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Biomedical subjects

G N Pandey

Publications and source records attributed to G N Pandey.

At least 91 records · Page 5Linked to original sources
PubMed1980

Effect of acute methadone withdrawal on prostaglandin E-stimulated 3H-cyclic adenosine monophosphate accumulation in human platelets.

The effect of acute methadone withdrawal was studied on PGE1-sensitive platelet adenylate cyclase of 8 former heroin addicts who had been stabilized with methadone. During acute methadone withdrawal there was a significant increase in PGE1-sensitive platelet adenylate cyclase activity, which correlated with the severity of withdrawal symptoms. This suggests that PGE1-sensitive adenylate cyclase and cyclic adenosine monophosphate (cyclic AMP) are involved in the human addictive process.

Adenylyl Cyclases↗
PubMed1979

Lithium transport across red cell membrane: a cell membrane abnormality in manic-depressive illness.

In the families of manic-depressive patients, relatives with a history of affective disorders had a significantly higher ratio of mean red cell lithium to plasma lithium in vitro than relatives with no such history. A genetically controlled abnormality in lithium-sodium transport, the mechanism that determines the lithium ratio, may play a role in the etiology of some forms of affective disorders.

Biological Transport↗
PubMed1979

Effect of neuroleptic drugs on lithium uptake by the human erythrocyte.

We studied the effects of neuroleptic and antidepressant drugs on Li+ uptake in human red cells to examine the reported neurotoxicity reported for lithium-neuroleptic combination treatment and its relationship to altered tissue Li+ levels. All the phenothiazines increased Li+ influx in red cells and steady-state Li+ distribution ratio in vitro. This effect was not observed with other drugs studied. It is suggested that increased levels of Li+ in the tissue caused by phenothiazines may be related to neurotoxic effects observed during Li+ -phenothiazine therapy.

Antidepressive Agents, Tricyclic↗
PubMed1979

Beta-adrenergic receptor function in affective illness.

In a study of beta-adrenergic receptor sensitivity, the authors determined the response of cyclic AMP synthesis to in vitro addition of norepinephrine (NE) and isoproterenol (IP) in leukocytes of patients with affective illness and schizophrenia and of normal controls. IP-stimulated increase in 3H-cyclic AMP synthesis in depressed patients was significantly lower than in normal subjects and schizophrenic patients. These results suggest that beta-adrenergic receptor sensitivity is reduced in depressive illness.

Adenylyl Cyclases↗
PubMed1978

Prediction of in vivo red cell/plasma Li+ ratios by in vitro methods.

Two incubation procedures were used for the determination, in vitro, of the steady-state Li+ ratio between red cells and external media. The Li+ ratio in vitro determined prior to Li+ therapy correlates significantly with the subsequent ratio in vivo between red cells and plasma in patients treated with Li+. The Li+ ratio determined in vitro in patients during Li+ therapy was significantly higher than the value determined during the pretreatment, drug-free period that correlated significantly with Li+ ratios in vivo. The in vitro procedure used thus could be applied in the prediction of the in vivo Li+ ratio, and possibly of the response to Li+, in patients before treatment is begun. It also could be used for studies on abnormalities and on the genetics of Li+ transport in affective illness.

Bicarbonates↗
PubMed1978

Lithium transport pathways in human red blood cells.

In human red cells, Li is extruded against its own concentration gradient if the external medium contains Na as a dominant cation. This uphill net Li extrusion occurs in the presence of external Na but not K, Rb, Cs, choline, Mg, or Ca, is ouabain-insensitive, inhibited by phloretin, and does not require the presence of cellular ATP. Li influx into human red cells has a ouabain-sensitive and a ouabain-insensitive but phloretin-sensitive component. Ouabain-sensitive Li influx is competitively inhibited by external K and Na and probably involves the site on which the Na-K pump normally transports K into red cells. Ouabain does not inhibit Li efflux from red cells containing Li concentrations below 10 mM in the presence of high internal Na or K, whereas a ouabain-sensitive Li efflux can be measured in cells loaded to contain 140 mM Li in the presence of little or no internal Na or K. Ouabain-insensitive Li efflux is stimulated by external Na and not by K, Rb, Cs, choline, Mg, or Ca ions. Na-dependent Li efflux does not require the presence of cellular ATP and is inhibited by phloretin, furosemide, quinine, and quinidine. Experiments carried out in cells loaded in the presence of nystatin to contain either only K or only Na show that the ouabain-insensitive, phloretin-inhibited Li movements into or out of human red cells are stimulated by Na on the trans side and inhibited by Na on the cis side of the red cell membrane. The characteristics of the Na-dependent unidirectional Li fluxes and uphill Li extrusion are similar, suggesting that they are mediated by the same Na-Li countertransport system.

