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PubMed1987

Biphasic effect of methadone on hepatic drug metabolism.

When methadone HCl (30 mg/kg, po) was given acutely to mice, it was found to inhibit drug metabolism as evidenced by a prolongation of hexobarbital sleeping time and zoxazolamine paralysis time. Pharmacokinetic studies revealed that this acute dose of the narcotic analgesic could also prolong the plasma half-life of aminopyrine without any change in its volume of distribution. When added to the incubation mixture containing 10,000 g mouse liver supernatant fraction and a complete system for measuring aminopyrine N-demethylase or aniline hydroxylase, methadone showed a dose-dependent inhibition of the enzymes; the former enzyme was inhibited to a greater extent than the latter one. However, subacute treatment of mice with methadone HCl (30 mg/kg, po, twice daily for 3 days) resulted in increases in liver weight, microsomal protein, and cytochrome P-450 content in consonant with the increased activities of four hepatic drug-metabolizing enzymes: aminopyrine N-demethylase, aniline hydroxylase, p-nitroanisole, O-demethylase, and benzphetamine N-demethylase. Moreover, both hexobarbital sleeping time and zoxazolamine paralysis time were shortened. The plasma half-life of aminopyrine was decreased. These changes were prevented by simultaneous administration of puromycin diHCl (80 mg/kg, ip). Methadone thus seems to act in a manner very similar to that of propoxyphene or SKF-525A, acting as a potent inhibitor of hepatic drug metabolism when given acutely and as an inducer when given subacutely.

Aminopyrine N-Demethylase↗
PubMed1985

Biochemical basis of enhanced drug bioavailability by piperine: evidence that piperine is a potent inhibitor of drug metabolism.

Piperine, a major active component of black and long peppers, has been reported to enhance drug bioavailability. The present studies were aimed at understanding the interaction of piperine with enzymatic drug biotransforming reactions in hepatic tissue in vitro and in vivo. Piperine inhibited arylhydrocarbon hydroxylation, ethylmorphine-N-demethylation, 7-ethoxycoumarin-O-deethylation and 3-hydroxy-benzo(a)pyrene glucuronidation in rat postmitochondrial supernatant in vitro in a dose-dependent manner. Piperine inhibition of these reactions in postmitochondrial supernatant from 3-methylcholanthrene- and phenobarbital-treated rats was similar to the controls. Inhibition by piperine of arylhydrocarbon hydroxylase (AHH) from 3-methylcholanthrene-treated rats was comparable to that observed with 7,8-benzoflavone. Piperine caused noncompetitive inhibition of hepatic microsomal AHH from the untreated and 3-methylcholanthrene-treated rats with a Ki of 30 microM which was close to the apparent Km of AHH observed in the controls. Similarly, the kinetics of inhibition of ethylmorphine-N-demethylase from control rat liver microsomes exhibited noncompetitive inhibition with an apparent Km of 0.8 mM and Ki of 35 microM. These studies demonstrated that piperine is a nonspecific inhibitor of drug metabolism which shows little discrimination between different cytochrome P-450 forms. Oral administration of piperine in rats strongly inhibited the hepatic AHH and UDP-glucuronyltransferase activities. The maximal inhibition of AHH observed within 1 hr restored to normal value in 6 hr. Pretreatment with piperine prolonged hexobarbital sleeping time and zoxazolamine paralysis time in mice at half the dose of SKF-525A. These results demonstrate that piperine is a potent inhibitor of drug metabolism.

Alkaloids↗
PubMed2006

Narcolepsy and the hypocretins.

