Impairment of renal function in rats with generalized lipidosis as induced by chlorphentermine. Cumene hydroperoxide-mediated lipid peroxidation in rat alveolar macrophages following induction of phospholipidosis with chlorphentermine. Effect of chlorphentermine on the pulmonary disposition of norepinephrine in the isolated perfused rabbit lung. Ionamin online references

Ionamin online research references

Arzneimittelforschung. 1981;31(5):795-9.
Impairment of renal function in rats with generalized lipidosis as induced by chlorphentermine.

Lullmann H, Lullmann-Rauch R, Mosinger EU.

The purpose of this work was to study the impact of experimentally induced lipidosis upon renal function. Rats were orally treated up to 12 weeks with the anorectic drug chlorphentermine at dosages of 20 and 50 mg/kg, respectively. During the course of treatments the following parameters were determined: plasma urea level, creatinine clearance, ability of the kidneys to concentrate the urine after acute deprivation of drinking water, and to dilute the urine after acute water load. Morphological examination confirmed generalized lipidosis affecting kidney and many other organs. Chronic treatments with both drug dosages caused a rise of plasma urea level. Treatment with the high dosage caused a significant reduction of creatinine clearance and significant impairment of both abilities to concentrate and to dilute the urine. The findings demonstrate that serve generalized lipidosis as induced by high doses of chlorphentermine is associated with significant impairment of renal function.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7196738&dopt=Abstract

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Toxicology. 1980;18(2):159-68.
Cumene hydroperoxide-mediated lipid peroxidation in rat alveolar macrophages following induction of phospholipidosis with chlorphentermine.

Reasor MJ.

Rats were treated for 4 weeks with chlorphentermine hydrochloride (30 mg/kg, i.p., 5 days/seek), a regimen which causes a profound phospholipidosis in the alveolar macrophages (AMs). The susceptibility of these lipid-laden cells to lipid peroxidation was examined and compared to AMs from control (untreated) rats. Lipid peroxidation was induced in cells in vitro by incubation with cumene hydroperoxide (10(-5) M--10(-3) M). A dose dependent increase in malonyl dialdehyde (MDA) formation was observed with both populations of AMs. Two to three times more MDA was found in lipidotic AMs than controls at the higher dose of cumene hydroperoxide. Under these conditions, less loss of cellular viability resulted with the lipidotic AMs than controls. The partial depletion of reduced glutathione in the cells led to an even greater MDA formation by both cell-types with the lipidotic AMs being more markedly affected. Both populations of AMs experienced a greater loss of viability associated with loss of reduced glutathione with the control AMs showing more toxicity than the lipidotic cells. Therefore, while the induction of phospholipidosis renders AMs more suspectible to lipid peroxidation, they show less of a loss in cellular viability than control cells. The previously reported augmentation in the antioxidant defense mechanisms in the lipidotic cells may be partially responsible for these results.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7256780&dopt=Abstract

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Exp Lung Res. 1981 May;2(2):71-84.
Effect of chlorphentermine on the pulmonary disposition of norepinephrine in the isolated perfused rabbit lung.

Angevine LS, Nabeshima T, Ho IK, Mehendale HM.

Chlorphentermine (CP) has been noted to cause primary pulmonary hypertension both clinically and experimentally. It was postulated that CP might affect the pulmonary clearance of endogenous vasoactive substances such as norepinephrine (NE). The uptake and metabolism of 14C-NE were followed in artificially ventilated isolated perfused rabbit lung preparations using a constituted perfusate with initial NE concentration of 5 micrograms/100 ml. Perfusate samples were analyzed for total radioactivity, metabolites, and parent compound. Preloading the lungs with 0.25 mM CP significantly increased the concentrations of total radioactivity, deaminated products, and decreased the concentration of normetanephrine in the perfusate. In addition, the accumulation of total radioactivity in the lung tissue after 60 min of perfusion was significantly decreased in CP-treated lungs. The proportion of deaminated metabolites in the lung tissue was slightly decreased while the percent of normetanephrine, and parent compound were significantly increased by the CP treatment. CP (0.1 mM) also inhibited the in vitro metabolism of NE by 79%. These results provide experimental evidence in support of a hindered pulmonary clearance of circulating NE by CP.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7274178&dopt=Abstract

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