Drugs online research references
Hepatology. 1996 Aug;24(2):419-23.
Inhibition of experimentally induced cirrhosis in rats by hypothyroidism.
Oren R, Dotan I, Papa M, Marravi Y, Aeed H, Barg J, Zeidel L, Bruck R, Halpern Z.
Department of Gastroenterology, Ichilov Hospital, Tel Aviv, Israel.
The coexistence of hyperkinetic circulation, hypermetabolism, and hyperactivity of the sympathetic nervous system is encountered in both cirrhosis and hyperthyroidism. Several drugs, such as propylthiouracil and propranolol, that are beneficial for treating some patients with chronic liver diseases are also prescribed for the treatment of thyrotoxicosis. We investigated the effects of experimentally induced hypo- and hyperthyroidism on the development of cirrhosis induced in rats by thioacetamide (TAA). We specifically examined whether hypothyroidism could prevent and hyperthyroidism could aggravate liver damage. Hypothyroidism induced by methimazole (MMI, 0.04%), propylthiouracil (PTU 0.05%), and by thyroidectomy was confirmed by a significant elevation of thyroid-stimulating hormone (TSH) levels. Hyperthyroidism (decreased TSH levels) was induced by eltroxin (ELT:50 micrograms/kg). Thirteen groups of 10 rats each were studied: euthyroid controls (3 groups: water, TAA 1.5 months, and TAA 3 months), hypothyroid (6 groups: MMI, PTU, surgical, MMI-TAA, PTU-TAA, surgical-TAA), and hyperthyroid (4 groups:ELT 1.5 months and 3 months, and ELT-TAA for 1.5 months and 3 months). Hepatic fibrosis (scored from 0 to 3) was significantly reduced (P < .0001) in hypothyroid rats as compared with euthyroid controls, and was aggravated in TAA-treated hyperthyroid rats (P < .0001). Quantitative microscopic analysis of liver biopsy specimens from all groups confirmed the semiquantitative histopathological scores (P < .001). Direct intrasplenic pressure measurement revealed a significant portal pressure elevation in the TAA and the ELT-treated rats (from 4.7 +/- 0.1 in the euthyroid group to 8.1 +/- 2.3 and 10.2 +/- 2.1 and 12.5 +/- 1.6 in the TAA, ELT and ELT-TAA groups, respectively). However, in the hypothyroid-TAA groups, the portal pressure was found to be within the euthyroid normal range (4.6 +/- 1.2 and 5.8 +/- 0.6 in the PTU-TAA and surgical-TAA, respectively). After 12 weeks, the mean spleen weight of rats receiving only TAA was significantly higher than the TAA-treated hypothyroid rats (P < .0001), indicating that the hypothyroid TAA-treated rats were less portal hypertensive. These results suggest that induced hypothyroidism can inhibit, whereas hyperthyroidism can aggravate, the development of cirrhosis in a rat model.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8690414&dopt=Abstract
Pharmacology. 1996 Nov;53(5):289-95.
Relaxant responses by optical isomers of ephedrine and methylephedrine in guinea pig tracheal smooth muscle.
Koike K, Kawasuji T, Saito H, Matsumoto M, Yasuda N, Niizawa S, Takayanagi I.
Department of Chemical Pharmacology, Toho University School of Pharmaceutical Sciences, Chiba, Japan.
The effects of optical isomers of ephedrine and methylephedrine on the guinea pig tracheal smooth muscle were studied. l-Ephedrine markedly caused a graded relaxation of the guinea pig trachea where the tone had been raised spontaneously. A rightward shift of the l-ephedrine concentration-response curve was observed for propranolol and butoxamine, and the pA2 values for propranolol and butoxamine were 8.55 and 6.38, respectively. d-Methylephedrine markedly caused a graded relaxation of the guinea pig trachea contracted with histamine. Propranolol and bupranolol did not affect the relaxant response to d-methylephedrine. d-Methylephedrine competitively antagonized the contractile responses to histamine, and the pA2 value for d-methylephedrine was 5.12. These results suggest that l-ephedrine-induced relaxation of the guinea pig trachea is mediated through beta 2-adrenoceptors, whereas d-methylephedrine relaxes the guinea pig trachea by blocking histamine receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8990487&dopt=Abstract
Circulation. 1977 Jun;55(6):872-80.
The effect of propranolol on microvascular injury in acute myocardial ischemia.
Kloner RA, Fishbein MC, Cotran RS, Braunwald E, Maroko PR.
The purpose of this study was to determine whether propranolol, which has been shown to reduce the extent of myocardial infarction, reduces microvascular injury which may play a role in exacerbating ischemia. Saline (10 dogs) or propranolol (2 mg/kg i.v., 7 dogs) was injected prior to a one hour occlusion of the left anterior descending coronary artery. Carbon black (1 ml/kg), which labels damaged and leaky vessels, was injected 5 min after release of the occlusion and allowed to circulate for two hours. By morphometric analysis of 1 micron thick sections, 75 +/- 12% of vessels and 84 +/- 7% of myocardial cells showed damage in untreated dogs; only 2 +/- 1% of vessels and 9 +/- 8% of myocardial cells showed damage in the propranolol-treated dogs (P less than 0.001). The number of carbon black-labeled vessels/10 fields/biopsy from comparable areas of ischemic tissue was 55 +/- 7 in untreated dogs and 27 +/- 3 in propranolol-treated dogs (P less than 0.001). The results suggest that propranolol not only protects the ischemic myocardial cell, but also significantly decreases the ischemic microvascular changes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=870245&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||