Properties of microsomal enzyme systems that reduce N-hydroxyphentermine. Sympathomimetic drugs: evaluation for acute central hypotensive activity in alpha-chloralose-anesthetized dogs and cats intravertebral artery administration,. Palmitic acid-1-14C incorporation and turnover in lung phospholipids of rats treated with chlorphentermine, RMI 10.393 and Ro 4-4318. Ionamin online references

Ionamin online research references

Drug Metab Dispos. 1976 Sep-Oct;4(5):436-41.
Properties of microsomal enzyme systems that reduce N-hydroxyphentermine.

Sum CY, Cho AK.

The reduction of N-hydroxyphentermine was studied in liver microsomes isolated from rat, guinea pig, and rabbit. The reduction requires a NADPH-generating system and was inhibited by oxygen and carbon monoxide. In the rat, the reduction was increased by phenobarbital pretreatment. Kinetic analysis of the reductase activity in rat liver microsomes suggests that the reduction of the hydroxylamine is mediated by at least two enzyme systems, one of which is a CO-sensitive system inducible by phenobarbital.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10142&dopt=Abstract

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Arch Int Pharmacodyn Ther. 1976 Aug;222(2):216-32.
Sympathomimetic drugs: evaluation for acute central hypotensive activity in alpha-chloralose-anesthetized dogs and cats intravertebral artery administration,.

Kaplan HR, Fox JH, Kopia GA, Commarato MA.

dl-Amphetamine, phentermine and their para-chloro derivatives were tested for acute central hypotensive activity after intra-vertebral artery (iva) infusions in alpha-chloralose-anesthetized cats and intact and carotid sinus denervated dogs. Iva clonidine (reference standard) caused immediate reductions in blood pressure and heart rate and carotid sinus denervation (CSD) enhanced the clonidine response. dl-Amphetamine and phentermine did not cause acute hypotensive responses in the dog or cat whereas their para-chloro derivatives did. The vasodepressor response to para-chloramphetamine was inconsistent and transient and not modified by CSD. The magnitude and duration of the chlorphentermine vasodepressor response was minimal in the intact and CSD dog compared to clonidine. In contrast, chlorphentermine in the cat (140-300 mug/kg) caused an acute hypotensive response comparable in magnitude to clonidine (0.6-1.0 mug/kg). The bradycardias observed after iva chlorphentermine were much less pronounced than those associated with iva clonidine at comparable vasodepressor doses. By the i.v. route, each drug caused only pressor responses in the dog and cat. Suppression of the pressor response (resulting from "spill-over" of these alpha-stimulants into the systemic circulation after iva dosing) in the dog with small doses of i.v. phenoxybenzamine did not unmask or enhance the vasodepressor or bradycardic actions to iva administration of drugs. Methysergide prevented the hypotensive response to chlorphentermine in the cat and partially suppressed the response to clonidine; the reverse was true after piperoxan. Lilly 110140 and para-chlorophenylalanine reduced or abolished the effects of iva chlorphentermine. In summary, (1) iva chlorphentermine and clonidine were the only alpha-sympathomimetics tested which were effective as hypotensive substances; (2) the cat was considerably more responsive to iva chlorphentermine than the intact or CSD dog; (3) iva clonidine was more bradycardic than iva chlorphentermine; and (4) both adrenergic and serotonergic components appear to be among the mechanisms involved in the acute iva hypotensive response to chlorphentermine in the cat.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=984975&dopt=Abstract

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Arch Toxicol. 1976 Jun 8;35(3):163-74.
Palmitic acid-1-14C incorporation and turnover in lung phospholipids of rats treated with chlorphentermine, RMI 10.393 and Ro 4-4318.

Karabelnik D, Zbinden G.

The effects of 3 lipidosis-inducing drugs on the incorporation and turnover of palmitic acid-1-14C in lung phospholipids was studied. In rats treated with 1 dose of chlorphentermine or RMI 10.393, the incorporation of palmitate-1-14C into most lung phospholipid fractions was moderately decreased, but markedly lowered after 1 dose of Ro 4-4318. Eight doses of chlorphentermine and RMI 10.393 strongly inhibited the incorporation of palmitate-1-14C into lung phospholipids, whereas with 8 doses of Ro 4-4318 the incorporation was highly increased. Thirty hours after the last of 3 injections of the labeled palmitic acid the turnover of most lung phospholipids was considerably lower in chlorphentermine- and RMI 10.393-treated rats than in controls. Ro 4-4318, however, induced a highly increased turnover of most phospholipids. After 54 h, this effect had practically disappeared. Our studies showed that phospholipid storage after treatment with chlorphentermine and RMI 10.393 is mainly due to decreased degradation of phospholipids, whereas increased synthesis accounts for the effect of Ro 4-4318.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=989288&dopt=Abstract

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