Online Pharmacy, Tramadol, Paxil, antibiotics, amoxicillin, zithromax, Rx Online, pharmaceuticals, DHEA, prescription medications, prescription drugs.

Drugs online research references

Am J Physiol Lung Cell Mol Physiol. 2000 May;278(5):L1039-44.
Amiodarone induces apoptosis of human and rat alveolar epithelial cells in vitro.

Bargout R, Jankov A, Dincer E, Wang R, Komodromos T, Ibarra-Sunga O, Filippatos G, Uhal BD.

Department of Medicine, Cook County Hospital, Chicago, Illinois 60612, USA.

The antiarrhythmic amiodarone (AM) and its metabolite desethylamiodarone (Des) are known to cause AM-induced pulmonary toxicity, but the mechanisms underlying this disorder remain unclear. We hypothesized that AM might cause AM-induced pulmonary toxicity in part through the induction of apoptosis or necrosis in alveolar epithelial cells (AECs). Two models of type II pneumocytes, the human AEC-derived A549 cell line and primary AECs isolated from adult Wistar rats, were incubated with AM or Des for 20 h. Apoptotic cells were determined by morphological assessment of nuclear fragmentation with propidium iodide on ethanol-fixed cells. Necrotic cells were quantitated by loss of dye exclusion. Both AM and Des caused dose-dependent necrosis starting at 2.5 and 0.1 microg/ml, respectively, in primary rat AECs and at 10 and 5 microg/ml in subconfluent A549 cells (P < 0.05 and P < 0.01, respectively). AM and Des also induced dose-dependent apoptosis beginning at 2.5 microg/ml in the primary AECs (P < 0.05 for both compounds) and at 10 and 5 microg/ml, respectively, in the A549 cell line (P < 0.01). The two compounds also caused significant net cell loss (up to 80% over 20 h of incubation) by either cell type at drug concentrations near or below the therapeutic serum concentration for AM. The cell loss was not due to detachment but was blocked by the broad-spectrum caspase inhibitor Z-Val-Ala-Asp-fluoromethylketone. Furthermore, the angiotensin-converting enzyme inhibitor captopril (500 ng/ml) and the angiotensin-receptor antagonist saralasin (50 microg/ml) significantly inhibited both the induction of apoptosis and net cell loss in response to AM. These results are consistent with recent work from this laboratory demonstrating potent inhibition of apoptosis in human AECs by captopril (Uhal BD, Gidea C, Bargout R, Bifero A, Ibarra-Sunga O, Papp M, Flynn K, and Filippatos G. Am J Physiol Lung Cell Mol Physiol 275: L1013-L1017, 1998). They also suggested that the accumulation of AM and/or its primary metabolite Des in lung tissue may induce cytotoxicity of AECs that might be inhibitable by angiotensin-converting enzyme inhibitors or other antagonists of the renin-angiotensin system.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10781436&dopt=Abstract

J Thorac Cardiovasc Surg. 2000 May;119(5):1030-8.
Captopril-induced glutamate release at the start of reperfusion after cold cardioplegic storage of pig hearts.

Randsbaek F, Kimose HH, Bjerre T, Moldrup U, Botker HE, Nielsen TT.

Department of Cardiology and Institute of Experimental Clinical Research, Skejby Hospital, Aarhus University Hospitals, University of Aarhus, Denmark.

OBJECTIVE: We sought to evaluate the effects of captopril on glucose-related metabolism during hypothermic cardioplegic storage and subsequent reperfusion. METHODS: We compared hearts from control pigs with hearts from pigs treated with increasing oral doses of captopril for 3 weeks (12.5-150 mg daily), an intravenous bolus (25 mg) before operation, and captopril-containing cardioplegic solution (1 mg/L). The hearts were excised after infusion of cold crystalloid cardioplegic solution and stored in saline solution (4 degrees C-6 degrees C). In one series we studied myocardial blood flow and arteriovenous differences in oxygen, glucose, lactate, glutamate, and alanine during 60 minutes of postcardioplegic blood reperfusion. In this series captopril-treated hearts were reperfused with captopril-containing blood (1 mg/L). In another series we obtained biopsy specimens from the left ventricle throughout 30 hours of hypothermic cardioplegic storage and monitored tissue content of energy-rich phosphates, glycogen, glutamate, and alanine. RESULTS: Captopril increased glutamate and alanine release 11- to 17-fold at the start of reperfusion (P <.001). Furthermore, captopril increased myocardial oxygen and glucose uptake during reperfusion (P <.001 for both), whereas lactate release and myocardial blood flow were unaffected by captopril. At the start of reperfusion, there was a positive correlation between glutamate release and glucose uptake in captopril-treated hearts (r = 0.66, P =.05). We found no statistically significant differences between captopril and control hearts in tissue content of adenosine triphosphate, glycogen, glutamate, alanine, or lactate during 30 hours of cardioplegic storage. CONCLUSIONS: The metabolic effects of captopril are strictly related to reperfusion, during which oxidative metabolism of glucose is improved. The captopril-induced increase in glutamate and alanine release at the start of reperfusion after cardioplegic storage may reflect a switch in metabolism of glucose-related amino acids.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10788826&dopt=Abstract

Klin Med (Mosk). 2000;78(3):42-6.
[Effects of angiotensin-converting enzyme (ACE) inhibitors on water-salt homeostasis in hypertensive patients living in Far North]

[Article in Russian]

Vershinina AM, Gapon LI, Bazhukhina IF, Teffenberg DV, Drozdov VV, Spitsina NA, Sergeichik OI.

The aim of the study was evaluation of ACE inhibitors (captopril and ramipril) effect on water-salt homeostasis in the treatment of patients with arterial hypertension (AH) living in the Far North of Russia. 100 male patients with mild and moderate AH were examined 2 weeks, 3 and 6 months after administration of captopril or ramipril. The drugs are shown to correct water-salt metabolism. This is explained by better renal function due to speeding up glomerular filtration and increased sodium excretion with urine, and by activity of humoral mechanisms (inhibited activity of plasma renin, low plasma concentration of aldosterone and its 24-h excretion). Comparison of captopril versus ramipril demonstrates advantages of prolonged ramipril in respect to regulation of water salt metabolism in the treatment of essential hypertension in the Far North.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10790965&dopt=Abstract

online pharmacies || Hair Million herbal formula for hair loss and hair growth || Amoxicillin || Tramadol || Paxil || Rx Drugs USA, Prescription Drugs Online Pharmacy || Zithromax || online pharmacy || Antibiotics and prescription medications online literature || Antibiotics