Narcolepsy is a chronic neurologic disease characterized by excessive daytime sleepiness and one or more of three additional symptoms (cataplexy, or sudden loss of muscle tone; vivid hallucinations; and brief periods of total paralysis) related to the occurrence of rapid eye movement (REM) sleep at inappropriate times. The daytime sleepiness typically presents as a sudden overwhelming urge to sleep, followed by periods of sleep that last for seconds or minutes, or even longer. During daytime sleep episodes, patients may exhibit "automatic behavior," performing conventionalized functions (eg, taking notes), but not remembering having done so once they are awake. About 10% of narcoleptics are members of familial clusters; however, genetic factors alone are apparently insufficient to cause the disease, inasmuch as the most common genetic disorder, a mutation in chromosome 6 controlling the HLA antigen immune complex, although seen in 90% to 100% of patients, also occurs in as many as 50% of people without narcolepsy. A dog model of narcolepsy exhibits a mutation on chromosome 12 that disrupts the processing of the peptide neurotransmitter hypocretin. No such mutation characterizes human narcolepsy; however, cerebrospinal fluid (CSF) hypocretin levels are profoundly depressed in narcoleptic patients, and a specific reduction in hypocretin-containing neurons has been described. One hypothesis concerning the pathophysiology of narcolepsy proposes that the HLA subtype resulting from the mutation on chromosome 6 increases the susceptibility of hypocretin-containing brain neurons to immune attack. Because hypocretin may normally participate in the maintenance of wakefulness, the loss of neurons that release this peptide might allow REM sleep to occur at inappropriate times, ie, while the patient is awake, in contrast to its normal cyclic appearance after a period of slow-wave sleep. The cataplexy, hallucinations, and/or paralysis associated with REM episodes normally are unnoticed-or, at least, not remembered-when the transition to REM follows slow wave sleep, as is normally the case; however, they are remembered when, in people with narcolepsy, the REM episode starts during a period of wakefulness. The association of narcolepsy with a deficiency in a specific neurotransmitter, in this case, hypocretin, is reminiscent of the associations between Parkinson disease and dopamine, or early Alzheimer disease and acetylcholine.

Animals↗
PubMed1980

Metabolite involvement in bromocriptine-induced circling behaviour in rodents.

Bromocriptine and apomorphine produced identical circling responses in rodents with medial forebrain bundle lesions. Rotation induced by bromocriptine, but not by apomorphine, was inhibited by prior treatment with reserpine or alpha-methyl-p-tyrosine suggesting a requirement for intact presynpatic events. Bromocriptine-induced circling also was inhibited by the catecholamine re-uptake blockers nomifensine and desmethylimipramine, supporting the role of presynaptic mechanisms. Bromocriptine-induced circling, but not apomorphine circling, was reduced by pre-treatment with SKF 525A, an inhibitor of monooxygenase enzymes, suggesting metabolite involvement in the turning response. This compound prolonged hexobarbitone sleeping times and zoxazolamine paralysis times in mice. These indices of drug metabolizing activity also were prolonged by pre-treatment with desmethylimipramine while nomifensine prolonged only hexobarbitone sleeping times and alpha-methyl-p-tyrosine had no effect on either index. The data suggest that a metabolite of bromocriptine may be of importance in causing circling and that uptake of bromocriptine (or a metabolite) into presynaptic catecholamine terminals may be necessary.

Amphetamine↗
PubMed1982

Oxygen saturation during sleep in patients with spinal cord injury.

Sleep is associated with moderate or severe arterial desaturation in many disease states. This study was undertaken to evaluate whether hypoxemia during sleep was a significant problem in the spinal cord injured patient. Eleven patients with cervical or thoracic cord injury who had significant respiratory deficiency were evaluated. The mean age was 29.2 +/- 14. Vital capacity (VC) for the group revealed a mean of 43.1 +/- 18.1% of predicted, inspiratory capacity (IC) was 51.6 +/- 20.2% of predicted, and expiratory reserve volume (ERV) was 23.6 +/- 24.7% of predicted. In eight patients blood gases revealed a mean PO2 of 81.5 +/- 8.4 mmHg and PCO2 of 38.9 +/- 3.4 mmHg. Sleep screening studies were done using the Hewlett-Packard ear oximeter. They were studied for a mean of 2.6 +/- 1.1 hours. The initial O2 saturation was 96.6 +/- 1.6% and dropped to a mean of 90.6 +/- 6.4%. Only 1/11 reached saturation to less than 85% and 2/11 reached levels lower than 90%. Only age was significantly correlated with amount of desaturation (p less than .01). The level of the lesion, and % predicted ERV were not. One of the two patients who had hypoxemia with sleep had unilateral diaphragmatic paralysis. It is concluded that young quadriplegic patients with normal diaphragmatic function have no severe desaturation during sleep, but older patients and patients with some diaphragmatic dysfunction should be screened for sleep desaturation.

