Comparison between Carbetocin and Oxytocin in Active Management of 3rd Stage of Labour in Preventing Post Partum Hemorrhage.

The third stage of labour is considered to be the most critical part of child birth due to the risk of post partum haemorrhage (PPH). To compare the effectiveness of carbetocin and oxytocin in the management of 3rd stage of labour in preventing post partum hemorrhage, this experimental clinical trial was conducted in the Department of Obstetrics and Gynecology, Sir Salimulla Medical College Hospital, Dhaka, Bangladesh from January 2015 to June 2016. Three hundred women undergoing normal vaginal delivery were consecutively enrolled. They were divided into two groups, one group was treated with carbetocin 100µg IV and another group was treated with oxytocin 10 unit IV. Post partum haemorrhage was developed in 23(15.3%) and 31(20.7%) patients in carbetocin and oxytocin groups respectively. Among these PPH patients, 17(73.9%) patients received oxytocin, 21(91.3%) patients received Ergometrin and 14(60.9%) patients received misoprostol in carbetocin group as additional drug. In oxytocin group 30(96.8) patients received ergometrin and 26(83.9) patients received misoprostol. Significantly higher number of patients was treated with balloon catheter in oxytocin group (77.4%) than carbetocin group (39.1%). Thirteen (41.9%) patients in oxytocin group and 4(17.4%) patients in carbetocin group needed to treat in ICU. In carbetocin Group I patient (4.3%) and in oxytocin Group II patients (6.5%) died. carbetocin is better than oxytocin in the management of 3rd stage of labour to prevent post partum haemorrhage (PPH).

Effect of l-ornithine l-aspartate against thioacetamide-induced hepatic damage in rats.

OBJECTIVE: To investigate the hepatoprotective activity of L-ornithine-L-aspartate against thioacetamide (TAA)-induced hepataopathy in rats. MATERIALS AND METHODS: The hepatoprotective activity of L-ornithine-L-aspartate (OA) at a dose of 2 g/kg, p.o. for 10 days was evaluated against TAA (250 mg/kg, i.p. for 2 days) induced hepatopathy in rats. Biochemical parameters such as serum aspartate transaminase, alanine transaminase, alkaline phosphatase, bilirubin and glutathione, thiobarbituric acid reactive substances, and protein in liver tissues were estimated to assess the liver function. RESULTS: TAA-induced pathogenic changes in the levels of the above indices were significantly (P < 0.01) reversed by the OA treatment. OA treatment also exhibited significant restoration of the hepatic architecture and lobular structure in histological evaluation of the rat liver sections. CONCLUSION: Ornithine aspartate exhibited significant hepatoprotective activity against TAA-induced hepatic damage in rats.

Neuropharmacological safety evaluation of jigrine: A polyherbal hepatoprotective formulation.

OBJECTIVE: Jigrine is a herbal hepatoprotective formulation containing aqueous extracts of 14 medicinal plants. Present study was designed to evaluate per se neuropharmacological effects of jigrine in mice. MATERIALS AND METHODS: Jigrine was evaluated in a number of pharmacological test paradigms, viz. open field arena, actophotometer, hole board, rotarod, traction test, grip strength test, spontaneous alternation behavior, passive avoidance task, and phenobarbital sleeping time. RESULTS AND CONCLUSIONS: Jigrine pretreatment (1 and 2 ml/kg, p.o.) did not produce any significant effect as compared to normal saline treated animals and was found to be free from any acute undesirable central effects at these two dose levels.

Hepatoprotective and behavioral effects of jigrine in galactosamine-induced hepatopathy in rats.

The hepatoprotective activity of jigrine, a polypharmaceutical herbal formulation, at a dose of 1 mL/kg/day p.o. was evaluated against galactosamine (400 mg/kg b.wt.)-induced hepatopathy in rats. Biochemical parameters such as alanine trasaminase (ALT), alkaline phosphatase (ALP), and bilirubin were estimated to assess liver function. Jigrine was also evaluated for its effect on the possible behavioral alterations secondary to liver damage produced by galactosamine (d-Gal) administration in rats. The d-Gal-induced elevation in serum levels of ALT, ALP, and bilirubin was significantly reduced (p values <0.01, <0.01, and <0.05, respectively) in jigrine- and silymarin-pretreated rats. Jigrine pretreatment also exhibited beneficial effects on d-Gal-induced behavioral abnormalities in rats. Silymarin (25 mg/kg/day p.o.) was used as reference standard. The biochemical observations were supplemented with histopathological examination of rat liver sections. Histopathological evaluation showed marked improvement in the livers of jigrine- and silymarin-treated animals.

Free radical scavenging and hepatoprotective activity of jigrine against galactosamine induced hepatopathy in rats.

