Drugs online research references
J Chromatogr. 1979 Jan 1;162(1):47-58.
Determination of propranolol and six metabolites in human urine by high-pressure liquid chromatography.
Pritchard JF, Schneck DW, Hayes AH Jr.
A method for the determination of propranolol and six of its metabolites, as well as their glucuronide and/or aryl sulfate conjugates in human urine is described. Propranolol and its basic and neutral metabolites are extracted into ether at pH 9.8, evaporated to dryness, reconstituted, separated on a reversed-phase, high-pressure liquid chromatographic system and quantitated using fluorescence detection. The aqueous urine aliquot is then made acidic and the acid metabolites extracted and measured using similar methods. The presence of 2% sodium metabisulfite in all urines collected is essential to ensure the stability of 4-hydroxy-propranolol during collection and storage. Preliminary data is presented from 24-h urine samples collected from three patients chronically receiving propranolol.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=762208&dopt=Abstract
Am J Respir Crit Care Med. 1997 Jul;156(1):217-22.
Impairment of neural nitric oxide-mediated relaxation after antigen exposure in guinea pig airways in vitro.
Miura M, Yamauchi H, Ichinose M, Ohuchi Y, Kageyama N, Tomaki M, Endoh N, Shirato K.
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Nitric oxide (NO), a neurotransmitter of inhibitory nonadrenergic noncholinergic (iNANC) nerves in airways, is a radical with a short half-life, and its function may be modified by airway inflammation. To test this hypothesis, we examined whether airway allergic inflammation affects iNANC responses mediated by NO in guinea pigs in vitro. Animals sensitized with ovalbumin (OA) were challenged with 0.03% OA (OA group) or saline (saline group) by inhalation on 3 consecutive days. On the day after the final challenge, iNANC responses elicited by electrical field stimulation (2 to 16 Hz) or relaxation responses to 3-morpholinosydnonimine (SIN-1), 10(-8) to 10(-4) M, were obtained in the tracheal strips precontracted by histamine (3 x 10(-6) M) in the presence of atropine and propranolol (both 10(-6) M). The INANC responses of the OA group were significantly attenuated compared with those of the saline group (p < 0.05), and the inhibitory effect of a NO synthase (NOS) inhibitor, Nm-nitro-L-arginine methyl ester, on the INANC responses was abolished in the OA group. SIN-1-induced tracheal smooth muscle relaxation was also significantly affected by antigen exposure (p < 0.05), the effect of which disappeared in the presence of a NO scavenger, carboxy PTIO (3 x 10(-6) M). The impairment of the INANC responses after antigen exposure was significantly restored by superoxide dismutase (1,000 U/ml), especially at lower frequencies. Histochemical demonstration of NADPH-diaphorase-positive nerves representing neural NOS density was not different between the two groups. These results suggest that allergic airway inflammation impairs neural NO-induced relaxation, presumably by inhibiting the access of neural NO to the airway smooth muscle.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9230751&dopt=Abstract
J Toxicol Clin Toxicol. 1995;33(4):337-42.
Combined use of glucagon and milrinone may not be preferable for severe propranolol poisoning in the canine model.
Sato S, Tsuji MH, Okubo N, Nishimoto C, Naito H.
Department of Anesthesiology, University of Tsukuba, Ibaraki, Japan.
In a previous study of propranolol poisoning, glucagon and milrinone significantly increased cardiac output, but the improvement caused by glucagon was almost entirely due to the chronotropic effect. This study investigates the combined effect of glucagon, in a dose not inducing tachycardia, and milrinone on beta-blocker poisoning. Following the administration of 10 mg/kg propranolol IV over ten minutes, dogs (N = 20) were divided into four treatment groups, group S (saline), group G (glucagon 2.5 micrograms/kg), group M (milrinone 100 micrograms/kg), and group G + M (glucagon 2.5 micrograms/kg plus milrinone 100 micrograms/kg). Hemodynamic parameters were observed over the next thirty minutes. Heart rate, cardiac output, and mean arterial pressure were decreased in all groups after the administration of propranolol. Heart rate, mean arterial pressure, cardiac output, and stroke volume recovered to the baseline values in group G + M. However, heart rate in group G + M showed a significant increase versus the other three groups. In a canine model of severe propranolol poisoning, the combined effect of glucagon 2.5 micrograms/kg and milrinone 100 micrograms/kg brought about a significant hemodynamic improvement, but it was accompanied by an excessive increase of heart rate. Combined therapy of milrinone and glucagon may not be preferable therapy in beta-blocker poisoning in the canine model.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7629900&dopt=Abstract
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