Adolescent↗
PubMed1994

[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords].

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.

Aged↗
PubMed1983

Drug metabolism and chemosensitization. Nitroimidazoles as inhibitors of drug metabolism.

The nitroimidazole misonidazole (MISO) and related compounds have been shown to enhance the response of tumours to cytotoxic agents, and often to improve their therapeutic indices. Previous experiments suggested inhibition of cytotoxic drug metabolism as a mechanism. We have now investigated the effects of MISO and related compounds on drug metabolism in mice, and the results can be summarised as follows. (1) MISO and related compounds inhibit drug-metabolising enzymes, as measured by pentobarbitone sleep-time and zoxazolamine paralysis-time. (2) Enzyme inhibition is primarily dependent on lipophilicity, with maximum inhibition exhibited by the most active chemosensitizers. (3) MISO significantly slowed the clearance of pentobarbitone, aminopyrine and the cytotoxic agent chlorambucil, but had no effect on renal function or protein binding. These data support the view that inhibition of cytotoxic drug metabolism may be an important factor in chemosensitization.

Aminopyrine↗
PubMed1986

Effect of praseodymium chloride on liver microsomal enzymes of rats.

A single i.v. dose (5 mg/kg) of a light lanthanon, praseodymium, prolonged the duration of hexobarbital-induced sleep and zoxazolamine-induced paralysis, as well as it modified pharmacokinetic parameters of hexobarbital and zoxazolamine, in rats. Half-lives (t1/2) and area under the curve (AUC) were increased, while elimination coefficient (beta) and clearance (Cl) were decreased. However, in daily doses of 1 mg/kg i.p. for 15 days, praseodymium did not alter pharmacological effects and pharmacokinetic parameters. The in vitro hydroxylation of hexobarbital and zoxazolamine by liver microsomes was inhibited when the animals were treated previously with a single i.v. dose (5 mg/kg) of praseodymium chloride. In these animals, the amount of cytochromes P-450 and b5 were reduced significantly, whereas that of NADPH-cytochrome c reductase remained unchanged. The pretreatment of animals with phenobarbital normalized the microsomal enzyme impairment caused by praseodymium.

Animals↗
PubMed2004

Sleep and arousal mechanisms in experimental epilepsy: epileptic components of NREM and antiepileptic components of REM sleep.

Neural generators related to different sleep components have different effects on seizure discharge. These sleep-related systems can provoke seizure discharge propagation during nonrapid eye movement (NREM) sleep and can suppress propagation during REM sleep. Experimental manipulations of discrete physiological components were conducted in feline epilepsy models, mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. The sleep-wake state distribution of seizures was quantified before and after discrete lesions, systemic and localized drug administration, and/or photic stimulation, as well as in relation to microdialysis of norepinephrine. We found that (1) neural generators of synchronous EEG oscillations--including tonic background slow waves and phasic "arousal" events (sleep EEG transients such as sleep spindles and k-complexes)--combine to promote electrographic seizure propagation during NREM and drowsiness, and antigravity muscle tone permits seizure-related movement; (2) neural generators of asynchronous neuronal discharge patterns reduce electrographic seizures during alert waking and REM sleep, and skeletal motor paralysis blocks seizure-related movement during REM; (3) there are a number of similarities between amygdala-kindled kittens and children with Landau-Kleffner Syndrome (LKS) that suggest a link among seizures, sleep disorders, and behavioral abnormalities/regression.

Amygdala↗
PubMed1994

Laryngeal electromyography with separated surface electrodes in patients with multiple system atrophy presenting with vocal cord paralysis.

