PubMed Health⌕ Search

Biomedical subjects

S S Parmar

Publications and source records attributed to S S Parmar.

160 records · Page 9Linked to original sources
PubMed1966

Decarboxylation of 2-keto fatty acids by brain.

An enzyme system consisting of washed acetone powder of pig brain, adenosine triphosphate, nicotinamide adenine dinucleotide, magnesium, fumaric acid, and ascorbic acid was found to catalyze the oxidative decarboxylation of 2-ketostearic acid. The products were carbon dioxide and heptadecanoic acid. Washing the enzyme powder with ethylene-diaminetetraacetate and other chelating agents destroyed the activity. Further properties of the enzyme system are described. It is believed that this enzyme system accounts in part for the 1-carbon degradation route for brain fatty acids.

Adenosine Triphosphate↗
PubMedDate not supplied

The role of dopamine (D2), alpha and beta-adrenoceptor receptors in the decrease in gastrointestinal transit induced by dopamine and dopamine-related drugs in the rat.

This study analyses the effects of dopamine receptor agonists and antagonists on rat gastrointestinal transit (GIT) in an attempt to identify the mechanisms involved. Dopamine (DA), apomorphine, quinpirole, bromocriptine and fenoldopam were given by subcutaneous (s.c.), intrathecal (i.t.), intracisternal (i.c.) and/or intraperitoneal (i.p.) routes. In general, DA (200 micrograms, i.t.), apomorphine (3, 5 and 10 mg/kg, s.c.; or 10, 30 and 100 micrograms, i.t.), and bromocriptine (1, 5 and 10 mg/kg, s.c.) elicited decreases in gastrointestinal transit which were significantly antagonized by the D2 receptor antagonists domperidone or alizapride (both 5 mg/kg, s.c.), but remained unaffected by the D1 receptor antagonist SCH 23390 (5 mg/kg, s.c.). Similarly, DA (50, 100 and 200 micrograms, i.c.) and apomorphine (12 and 50 micrograms; i.c.) produced dose-dependent decreases in gastrointestinal transit amenable to blockade by the classical DA receptor antagonist haloperidol (10 micrograms, i.c.). The responses to apomorphine (3, 5 and 10 mg/kg, s.c.) were unaltered by 6-hydroxydopamine (100 mg/kg, i.p.)-induced sympathectomy but were antagonized by both propranolol (1 mg/kg, s.c.) and phentolamine (5 mg/kg, s.c.). Significantly, after bilateral (cervical) vagotomy, gastrointestinal transit was markedly reduced, but apomorphine (5 mg/kg, s.c.) apparently further reduced gastrointestinal transit. The D1 agonists fenoldopam (5, 10 and 20 mg/kg, s.c.) significantly reduced GIT. Fenoldopam-induced antitransit effects were markedly modified by the D1 receptor antagonist, SCH 23390 (5 mg/kg, s.c.); only the response induced by 5 mg/kg of fenoldopam was apparently antagonized by SCH 23390. The mixed D2 and D3 receptor agonist quinpirole (4 and 8 mg/kg, s.c.; or 8 mg/kg, i.p.; 200 micrograms, i.t.) did mimic DA eliciting significant reductions in gastrointestinal transit which, however, were not antagonized by domperidone (5 mg/kg, s.c.). Taken together, the present results support the contention that the decrease in rat gastrointestinal transit induced by DA and apomorphine may be mediated by an interaction with central and/or peripheral D2 receptors. The presence of dopamine receptors (D2) in the alimentary canal are strengthened by antitransit effect of fenoldopam and bromocriptine in the gastrointestinal tract.

Animals↗
PubMedDate not supplied

Serotonin in toxaemia of pregnancy.

Serotonin (5-hydroxytryptamine) contents of maternal blood, fetal cord blood, and placenta from thirty-five patients with toxaemia of pregnancy and forty normal pregnant subjects were estimated. Placental monoamine oxidase activity from ten normal and ten toxaemic cases were also estimated. An increased content and uptake of serotonin by platelets in maternal blood from toxaemic patients were observed and there was a concomitant reduction in platelet count. Raised levels of serotonin and a decrease in monoamine oxidase levels were observed in placentas of the toxaemic group. The levels of serotonin in fetal cord blood were significantly higher than those in normal maternal blood. It is suggested that the fetus could be the source of increased serotonin in this syndrome, due to the decrease in monoamine oxidase activity in the toxaemic placenta. An abnormality in indole amine metabolism may contribute to the pathology associated with toxaemia of pregnancy.

Adult↗