Adenosine Triphosphate↗
PubMed1978

A heritable disorder of lithium transport in erythrocytes of a subpopulation of manic-depressive patients.

The in vivo RBC/plasma Li+ ratio is determined by the equilibrium between Li+ influx (ouabain-sensitive Na+-K+ pump and ouabain-insensitive leakage pathways) and Li+ efflux (phloretin-sensitive Li+-Na+ counterflow). A study of RBC Li+ transport via these pathways showed that a deficiency of Li+-Na+ counterflow was responsible for the high in vivo ratio (1:1) observed in a manic patient. This defect was related to an alteration in the membrane Na+ exchange system and was under genetic control. The level of counterflow before lithium therapy was an excellent predictor (r = .88) of the in vivo Li+ ratio and was deficient in approximately one-fourth of manic-depressive patients but not in controls, schizophrenics, or unipolar depressed patients.

Adult↗
PubMed1977

Urinary cyclic AMP excretion by methadone subjects during gradual and acute withdrawal.

Laboratory and animal investigations have supported the hypothesis that levels of cyclic AMP are stable during tolerance to narcotic drugs and increased during withdrawal. In order to test this hypothesis, serial 24-h urinary excretion of cyclic AMP by long-term methadone addicts was determined during a period of stable methadone intake, a period of gradual withdrawal, and a period of acute withdrawal. Cyclic AMP excretion during stable methadone intake is identical to that of normal control subjects. Neither gradual nor acute withdrawal appears to affect the urinary excretion of cyclic AMP. These data agree with previous reports in the literature which suggest that cyclic AMP levels are not altered during tolerance to narcotics, but do not support the hypothesis that levels of the nucleotide might be increased during withdrawal.

Adult↗
PubMed1977

Abnormal lithium and sodium transport in erythrocytes of a manic patient and some members of his family.

This paper compares the transport of Li(+) and Na(+) in erythrocytes from a patient with mania and from members of his family to that in erythrocytes from normal humans. In normal human erythrocytes, Li(+) is transported by at least three operationally distinct pathways: one inhibited by ouabain (ouabain-sensitive), one by phloretin (phloretin-sensitive), and one not inhibited by either compound (insensitive). Li(+) can be driven up its electrochemical potential gradient by an oppositely directed electrochemical potential gradient for Na(+)-i.e., Li(+)/Na(+) counterflow can occur-through the phloretin-sensitive pathway but not through the other two pathways. Because ouabain-sensitive Li(+) transport is negligible under physiological conditions, Li(+) distribution between erythrocytes and plasma in vivo depends mainly on the balance between Li(+)/Na(+) counterflow and the insensitive pathway(s) of Li(+) transport. The steady-state ratio of Li(+) concentration in the erythrocytes to that in the plasma of the patient was between 2 and 3 times higher than the comparable ratio in normal persons. The phloretin-sensitive Li(+)/Na(+) counterflow system was almost absent in the erythrocytes of the patient. Furthermore, unlike those from normal individuals, the patient's erythrocytes showed no external Li(+)-stimulated, phloretin-sensitive, ouabain-insensitive Na(+) efflux. The magnitudes of the ouabain-sensitive and insensitive pathways for Li(+) transport in the patient's erythrocytes were within normal limits. The decreased Li(+)/Na(+) counterflow in the patient's erythrocytes was probably not due to the presence of an inhibitor in the plasma of the patient but rather to an intrinsic defect in the erythrocytes. Because the father and several siblings of the patient showed a similar abnormality in erythrocyte Li(+)/Na(+) transport, it is probable that this defect is inherited.

Adolescent↗