly was accompanied by an increase of HR and PR and a decrease of CO and SV, whereas BP remained unchanged or somewhat declined. Infusion of further amounts of the CNS depressants caused a dose-dependent decrease of HR, CO and BP but did not influence SV whereas PR declined but did not fall considerably beyond the values in awake rats. A strong decline of CO, SV and BP but no change of HR and PR occurred after pithing in rats. Anesthetic doses of hexobarbital, pentobarbital, secobarbital, secbutabarbital, methaqualone, and guaiphenesine produced no hemodynamic effects in pithed rats. Chloral hydrate, urethane, ethanol, meprobamate, diazepam, and chlorpromazine, on the other hand, in anesthetic doses depressed the CO and BP of pithed rats without influencing PR. In toxic doses, the CNS depressants caused comparable hemodynamic changes in pithed as in anesthetized rats. CONCLUSION: Hemodynamic failure induced by narcotic doses of CNS depressants is mainly due to a depression of the vasomotor center(s) and an impairment of cardiovascular reflex control, that after toxic doses is mainly caused by the direct cardiovascular-depressive actions of these drugs.

Animals↗
PubMed1979

Studies on the mechanism of paracetamol-induced protection against paracetamol hepatotoxicity.

In rats, 3 days treatment with paracetamol (1 oral dose of 1 g/kg daily) produced a complete protection against the hepatotoxic actions of a further dose of paracetamol as documented by determination of serum enzyme activities (glutamic-oxaloacetic transaminase, (GOT), glutamic-pyruvic transaminase (GPT), sorbitol dehydrogenase (SDH), bromsulphthalein retention and histological investigations. Subacute paracetamol treatment decreased liver glutathione levels by 46%, liver microsomal cytochrome P-450 content by 23%, hepatic hydroxylation of aniline by 29% and hepatic demethylation of aminopyrine by 46%. It afforded also some protection against the hepatotoxic actions of carbon tetrachloride, bromobenzene and thioacetamide, but did not influence the antiphlogistic activity of paracetamol (carrageenan paw edema test). Plasma and liver concentrations of free paracetamol after oral administration of 1 g/kg paracetamol were somewhat higher in the subacutely paracetamol-pretreated rats than in the non-pretreated control animals whereas no differences in the concentrations of conjugated paracetamol were found between the 2 groups. Pretreatment with paracetamol did not influence the urinary excretion of free paracetamol but caused some shift in the urinary excretion of paracetamol conjugates: pretreated rats excreted 23% less of the paracetamol glucuronide and sulfate and 33% more of the paracetamol mercapturate than the control animals. A depression of the microsomal mixed-function oxidase activity is presumed to be the main cause of the paracetamol-induced protection against paracetamol hepatotoxicity.

Acetaminophen↗
PubMed1978

[Cardiotoxicity of bromethylbutyramide (carbromide) (author's transl)].

Bromethylbutyramide (Carbromide), a quantitatively important metabolite of carbromal, diminished the contractility of electrically driven and the frequency of spontaneously beating guinea-pig atria. The negative inotropic action of bromethylbutyramide occurred at concentrations which are reached in human carbromal poisoning. The cardiodepressive actions of bromethylbutyramide and carbromal may be important for the course and the ending of severe carbromal intoxications.

Animals↗
PubMed1978

Increased carbon tetrachloride hepatotoxicity after low-level ethanol consumption.

Male rats provided with a 5 or 15% (v/v) ethanol solution as the sole source of fluid consumed ethanol at a rate of 11.4 or 24.9% of total calories (4.2 or 8.3 g/kg daily). After ethanol consumption lasting 1, 2 and 3 weeks the hepatotoxicity of CCl4 (0.1 ml/kg i.p.) was elevated by determination of serum activities of glutamic-oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase ( GPT), sorbitol dehydrogenase (SDH) and histological investigations. Carbon tetrachloride (CCl4)-induced liver damage was significantly greater in rats provided with ethanol than in the tap-water consuming controls. This potentiation of CCl4 hepatotoxicicty was fully developed already after a 1-week exposition to ethanol and was greater in the 15% than in the 5% ethanol group. Ethanol alone did not influence serum enzyme activities but increased microsomal aniline hydroxylation. There was, however, no clear-cut parallelism between potentiation of CCl4 hepatotoxicity and activation of aniline hydroxylation.

Aniline Hydroxylase↗
PubMed1978

The influence of ethanol pretreatment on the effects of nine hepatotoxic agents.

The hepatotoxic effects of carbon tetrachloride (0.01 ml/kg i.p.), thioacetamide (50 mg/kg intraperitoneally), paracetamol (0.5 g/kg intraperitoneally), and allyl alcohol (0.05 ml/kg intraperitoneally) as estimated by determination of serum enzyme activities (GOT, GPT, SDH) were enhanced in mice treated with one oral dose of 4.8 g/kg ethanol 16 hrs. previously. Pretreatment of mice with ethanol did not increase the hepatotoxic actions of bromobenzene (0.25 ml/kg intraperitoneally), phalloidin (1.5 mg/kg intraperitoneally), alpha-amanitin (0.75 mg/kg intraperitoneally), and praseodymium (12 mg/kg intravenously) though there was a trend to higher enzyme activities in the case of bromobenzene. In guinea-pigs ethanol also aggravated CCl4-induced liver damage, but only strengthened the hepatotoxic activity of D-galactosamine (150 mg/kg intraperitoneally). Treatment with 4.8 g/kg ethanol did not influence liver glutathione levels in mice but increased aniline hydroxylation in the 9000 x g liver homogenate supernatant of mice and guinea-pigs. A dose of 2.4 g/kg ethanol, on the other hand, neither increased aniline hydroxylase activity nor enhanced carbon tetrachloride-induced hepatotoxicity in mice. It is assumed that the enhanced sensitivity to hepatotoxic agents after treatment with ethanol may be due to an enhanced microsomal activation of these substances.

Acetaminophen↗
PubMed1978

Relations between hepatotoxicity and pharmacokinetics of paracetamol in rats and mice.

A dose-dependent increase of paracetamol serum half-life (t1/2) was found after oral and intravenous application in rats and oral application in mice. The hepatotoxic effects of paracetamol were not correlated with this prolongation of t1/2. Dithiocarb protected rats against paracetamol liver damage but did not change paracetamol t1/2. Paracetamol t1/2 was not influenced either by a hepatotoxic dose of carbon tetrachloride. In conclusion, the dose-dependent prolongation of paracetamol serum half-life is not due to paracetamol-induced liver damage but merely the consequence of saturated elimination processes.

Acetaminophen↗