When recording the activity of the posterior cricoarytenoid muscle (PCA) with surface electrodes, there is contamination from the surrounding muscles such as the cricopharyngeal muscle. We therefore devised a new oesophageal catheter electrode of the separate type, having three individual surface electrodes for the PCA, cricopharyngeal muscle and diaphragm. The records obtained with this catheter demonstrated satisfactory separation between PCA and cricopharyngeal muscle activities. We used this catheter in patients with multiple system atrophy presenting with vocal cord paralysis, who were awake or asleep. There were two interesting electromyographical findings, which were inspiratory activity of the adductor muscle (the thyroarytenoid muscle) and fade-out of the abductor muscle, that is, PCA activity during sleep. Although vocal cord paralysis is one of the most serious life-threatening complications, the precise mechanism has not been clarified. We believe that our catheter may be useful in investigating the mechanism of vocal cord paralysis which could cause sudden death in neurodegenerative disorders, including multiple system atrophy.

Aged↗
PubMed1987

Sleep in restrictive lung disease.

Restrictive lung disease patients exhibit a wide range of breathing and oxygenation abnormalities during sleep. The combination of degree of restriction, whether it is intrapulmonary or extrapulmonary, and confounding factors, such as obesity, age, and sex, will ultimately determine the degree of disturbed nocturnal physiology. The sleep literature is still sparse in most restrictive diseases. For patients with interstitial lung disease, the role of nocturnal oxygen in chronic established fibrosis, and also in acute alveolitis (e.g., farmer's lung, bird fancier's lung, etc.), has not been addressed. As fibrotic lung disease progresses, the degree of nocturnal desaturation and breathing dysrhythmias will progress. Changes in sleep architecture are likely related to the progression of the disease, but this is not known with certainty. Long-term evaluation of sleep and breathing in interstitial lung disease will give further insight into whether or not sleep changes are primary or secondary events. For kyphoscoliosis patients, again, we need more information on sleep as the thoracic deformity changes. In addition, the use of drugs (acetazolomide, medroxyprogesterone, and almitrine) and/or nasal CPAP to treat nocturnal desaturation needs to be assessed in a controlled fashion. In neuromuscular disease, the dynamics of gas exchange and sleep structure need to be defined in a larger group of patients. Factors such as degree of muscle weakness, degree of underlying lung diseases, and medications must be taken into consideration. Nocturnal hypoxemia may cause muscle weakness and fatigue, which in time, could cause more nocturnal hypoventilation and further hypoxemia. Supplemental nocturnal oxygen should be evaluated in this population.

Female↗
PubMed1988

A syndrome of REM and non-REM sleep reduction and lateral gaze paresis after medial tegmental pontine stroke. Computed tomographic scans and anatomical correlations in four patients.

A common pattern of reduction in both rapid eye movement and non-rapid eye movement sleep associated with various lateral gaze paralyses was present in four cases of brain-stem stroke. From computed tomographic scan data, clinical inferences, and, in two cases, neuropathologic sections, the common lesions were localized in the medial pontine tegmentum, ie, the inner part of the gigantocellular and pontis centralis caudalis nuclei. These data in humans were compared with lesions obtained experimentally in cats.

Adult↗
PubMed1986

Digitoxin metabolism by liver microsomal cytochrome P-450 and UDP-glucuronosyltransferase and its role in the protection of rats from digitoxin toxicity by pregnenolone-16 alpha-carbonitrile.

