Drugs online research references
J Neural Transm Gen Sect. 1992;90(3):241-7.
Effects of muscarinic receptor agonists and antagonists on rat brain serotonergic activity.
Bhattacharya SK, Sen AP.
Department of Pharmacology, Banaras Hindu University, Varanasi, India.
The effects of some muscarinic M1 and M2 receptor agonists and antagonists on rat brain serotonergic activity was assessed by noting their effects on the levels of 5-hydroxytryptamine (5-HT) and its major metabolite, 5-hydroxyindole acetic acid (5-HIAA), estimated by a high pressure-liquid chromatographic (HPLC) technique. The muscarinic M1 receptor agonists, arecholine and McN-A-343, and the M2 receptor agonists, gallamine and AF-DX 116, induced a dose-related decrease in the concentrations of both 5-HT and 5-HIAA. On the contrary, scopolamine and the selective M1 receptor antagonist, pirenzepine, increased the levels of the amine and its metabolite. The anti-cholinesterase agent, physostigmine, and the putative M2 receptor agonist, carbachol, induced a dose-related dual effect, with the smaller doses decreasing and the higher doses increasing 5-HT and 5-HIAA concentrations. The results indicate that an inverse relationship exists between the cholinergic and serotonergic neurotransmitter systems in the rat brain due to the likely presence of muscarinic heteroreceptors on serotonergic neurones. The data also indicates that though physostigmine and carbachol may function as M2 receptor agonists, they lose their receptor specificity on dose increment.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1283683&dopt=Abstract
Indian J Exp Biol. 1991 Mar;29(3):237-40.
Effects of muscarinic receptor agonists and antagonists on response of non-extensor rats to maximal electroshock.
Bhattacharya SK, Sen AP, Mitra SK.
Department of Pharmacology, Banaras Hindu University, Varanasi, India.
Rats which do not respond consistently to maximal electroshock by exhibiting the classical hindlimb extensor response, are designated as 'flexors', and can serve as a useful experimental model for investigating seizure mechanisms. 20-25% Charles Foster rats exhibit the flexor status and were used in this study. The flexor rats were converted to extensors by acetylcholine (icv), physostigmine (ip) and the selective muscarinic M1 receptor agonists, arecholine (ip) and McN-A-343 (icv). This conversion of flexors to extensors was significantly attenuated by M1 receptor antagonists scopolamine (ip) and pirenzepine (icv). The M2 receptor agonist, carbachol (icv), had no effect in lower doses but induced conversion of flexor rats to the extensor status only in very high doses which may be due to loss of receptor specificity on dose increment. The M2 receptor antagonists, gallamine (icv) and AF-DX 116 (ip), also induced significant conversion of flexors to extensors, which was dependent upon the availability of neuronal acetylcholine since the effects were attenuated following pretreatment with hemicholinium, an inhibitor of acetylcholine synthesis. The results suggest that the central cholinergic system has a facilitatory pro-convulsant effect, mediated through the muscarinic M1 receptors, an action modulated by the M2 receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1874538&dopt=Abstract
J Cardiothorac Anesth. 1990 Aug;4(4):425-9.
Effect of premedication on arterial oxygen saturation in children with congenital heart disease.
DeBock TL, Davis PJ, Tome J, Petrilli R, Siewers RD, Motoyama EK.
Department of Anesthesiology, Children's Hospital of Pittsburgh, PA 15213-2583.
The effect of a standardized intramuscular premedication (morphine, 0.1 mg/kg, scopolamine, 13 micrograms/kg, and secobarbital, 2.5 mg/kg) on the arterial oxygen saturation of hemoglobin was evaluated in 33 patients with congenital heart disease by use of the Nellcor pulse oximeter. Sixteen patients had noncyanotic congenital heart disease and 17 patients had cyanotic congenital heart disease. In the noncyanotic congenital heart disease group, pulse oximeter saturations decreased from 98.1% +/- 1.5% (mean +/- SD), before premedication, to 96.5% +/- 1.5% following premedication. Although this decrease was statistically significant (P less than 0.05), it was determined to not be clinically meaningful. In the patients with cyanotic congenital heart disease, oxygen saturation increased from 73.5% +/- 11.8 to 74.7% +/- 10.2 following premedication, but this change was not statistically significant. The effect of premedication on SaO2 was highly variable in patients with cyanotic heart disease; although the group mean appeared to increase, 6 of the 17 patients had decreases in saturation and the decrease exceeded 10% in saturation in 3 of them. Therefore, oxygen saturation should be monitored following premedication in patients with cyanotic heart disease and oxygen administered as needed.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2132337&dopt=Abstract
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