Drugs online research references
Res Commun Mol Pathol Pharmacol. 1994 Oct;86(1):99-110.
Biological effects of diesel exhaust particles (DEP) on isolated cardiac muscle of guinea pigs.
Sakakibara M, Minami M, Endo T, Hirafuji M, Murakami S, Mori Y, Sagai M.
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Health Sciences University of Hokkaido, Japan.
Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) could produce superoxide anions in an in vitro study. Furthermore, mice instilled intratracheally with DEP showed high mortality at low doses. The cause of death was lung edema with damage to the lung endothelial cells. In order to elucidate the mechanism of the onset of mortality induced by DEP, we examined the direct action of DEP on the isolated atrium of guinea pigs. A light-duty (2740cc), four cylinder diesel engine was used. The DEP were collected on fiberglass filter. DEP caused a negative inotropic action that was followed by the cardiac arrest of the isolated left atrium. These actions were not inhibited by propranolol, atropine, verapamil, diltiazem, diphenhydramine, indomethacin, superoxide dismutase or catalase. The precise mechanism of cardiac arrest is unknown. However, these results suggest that cardiac toxicity induced by DEP might be involved in lung edema.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7531585&dopt=Abstract
Biochim Biophys Acta. 1995 Sep 14;1258(2):169-76.
Characterization and partial purification of phospholipase D from human placenta.
Vinggaard AM, Hansen HS.
Department of Biological Sciences, Royal Danish School of Pharmacy, Copenhagen.
We report the existence in the human placenta of a phosphatidylcholine-hydrolyzing phospholipase D (PLD) activity, which has been characterized and partially purified. Triton X-100 effectively solubilized PLD from the particulate fraction of human placenta in a dose-dependent manner. However, Triton X-100 caused decreasing enzyme activities. Maximum transphosphatidylation was obtained with 2% ethanol. The enzyme was found to have a pH optimum of 7.0-7.5 and an apparent Km of 33 mol% (or 0.8 mM). Ca2+ and Mg2+ was not required for the enzyme activity. Addition of phosphatidyl-4,5-bisphosphate, but not phosphatidylethanolamine, to the substrate mixture gave rise to a pronounced dose-dependent increase in PLD activity (EC50 = 0.3 mol%), suggesting a regulatory role of this phospholipid in PLD action. The enzyme was inhibited by sodium oleate when partly or fully substituting for octylglucoside in the substrate mixture. The PLD activity was enriched 15-fold by solubilization and purification on a DEAE-Sepharose column. N-Ethylmaleimide (10 mM) markedly inhibited the purified enzyme, indicating the presence of free thiol groups on PLD. Sphingosine (20 microM) and (+/-) propranolol (53 microM) had no direct effect on PLD activity. The present results form the basis for further purification of a PLD from human tissue.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7548180&dopt=Abstract
Pol J Pharmacol Pharm. 1978 Nov-Dec;30(6):799-818.
Effect of catecholamines and adrenergic antagonists on blood glucose, free fatty acids and liver glycogen levels in fed rats.
Bugajski J, Hano J, Zdebska A.
In fed rats the effects of catechloamines and adrenergic antagonists on blood glucose, free fatty acids (FFA), and liver glycogen levels were investigated in order to determine the role of alpha- and beta-adrenergic receptors in metabolic responses to catechloamines. Hyperglycemic responses to dopamine (DA), noradrenaline (NA), adrenaline (A) and isoprenaline (ISP) were dose-related and accompained by a depletion of liver glycogen. The relative potencies in producing hyperglycemia and in causing liver glycogenolysis were in descending order of potency, A, NA, DA and ISP. Hyperlipemic response was most potent to NA and DA, weaker to ISP, and least potent to A. Phentolamine antagonized completely both hyperglycemia and hepatic glycogen depletion induced by all catecholamines. Propranolol impaired only hyperglycemic responses to A and ISP. Phentolamine antagonized hyperlipemia induced by DA and NA but only partially impaired hyperlipemia after A. Propranolol only partially antagonized hyperlipemic responses to NA and ISP without influencing DA--and A-induced hyperlipemia. The results indicate that in fed rats hyperglycemic responses to catecholamines are mediated mainly by an alpha-adrenergic receptor, and hyperlipemic responses do not fit inton the alpha-receptor or beta-receptor classification.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=755244&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||