The aim of the present study was to investigate whether the mechanism by which pregnenolone-16 alpha-carbonitrile (PCN) protects rats from digitoxin toxicity was dependent on the induction of liver microsomal cytochrome P-450p and/or the UDP-glucuronosyltransferase active toward digitoxigenin monodigitoxoside (UDP-GT-dt1). Evidence is presented that suggests troleandomycin is a selective inhibitor of cytochrome P-450p in vivo, based on the pattern of inhibition observed when zoxazolamine paralysis time and hexobarbital sleeping time were measured in rats treated with different cytochrome P-450 inducers. A single dose of troleandomycin completely reversed the ability of PCN to protect rats from digitoxin toxicity, establishing the importance of cytochrome P-450p induction in the protective effect of PCN. The postpubertal decline in constitutive cytochrome P-450p levels in female but not male rats was paralleled by a female-specific, age-dependent decline in the rate of digitoxin sugar cleavage (i.e., digitoxosyl oxidation of digitoxin to 15'-dehydrodigitoxin and digitoxosyl cleavage to digitoxigenin bisdigitoxoside). This resulted in a marked sex difference in the rate of digitoxin sugar cleavage catalyzed by liver microsomes from mature rats (male/female approximately 6). However, no sex difference in digitoxin toxicity was observed in either immature or mature rats. In contrast to cytochrome P-450p, liver microsomal UDP-GT-dt1 activity increased dramatically with age in both male and female rats (mature/immature approximately 10). However, no age differences in digitoxin toxicity were observed in rats of either sex. The results indicate that cytochrome P-450p and UDP-GT-dt1 can be independently regulated in rat liver and that large changes in the constitutive levels of these microsomal enzymes have no effect on digitoxin toxicity. This suggests that the induction of cytochrome P-450p and UDP-GT-dt1 does not fully account for the mechanism by which PCN protects rats from digitoxin toxicity.

Age Factors↗
PubMed1989

Effect of exogenous pyruvate on acrylamide neuropathy in rats.

The protective effect of exogenous sodium pyruvate on the distal-proximal progression of experimental acrylamide neuropathy in rats was examined. Incorporation of 2% (w/w) sodium pyruvate powder in the diet of rats receiving subcutaneous injections of an aqueous solution of acrylamide (35 mg/kg/day, 5 days/week) retarded the onset and development of functional, morphological, and biochemical measures of acrylamide neuropathy. Pyruvate supplementation did not alter hexobarbital sleep time or zoxazolamine paralysis time, two in vivo measures of microsomal mixed-function oxidase activity, and the disposition of radioactivity in plasma or sciatic nerve following subcutaneous injection of [14C]acrylamide. Although acrylamide can interfere with energy metabolism at a variety of sites where pyruvate can rescue neurons (axons), the data of this study are consistent with our earlier hypothesis that acrylamide neuropathy may be associated with a glycolytic deficit. The exact site of pyruvate protection is unknown. Exogenous pyruvate is perhaps utilized by axons to circumvent toxin-induced glycolytic inhibition and provide chemical energy for fast axonal transport.

Acrylamide↗
PubMed1984

Effect of cigarette smoking on hepatic biotransformations in rats.

Adult male rats were nose-only exposed to cigarette smoke for 20 min each day for 6 months. Smoke inhalation was confirmed by urinary excretion of nicotine (4.5 micrograms/rat/day) and elevated blood carboxyhemoglobin (13.3%). Phenobarbital- and 3-methylcholanthrene-treated rats were included as positive controls for assessing hepatic enzyme induction. Cigarette smoke did not induce statistically significant alterations in hepatic enzyme activity when measured in vivo (pentobarbital sleep time and zoxazolamine paralysis time) or in vitro (oxidation, hydrolysis, glucuronidation, and glutathione conjugation). In some cases, the smoke-exposed rats did exhibit higher microsomal enzyme activity than did the controls, but this increase was also evident in the sham-control group. Therefore, these increases were attributed to stress and not to smoking per se. Additional evidence of stress associated with manipulation of the animals was the smaller percentage weight gains of the smoke-exposed and sham control rats over the 6-month period as compared to the controls (12, 35, and 50%, respectively). Smoking reduced hepatic glutathione by as much as 15%, but the glutathione transferase activity was not affected. These studies showed that chronic exposure of rats to cigarette smoke did not alter hepatic biotransformation processes, but do suggest that smokers may be less efficient than nonsmokers in the deactivation of xenobiotics by glutathione conjugation mechanisms.

Animals↗