Jigrine a polypharmaceutical herbal hepatoprotective formulation containing aqueous extracts of 14 medicinal plants is used in Indian system of medicine (Unani). Jigrine was evaluated for its hepatoprotective activity against galactosamine induced hepatopathy in rats. Galactosamine induced hepatotoxicity resembles human viral hepatitis. Biochemical parameters like AST, ALT and urea in serum, TBARS and glutathione in liver and whole blood glutathione were estimated to assess liver function. DPPH-free radical scavenging activity of jigrine was also evaluated. Biochemical data exhibited significant hepatoprotective activity of jigrine against galactosamine. Silymarin used as reference standard also exhibited significant hepatoprotective activity against galactosamine. The biochemical observations were supplemented with histopathological examination of rat liver sections.

Evaluation of hepatoprotective potential of jigrine post-treatment against thioacetamide induced hepatic damage.

Jigrine a polypharmaceutical herbal formulation containing aqueous extracts of 14 medicinal plants developed on the principles of unani system of medicine is used for liver ailments. The hepatoprotective potential of jigrine post-treatment at the dose of 0.5 ml/kg per day p.o. for 21 days was evaluated against thiocetamide induced liver damage in rats. Biochemical parameters like AST, ALT in serum and TBARS and glutathione in tissues were estimated to assess liver function. Data on the biochemical parameters revealed hepatoprotective potential of jigrine post-treatment against thioacetamide induced hepatotoxicity in rats. Silymarin used as reference standard also exhibited significant hepatoprotective activity on post-treatment against thioacetamide-induced hepatotoxity in rats. The biochemical observations were supplemented with histopathological examination of rat liver sections.

Histamine and selective H3-receptor ligands: a possible role in the mechanism and management of epilepsy.

The interaction of selective histamine H3-receptor agonist R(alpha)-methyl-histamine (RAMH) and antagonist thioperamide (THP) with some antiepileptic drugs [AED; phenytoin (PHT), carbamazepine (CBZ), sodium valproate (SVP), and gabapentin (GBP)] was studied on seizures induced by maximal electroshock (MES) and pentylenetetrazole (PTZ) in mice. It was found that subeffective dose of THP in combination with the subeffective doses of PHT and GBP provided protection against MES and/or PTZ-induced seizures. Further, RAMH reversed the protection afforded by either PHT or GBP on MES and/or PTZ seizures. In another set of experiments, the histamine content was measured in the whole brain and in different brain regions including cerebral cortex, hypothalamus, brain stem and cerebellum following convulsant (MES and PTZ) and AED treatment. It was seen that while MES exhibited a tendency to enhance brain histamine levels, PTZ showed the opposite effect. AEDs either increased (PHT and GBP) or decreased (SVP) brain histamine content in different regions to varying degrees. The results indicate a role for histamine in seizures and in the action of AEDs and suggest that selective H3-receptor antagonists may prove to be of value as adjuncts to conventional AEDs.

Patterns of prescriptions and drug use in two tertiary hospitals in Delhi.

The study was carried out to assess prescribing trends in outpatients at Dr. R.P. Centre for Ophthalmic Sciences (RPC) and other OPD's of All India Institute of Medical Sciences (AIIMS) and Safdarjung hospitals, two premier hospitals in Delhi. Prescriptions of 500 patients were audited and analysed under heads of average number of drugs per patient, percentages of drugs prescribed by generic name, antibiotics, injections, drugs from WHO recommended essential drug list, availability of drugs etc. using WHO basic drug indicators. Prescription analysis showed that 75 to 95% drugs were prescribed from essential drug list. The average number of drugs per prescription was 1.42 to 4.07. Percentage of antibiotics prescribed varied from 14.39% to 22.28%. The use of injections was from nil to 4.4%. Availability of drugs was however, not satisfactory. Though maximum drugs were prescribed from essential drug list, the results indicate that there is a considerable scope for improving prescribing habits according to rational drug use and to provide a feed back to hospital authority for making maximum number of drugs available to the patients.

Protection from phenytoin-induced cognitive deficit by Bacopa monniera, a reputed Indian nootropic plant.

Many epileptic patients suffer from cognitive impairments; both the underlying pathology and antiepileptic drug therapy can cause such deficits. Phenytoin, one of the widely used anticonvulsants, is known to adversely affect cognitive function. A reputed Indian nootropic plant Bacopa monniera (BM) was evaluated alone and in combination with phenytoin for its effect on (a) passive-avoidance (PA) task; (b) maximal electroshock seizures; and (c) locomotor activity in mice. Phenytoin (PHT, 25 mg/kg po x 14 days) adversely affected cognitive function in the PA task. BM extract (40 mg/kg x 7 days), given along with phenytoin in the second week of the two-week regimen, significantly reversed PHT-induced impairment. Both acquisition and retention of memory showed improvement without affecting its anticonvulsant activity. The observed cognitive effects of PHT and BM were found to be independent of motor stimulation. The results provide evidence for potential corrective effect of BM in cognitive deficit associated with PHT therapy.

