Ionamin online research references
Biochim Biophys Acta. 1988 Feb 4;958(2):163-71.
Association of chlorphentermine with phospholipids in rat alveolar lavage materials, alveolar macrophages and type II cells.
Ma JY, Ma JK, Weber KC, Bowman L, Reasor MJ, Miles PR.
Appalachian Laboratory for Occupational Safety and Health, Biochemistry Section, Morgantown, WV 26505.
Administration of chlorphentermine to rats leads to an increase in the phospholipid content of pulmonary surfactant materials and alveolar macrophages. It is known that this drug binds to pure phospholipids and prevents their degradation by phospholipases. Therefore, experiments were carried out to determine if chlorphentermine binds to surfactant phospholipids in vitro and to measure the in vivo association of drug with phospholipids in alveolar lavage materials from rats injected with [14C]chlorphentermine. The presence of chlorphentermine in alveolar macrophages, type II cells and other small pneumocytes (a population of lung cells which does not include alveolar macrophages or type II cells) from treated animals was also assessed. Binding of the drug to surfactant phospholipids, as measured with the fluorescent probe, 1-anilino-8-naphthalene sulfonate, occurs in vitro and does not differ in various subfractions of alveolar lavage materials isolated by differential centrifugation. Following daily administration of chlorphentermine to rats for 3 days, the drug appears to be associated with surfactant phospholipids such that the molar ratio is 1:100 (chlorphentermine/phospholipid). Chlorphentermine is also associated with alveolar macrophages (molar ratio, 1:18) and type II cells (molar ratio, 1:33). Not much drug is associated with the population of other lung cells (molar ratio, 1:333). In alveolar macrophages, approx. 70% of the drug seems to be bound to phospholipid and/or sequestered in subcellular organelles. However, only 20% of the chlorphentermine is bound and/or sequestered in type II cells. The results of these experiments suggest that following chlorphentermine administration, the drug is associated with phospholipids in acellular pulmonary lavage materials, alveolar macrophages and type II cells. This drug-phospholipid interaction may impair phospholipid degradation and lead to a phospholipidosis in surfactant materials and alveolar macrophages.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3337832&dopt=Abstract
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Anesthesiology. 1988 Mar;68(3):363-6.
The effect of vasopressor agents upon uterine artery blood flow velocity in the gravid guinea pig subjected to ritodrine infusion.
Chestnut DH, Ostman LG, Weiner CP, Hdez MJ, Wang JP.
University of Iowa College of Medicine, Iowa City.
The purpose of the present study was to assess the effects of intravenously administered vasopressors upon uterine artery blood flow velocity (UBFV) in the gravid guinea pig subjected to ritodrine infusion. Fourteen experiments were performed in 14 chronically instrumented pregnant guinea pigs near term. Immediately following a 1-h intravenous infusion of ritodrine (0.05-0.20 mg.kg.min-1), each animal received an intravenous bolus of vasopressor solution: 1) epinephrine, 0.001 mg/kg; 2) phenylephrine, 0.01 mg/kg; 3) mephentermine, 1.0 mg/kg; 4) ephedrine, 1.0 mg/kg; or 5) placebo. The experimental sequence was performed five times, so that each animal received all five solutions. The vasopressor sequence was randomly altered between animals. Infusion of ritodrine increased maternal heart rate 18 +/- 1% (P less than .0001), decreased maternal mean arterial pressure (MMAP) 4 +/- 1% (P less than .01), and decreased UBFV 5 +/- 1% (P less than .001). The four active vasopressor solutions resulted in similar, though not equivalent, increases in MMAP. Further, the MMAP response to each active vasopressor differed from the response to placebo (P less than .0001). Epinephrine and phenylephrine each significantly decreased UBFV (P less than .002). Ephedrine clearly preserved UBFV, whereas mephentermine appeared to result in an intermediate response.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3344991&dopt=Abstract
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Immunopharmacol Immunotoxicol. 1988;10(1):1-19.
Chlorphentermine suppresses the phosphatidylinositol pathway in concanavalin A-activated mouse splenic lymphocytes.
Sauers LJ, Wierda D, Reasor MJ.
Department of Pharmacology and Toxicology, West Virginia University Medical Center, Morgantown 26506.
We have previously demonstrated that the chlorphentermine (CP)1-induced impairment in lymphocyte blastogenesis involves drug-induced inhibition of an event which occurs very early during lymphocyte activation. An early event, which is associated with mitogen-induced lymphocyte activation, involves the hydrolysis of phosphatidylinositol by phospholipase C to yield inositol phosphates and diacylglycerol as products. Inositol phosphates and diacylglycerol then function as mediators of a trans-membrane signal for the continuation of the cellular response. It was the purpose of the present study to determine the effects of CP on this phosphatidylinositol pathway. We demonstrated that formation of inositol phosphates in lymphocytes increases progressively above control over a 2 hour period following concanavalin A (Con A)-stimulation. In contrast, lymphocytes pre-incubated with 10(-5)M CP for 60 min, then stimulated with Con A for 2 hours in the presence of 10(-5)M CP, exhibit a significantly depressed inositol phosphate formation. In addition, CP also inhibited the activity of phospholipase C (IC50 = 0.58 mM), the enzyme responsible for the formation of inositol phosphates during lymphocyte activation. Further, lymphocytes activated in a manner that bypasses the phosphatidylinositol pathway are not inhibited by 10(-7)M or 10(-9)M CP as are cells activated with Con A. These results suggest that the suppression of the phosphatidylinositol pathway may be involved in the inhibition by CP of lymphocyte blastogenesis induced by Con A.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3361070&dopt=Abstract
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