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Biomedical subjects

F Karoum

Publications and source records attributed to F Karoum.

At least 127 records · Page 7Linked to original sources
PubMed1981

A comparative study on the effects of morphine on central, peripheral and ganglionic stores of catecholamines.

The turnover and metabolism of catecholamines after i.p. administration of 10 (low dose) or 40 (high dose) mg/kg of morphine sulfate were measured in the brain, lumbar spinal cord, heart, celiac and superior cervical ganglia (SCG) of demedullated rats with unilaterally decentralized SCG. Demedullation significantly increased norepinephrine concentration and turnover in both sham operated and decentralized SCG, but demedullation failed to change the turnover of dopamine (DA) in both ganglia. Low doses of morphine only increased DA metabolism in the caudate nucleus. High doses of morphine failed to change the turnover of norepinephrine stored in heart and sympathetic ganglia but produced variable changes in norepinephrine turnover in the spinal cord and brain. High doses of morphine significantly increased DA turnover and metabolism in the celiac ganglion, SCG, caudate nucleus and the spinal cord of demedullated rats. These effects of morphine were antagonized by naloxone. DA metabolism in decentralized SCG of demedullated and SCG of intact rats remained unchanged after high doses of morphine. The action of morphine on DA metabolism was facilitated by demedullation, suggesting that the adrenal medulla secretes a modulator that can counteract the effects of opiate ligands on ganglionic small intensely fluorescent cells. Atropine and hexamethonium failed to antagonize the increase in the metabolism of ganglionic DA produced by morphine; and the increase in ganglionic DA metabolism caused by oxotremorine was not antagonized by naloxone, thus confirming a disassociation between the action on ganglionic DA mediated by cholinergic and opiate receptors. Since decentralization of the SCG abolishes the increase in DA metabolism induced by morphine, stimulation of extraganglionic opiate receptors reflects the metabolism of DA located in small intensely fluorescent cells.

Adrenal Medulla↗
PubMed1980

Modulation of nicotinic receptors by opiate receptor agonists in cultured adrenal chromaffin cells.

Morphological, physiological and pharmacological evidence indicates that opioid peptides, which in the brain are located intraneurally, may function as neurotransmitters. Similar evidence is not yet available for the opioid peptides that are stored in chromaffin cells of adrenal medulla and in axon terminals located in adrenal medulla and sympathetic ganglia. The present report contributes evidence suggesting that the opioid peptides which are stored in the axon terminals of the splanchnic nerves located in adrenal medulla may function as neuromodulators of the acetylcholine receptors located on chromaffin cells that are involved in catecholamine release. We support this functional role of the opioid peptides by showing that primary cultures of chromaffin cells of bovine medulla contain opiate receptors. When these receptors are occupied by specific agonists, the number of nicotinic receptors and the amount of catecholamine released by maximal doses of nicotine are reduced. Thus, like in other neuronal systems also in adrenal medulla, the action of opioid peptides is inhibitory. The specificity of this action is in part supported by the inability of opiate receptor agonists to reduce the Ca2+-dependent release of catecholamines elicited by K+ ions.

Adrenal Medulla↗
PubMed1980

Restoration of dopaminergic function by grafting of fetal rat substantia nigra to the caudate nucleus: long-term behavioral, biochemical, and histochemical studies.

Motor deficits produced in rats by unilateral substantia nigra lesions have been found to be reduced by grafts of fetal rat substantia nigra to the dopamine denervated caudate nucleus. In the present study these grafts were examined behaviorally, histochemically, and biochemically over six to 10-month periods. The grafts were found to survive in a healthy condition and contain catecholaminergic cells and fibers after eight to ten months. Concentrations of dopamine in adjoining parts of the caudate nucleus were increased when examined six months after grafting. Apomorphine induced rotation was reduced by the grafts, and these reductions persisted for at least six months. Although signs of aging were observed in the brains of the host animals when sacrificed eight to ten months after grafting, the grafts remained healthy and showed no signs of aging or deterioration. It is concluded that substantia nigra grafts can become permanent, functional constituents of the brains of host animals with prior substantia nigra lesions.

Animals↗
PubMed1980

Differential sensitivity of hypothalamic dopaminergic and noradrenergic neurones to pharmacological manipulation.

The effects of apomorphine (Apo), haloperidol (Hal), reserpine, phenyoxybenzamine, oxotremorine and scopolamine on hypothalamic caatecholamines and metabolites were assessed. All these drugs, except Apo, significantly changed the hypothalamic concentration of 3-methoxy-4-hydroxyphenylglycol (MHPG), thus suggesting parallel changes in noradrenaline (NA) metabolism and turnover. Hal increased MHPG, an effect which was reversed by Apo pretreatment. Oxotremorine and scopolamine respectively increased and decreased MHPG, reserpine decreased NA and increased MHPG. Phenoxybenzamine increased MHPG without altering NA concentrations. Dopamine and its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were not changed by Apo and Hal, but were influenced by the other drugs. These results indicate that NA in the hypothalamus is influenced by both cholinergic and dopaminergic events occurring in the brain and that dopaminergic neurones in this organ are different in their biochemical and pharmacological characteristics from neurones present in other central and peripheral systems.