Thioperamide, a selective histamine H3 receptor antagonist, protects against PTZ-induced seizures in mice.

The effect of selective histamine H3-receptor antagonist thioperamide was studied on PTZ-induced seizures in mice. Thioperamide significantly protected clonic seizures induced by PTZ in a dose-dependent manner. The effect of thioperamide was completely countered by pretreatment with R (alpha)-methylhistamine (RAMH), a selective H3-receptor agonist suggesting that the observed effect of thioperamide was elicited by histamine H3-receptors. RAMH alone did not significantly modify PTZ seizures. The findings are consistent with a role for the histaminergic neuronal system in seizures and suggest that H3-receptors may play an important role in modulating clonic seizures induced by PTZ in mice.

Modulation of hippocampal acetylcholine release and spontaneous alternation scores by intrahippocampal glucose injections.

Recent evidence indicates that systemic glucose treatment enhances memory while producing a corresponding increase in hippocampal acetylcholine (ACh) output. The present experiments examined whether unilateral intrahippocampal infusions of glucose would enhance spontaneous alternation performance and whether there would be a corresponding increase in ACh output in the ipsilateral and contralateral hippocampus. Extracellular ACh was assessed in samples collected at 12 min intervals using in vivo microdialysis with HPLC with electrochemical detection. Twelve minutes after a unilateral infusion of artificial cerebrospinal fluid (CSF) or glucose (6.6 mM), rats were tested in a cross maze for spontaneous alternation behavior with concurrent microdialysis collection. In two experiments, glucose infusions significantly increased alternation scores (67.5 and 59%) compared with CSF controls (42.4 and 39.5%, respectively). In both experiments, behavioral testing resulted in increased ACh output in the hippocampus. Glucose administration at the time of alternation tests enhanced ACh output beyond that of behavioral testing alone both ipsilateral (+93.8%) and contralateral (+85%) to the infusion site, as compared with ACh output (+36.1% and +55.5%) of CSF controls. Glucose infusions did not affect hippocampal ACh output in rats kept in a holding chamber. These results suggest that glucose may enhance alternation scores by modulating ACh release. The findings also indicate that unilateral glucose infusions increase hippocampal ACh output both ipsilateral and contralateral to the site of injection. Furthermore, glucose increased ACh output only during maze testing, suggesting that specific behavioral demands, perhaps requiring activation of cholinergic neurons, determine the efficacy of glucose in modulating ACh release.

Muscimol increases acetylcholine release by directly stimulating adult striatal cholinergic interneurons.

Because GabaA ligands increase acetylcholine (ACh) release from adult striatal slices, we hypothesized that activation of GabaA receptors on striatal cholinergic interneurons directly stimulates ACh secretion. Fractional [3H]ACh release was recorded during perifusion of acutely dissociated, [3H]choline-labeled, adult male rat striata. The GabaA agonist, muscimol, immediately stimulated release maximally approximately 300% with EC50 = approximately 1 microM. This action was enhanced by the allosteric GabaA receptor modulators, diazepam and secobarbital, and inhibited by the GabaA antagonist, bicuculline, by ligands for D2 or muscarinic cholinergic receptors or by low calcium buffer, tetrodotoxin or vesamicol. Membrane depolarization inversely regulated muscimol-stimulated secretion. Release of endogenous and newly synthesized ACh was stimulated in parallel by muscimol without changing choline release. Muscimol pretreatment inhibited release evoked by K+ depolarization or by receptor-mediated stimulation with glutamate. Thus, GabaA receptors on adult striatal cholinergic interneurons directly stimulate voltage- and calcium-dependent exocytosis of ACh stored in vesamicol-sensitive synaptic vesicles. The action depends on the state of membrane polarization and apparently depolarizes the membrane in turn. This functional assay demonstrates that excitatory GabaA actions are not limited to neonatal tissues. GabaA-stimulated ACh release may be prevented in situ by normal tonic dopaminergic and muscarinic input to cholinergic neurons.

Glutathione as a cerebral substrate in depressive behavior.

Behavioral depression through inescapable foot shock stress in Swiss albino mice was measured on the basis of their performance in an open field test (OFT) and a forced swimming test (FST). Glutathione (GSH) and various antidepressants (imipramine, maprotiline, fluvoxamine, trazodone, and alprazolam) were able to, either fully or partly, prevent and/or reverse the shock-induced behavioral depression. The GSH level was measured in the cerebral cortex, cerebellum, brain stem, and the hypothalamus in shocked mice to ascertain a possible correlation between brain GSH and stress-induced depression, under conditions of preshock and postshock antidepressant treatments as well as in the absence of the drugs. There was an appreciable depletion of cortical GSH in shocked mice that was corrected to varying degrees by the different antidepressants. The results suggest a close link between stress-induced behavioral depression, increased monoaminergic utilization, oxidative stress, and brain GSH.