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At least 217 records · Page 12Linked to original sources
PubMed1987

Effects of pharmacological and non-pharmacological interventions on ventricular late potentials.

The purpose of this paper is to review the presently available information on the effect of antiarrhythmic drugs and of map-guided antitachycardia surgery on ventricular late potentials. Studies in experimental myocardial infarction have shown that antiarrhythmic drugs are able to prolong regional low-amplitude fractionated electrical activity. However, no correlation between changes in duration of low-amplitude electrical activity and antiarrhythmic drug efficacy could be demonstrated. A similar lack of correlation between changes in duration of late potentials as recorded by the signal averaging technique from the body surface and inducibility or suppression of ventricular tachycardia were observed. Neither changes in duration or amplitude nor in the frequency content of ventricular late potentials showed an unequivocal correlation with drug efficacy. By contrast, there is convincing evidence that exclusion of arrhythmogenic tissue by map-guided antitachycardia surgery correlates with the loss of late potentials postoperatively in a high percentage of cases. If, however, late potentials persist after surgery, there is a high chance of ventricular tachycardia being still inducible postoperatively. A loss of ventricular late potentials by surgery may be the result of isolation of the arrhythmogenic tissue, devitalization and/or removal. In conclusion, there is presently no convincing evidence that any of the parameters for characterization of ventricular late potentials is clinically useful to predict the efficacy of antiarrhythmic drug therapy. On the other hand, ventricular late potentials have proved useful for prediction of the success of map-guided antitachycardia surgery.

Anti-Arrhythmia Agents↗
PubMed1988

Clinical pharmacology of oral and i.v. N-methylformamide: a pharmacologic basis for lack of clinical antineoplastic activity.

N-Methylformamide (NMF) has been an agent of considerable interest to oncologists because of its broad spectrum of preclinical antitumor activity, tumor-differentiating abilities, and radiosensitizing and chemosensitizing properties. In this report, the pharmacokinetics of NMF are described, based on data from two phase I studies exploring both iv and oral routes of administration. Mean peak NMF plasma concentrations at recommended phase II doses were 0.46 mmol/L for NMF administered orally, 600 mg/m2 three times/week X 4 weeks every 6 weeks, and 2.78 mmol/L for NMF administered as a weekly iv bolus at 2,000 mg/m2 X 3 weeks every 4 weeks. These NMF concentrations were significantly lower than the concentrations that have been demonstrated to induce antineoplastic and relevant biologic effects in preclinical studies. Plasma disappearance curves were biphasic in the majority of patients; however, 25% of the curves were best fit by a monoexponential kinetic model. Mean alpha half-life and beta half-life values (+/- SE) were 10 +/- 2 and 732 +/- 93 min, respectively. Volumes of distribution for the theoretical central compartment (Vc) and at steady-state (Vss) were 13.8 +/- 1.1 L/m2 and 18.7 +/- 1.1 L/m2, respectively. The mean plasma clearance of NMF was 19.1 +/- 2.1 mL/min per square meter, and the relative contributions to parent compound disposition by respiratory and renal routes were insignificant. No metabolites were identified. Gastrointestinal absorption of oral NMF was rapid and nearly complete; oral bioavailability was calculated to be 0.87. Pharmacodynamic associations were observed between the magnitude of the area under the plasma disappearance curves and hepatotoxicity, the dose-limiting toxic effect of iv NMF, and the symptom complex of nausea, vomiting, and malaise, which precluded dose escalation of oral NMF.

Administration, Oral↗
PubMed2000

Pharmacology department: pharmacologic approaches to abnormal blood lipids.

There are currently four classes of drugs available to treat dyslipidemia: niacin, bile acid-binding resins, 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, and fibric acid derivatives. Each acts at a unique point in a complex set of interrelated lipid metabolic pathways. The mechanism of action and adverse effects of these four classes are reviewed briefly. The efficacy of antioxidants and the importance of compliance issues are described.

Anion Exchange Resins↗
PubMed2003

The pharmacology and clinical pharmacology of 3,4-methylenedioxymethamphetamine (MDMA, "ecstasy").

The amphetamine derivative (+/-)-3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is a popular recreational drug among young people, particularly those involved in the dance culture. MDMA produces an acute, rapid enhancement in the release of both serotonin (5-HT) and dopamine from nerve endings in the brains of experimental animals. It produces increased locomotor activity and the serotonin behavioral syndrome in rats. Crucially, it produces dose-dependent hyperthermia that is potentially fatal in rodents, primates, and humans. Some recovery of 5-HT stores can be seen within 24 h of MDMA administration. However, cerebral 5-HT concentrations then decline due to specific neurotoxic damage to 5-HT nerve endings in the forebrain. This neurodegeneration, which has been demonstrated both biochemically and histologically, lasts for months in rats and years in primates. In general, other neurotransmitters appear unaffected. In contrast, MDMA produces a selective long-term loss of dopamine nerve endings in mice. Studies on the mechanisms involved in the neurotoxicity in both rats and mice implicate the formation of tissue-damaging free radicals. Increased free radical formation may result from the further breakdown of MDMA metabolic products. Evidence for the occurrence of MDMA-induced neurotoxic damage in human users remains equivocal, although some biochemical and functional data suggest that damage may occur in the brains of heavy users. There is also some evidence for long-term physiological and psychological changes occurring in human recreational users. However, such evidence is complicated by the lack of knowledge of doses ingested and the fact that many subjects studied are or have been poly-drug users.

Animals↗