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Biomedical subjects

V Gopalakrishnan

Publications and source records attributed to V Gopalakrishnan.

82 records · Page 5Linked to original sources
PubMed1982

Effect of cholinergic drugs on acute and chronic morphine dependence.

The effect of both centrally and peripherally acting cholinergic drugs on acute and chronic morphine dependence was investigated. The quaternary ammonium drugs, neostigmine and atropine methyl bromide which cross the blood-brain barrier with difficulty, significantly altered the withdrawal jumping and wet shakes in a similar manner to that exhibited by centrally acting tertiary drugs viz. physostigmine and atropine sulphate. The cholinergic agonists inhibited the withdrawal signs while the antagonists enhanced the same. This suggests that the peripheral cholinergic mechanisms are also involved apart from the central mechanisms in the phenomena of acute and chronic morphine dependence.

Animals↗
PubMed1981

Effect of prolactin and bromocriptine on intestinal transit in mice.

In vivo administration of relatively high concentrations of prolactin (PRL) enhanced gastrointestinal propulsion in mice. Pretreatment with atropine significantly abolished this effect of PRL while physostigmine enhanced it. The evidence confirms a cholinomimetic action for higher concentrations (20 microgram) of PRL on the intestinal tract. Bromocriptine per se produced a dose-dependent depression in transit while a combination of PRL and bromocriptine failed to significantly alter the transit as compared to the control.

Animals↗
PubMed1981

Contractile effect of prolactin on guinea pig isolated ileum.

Prolactin (PRL) at high concentrations contracted the guinea pig isolated ileum. The maximum response elicited by PRL was 44% of that of histamine-induced responses. There was no significant difference in potency between PRL preparations obtained from two different sources. PRL responses were nullified by denaturation or proteolytic digestion of the hormone. The contractile response was antagonised by atropine and potentiated by neostigmine, but unaffected by the prostaglandin antagonist SC-19220. The pA2 values of atropine against PRL and ACh were similar. Preincubation with morphine, which inhibits ACh release, produced slight inhibition of PRL-evoked contractions. Even high concentrations of PRL failed to produce any response in neostigmine-treated frog rectus muscle preparations. This suggests that PRL may produce contractions through a cholinergic mechanism involving muscarinic receptors. Enhanced gut motility reported earlier for hyperprolactinemic states may be attributed to this cholinomimetic effect of PRL on the intestinal tract.

Acetylcholine↗
PubMed1980

Effect of prolactin on human red cell sodium transport.

Incubation of red cells with higher concentrations of prolactin in vitro enhanced the cellular sodium level and produced a significant reduction in erythrocyte membrane adenosine triphosphatase activity. This effect was dose and time-dependent. It is the result of an inhibition of the active sodium pump similar to that produced by ouabain, suggesting altered red cell function and electrolyte balance in hyperprolactinemic states.

Biological Transport↗
PubMed1980

Changes in the sensitivity of smooth muscle to neurotransmitter during acute morphine treatment and its association with analgesia.

Acute in vivo administration of morphine to mice produced dose- and time-dependent subsensitivity to acetylcholine in ileum and supersensitivity to norepinephrine in vas deferens. These responses were specific to the agonist as potassium chloride-induced responses were not altered. A correlation was observed between the analgesia and the sensitivity changes produced by morphine. The sensitivity changes were mediated through opiate receptors as naloxone antagonised the effect of morphine.

Acetylcholine↗