Ionamin online research references
J Appl Physiol. 1989 May;66(5):2437-45.
Effects of drug-induced pulmonary phospholipidosis on lung mechanics in rats.
Camus P, Joshi UM, Lockard VG, Petrini MF, Lentz DL, Mehendale HM.
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216-4505.
Chronic administration of amphiphilic drugs to rats induces pulmonary phospholipidosis (P), a disease characterized by accumulation of phospholipids and large foamy macrophages in alveolar spaces. We investigated whether P induced by chlorphentermine (CPH) causes changes in lung volumes and mechanics in this species. Groups of rats were fed CPH (50 mg.kg-1.day-1) for 1, 2, 3, 5, 9, and 14 wk. After each treatment period, lung volumes and mechanics were studied in the anesthetized, paralyzed, supine rat. Partial pressure-volume (PV) curves were developed at 3 and 6 ml above functional residual capacity (FRC; PV3, PV6), followed by maximal [up to total lung capacity (TLC)] PV curves. FRC was determined by saline displacement. Lungs were then fixed for histopathological examination. A subgroup of animals was allowed a recovery period of 6 wk, after the 9 wk of CPH administration. Pair-fed rats served as controls (CTR) at each time point. Lung weight increased in CPH-treated (CPH-T) rats from 1.5 +/- 0.2 (SD) g at week 1 to 5.8 +/- 1.4 g at week 14, reflecting the development of P. TLC, FRC, transpulmonary pressure at FRC, the shape of maximal PV curves, and static expiratory lung compliance computed from maximal PV data points did not change in CPH-T rats. However, partial PV curves of CPH-T lungs (particularly PV3) were shifted downward and to the right of those of CTR at 2, 3, 5, and 9 wk, indicating increased recoil pressure in phospholipidotic lungs at these time points.(ABSTRACT TRUNCATED AT 250 WORDS)
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2745304&dopt=Abstract
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Proc Soc Exp Biol Med. 1988 May;188(1):35-9.
Role of phospholipase C in chlorphentermine-induced pulmonary phospholipidosis in rat.
Kacew S.
Department of Pharmacology, Faculty of Health Sciences, School of Medicine, University of Ottawa, Ontario, Canada.
Daily, oral administration of chlorphentermine (60 mg/kg) for 5 days to rats produced a significant increase in the concentration of whole lung total phospholipid as well as sphingomyelin, phosphatidylserine, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol, and phosphatidylcholine. Similarly, a significant elevation in total and all individual phospholipid components was found in the lysosomal fraction of chlorphentermine-treated rat lung. In contrast, the activities of pulmonary Na+,K+-ATPase and alkaline phosphatase, enzymatic markers of membrane function, were not markedly affected by chlorphentermine treatment. The observed lung phospholipidosis was accompanied by inhibition of phospholipase C activity. Regardless of the phospholipid substrate, chlorphentermine significantly decreased pulmonary phospholipase C to approximately the same extent. Our data show that accumulation of phospholipid in whole lung and lysosomes is associated with an inhibition of phospholipase C activity.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2835777&dopt=Abstract
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Exp Lung Res. 1988;14(5):619-36.
Effects of chlorphentermine and nitrogen dioxide on murine alveolar macrophages.
White SM, DeNicola DB, Rebar AH, Born GS, Kessler WV.
Department of Medicinal Chemistry and Pharmacognosy, Purdue University, West Lafayette, Indiana 47907.
Male Swiss-Webster mice were treated daily for 14 days with either 120 mg/kg chlorphentermine (CP) to produce pulmonary lipidosis or an equal volume of water. Animals in each treatment group were then exposed by whole-body inhalation to either air or NO2 for 48 h. Immediately following exposure, alveolar macrophages (MPs) were collected from each animal by bronchoalveolar lavage. Assays performed on adherent viable MPs showed some changes in metabolic reduction, phagocytosis, and killing activity. 5'-Nucleotidase activity and yeast phagocytosis and killing assays suggested that CP elicited an increase in phagocytosis over control levels. Although the percentage metabolic reduction and microbicidal killing activities following CP were not increased when compared to controls, absolute reduction and killing (percentage values times total MPs) were significantly increased. These increased functions seemed to be highly dependent on the large increase in the total number of MPs induced by CP. It is possible that the large accumulation of MPs in the airways of the lipidotic lung may help protect the alveolar epithelium from NO2 by quenching free radicals produced during NO2-induced lipid peroxidation.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2852102&dopt=Abstract
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