Animals↗
PubMed1979

Phenylethylamine in paranoid chronic schizophrenia.

Phenylethylamine (PEA) is an endogenous amine that is structurally and pharmacologically related to amphetamine. Urinary PEA excretion is significantly higher in paranoid chronic schizophrenics than in nonparanoid chronic schizophrenics and normal controls. Diet, hospitalization, and medication do not account for differences in PEA concentrations. These findings offer some indication that PEA may be an endogenous amphetamine.

Chronic Disease↗
PubMed1979

Activation of rat sympathetic ganglia SIF cell dopamine metabolism by muscarinic agonists.

The biochemical responsiveness of the dopamine-containing small intensely fluorescent (SIF) cells to cholinoceptive drugs was evaluated in rat superior cervical ganglion (SCG), middle-inferior cervical ganglion and celiac ganglion. Amines and metabolites were analyzed by mass fragmentography. The major metabolite of dopamine (DA) in all ganglia was 3,4-dihydroxyphenylacetic acid (DOPAC). Stimulation of muscarinic receptors with carbachol induced a 3-10 fold increase of DOPAC concentration in the ganglia, the celiac ganglion being the most responsive and the SCG being the least. Pretreatment with atropine blocked the rise of DOPAC. The rise of DOPAC after activation of muscarinic receptors was not the consequence of blocking the removal of this acid from the ganglion. We concluded that DA metabolism in SIF cells is enhanced by stimulation of muscarinic receptors and that the magnitude of the DOPAC increase in a ganglion may reflect the importance of DA in ganglionic transmission.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Adrenergic and dopaminergic response to chronic chair restraint in the rhesus monkey.

Prolonged chair restraint and social isolation in the rhesus monkey led to a reduction in the urinary excretion of HVA (4-hydroxy-3-methoxyphenylacetic acid), DOPAC (3,4-dihydroxyphenylacetic acid), VMA methoxy-4-hydroxymandelic acid), and MHPG (3-methoxy-4-hydroxyphenylethylglycol) over a 3 week period. This adaptation to a chronically "stressful" situation corresponds to earlier studies on the rhesus monkey indicating a gradual reduction in the urinary excretion of norepinephrine and epinephrine after initiation of restraint. The following basic information on the urinary excretion of catecholamine metabolites was obtained: (1) the rate of excretion of the dopamine metabolites (HVA and DOPAC) is about four times higher than the rate of excretion of adrenergic metabolites (VMA and MHPG): (2) MHPG is the major adrenergic metabolite in the rhesus monkey; and (3) the excretion rates of the urinary metabolites varied considerably between animals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

The dynamics of dopamine metabolism in various regions of rat brain.

Dopamine metabolism was studied in various regions of rat brain by following the decline of 3,4-dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylacetic acid (HVA) from brain after treatment with pargyline, or from the accumulation of the acids after treatment with probenecid. The decline of DOPAC and HVA after pargyline treatment appeared exponential in all regions of brain studied with half-lives of about 13 min for HVA and 6.5 min for DOPAC. DOPAC was the major metabolite of dopamine, with various brain regions producing between 2-5 times more DOPAC than HVA. HVA accumulated after treatment with probenecid but the accumulation in 1 h did ot account for all of the HVA apparently eliminated from brain. DOPAC accumulated in some regions of brain (medulla, hypothalamus and midbrain) and not in others (cerebellum, cortex, striatum and hippocampus) after probenecid treatment. We conclude that dopamine metabolism is not uniform in brain and that the accumulation of DOPAC and HVA in brain after probenecid treatment only accounts for a minor fraction of the dopamine formed in brain.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1977

Presence of free, sulfate and glucuronide conjugated 3-methoxy-4-hydroxyphenylglycol (MHPG) in human brain, cerebrospinal fluid and plasma.

The concentration of the free, glucuronide and the sulfate conjugated forms of 3-methoxy-4-hydroxyphenylglycol (MHPG) were measured in human plasma, cerebrospinal fluid (CSF) and brain by mass fragmentography. All three forms of MHPG were detected in the media analyzed. Free MHPG was found to be the predominant form in both the brain and the CSF. The sulfate conjugate of MHPG constitutes about 15% of the total MHPG in the CSF while in the brain the percentage varies between 30% in the hypothalamus and cortex and 80% in the substantia nigra. The concentration of the glucuronide conjugate of MHPG measured in the brain and CSF represents about 5% of the total MHPG concentration. In the plasma free MHPG and its glucuronide and sulfate conjugates are present in about equal concentrations. The relative concentrations of the three forms of MHPG measured in plasma, CSF and brain were compared with their concentrations in the urine from previously published results. From this comparison the diagnostic significance of each of the three forms of MHPG in the clinical assessment of central norepinephrine metabolism is discussed.

Adult↗