Biomedical subjects

D E Mann

Publications and source records attributed to D E Mann.

At least 73 records · Page 4Linked to original sources

PubMed1984

Serial electrophysiologic testing with a permanent pacemaker after acute myocardial infarction.

Electrophysiologic testing in patients after acute myocardial infarction may predict subsequent sudden death. We used a permanent pacemaker for repetitive electrophysiologic testing in a patient after acute infarction. Programmed, twice-threshold ventricular extrastimulation at two weeks after anteroseptal infarction failed to induce ventricular tachycardia. Subsequent programmed extrastimulation induced sustained ventricular tachycardia on four occasions (6, 16, 29 and 65 weeks) after infarction. As yet (20 months), spontaneous ventricular tachycardia has not occurred. Firm conclusions cannot be drawn from a single case. However, our patient developed a stable ventricular tachycardia circuit which was not apparent at two weeks. Thus, a single electrophysiologic study performed acutely after infarction may not accurately describe the potential for ventricular tachycardia or fibrillation. Serial electrophysiologic testing with an implantable externally triggered pacemaker may more accurately describe the potential for sudden death post-infarction in a few high-risk patients. This report shows that induction of ventricular tachycardia after acute infarction may not predict outcome.

Adult↗

PubMed1984

Comparative effect of disopyramide and ethmozine in suppressing complex ventricular arrhythmias by use of a double-blind, placebo-controlled, longitudinal crossover design.

This placebo-controlled, double-blind, longitudinal crossover study compares the efficacy of disopyramide and ethmozine, a new investigational drug, in suppressing frequent (40 or more per hour) ventricular premature depolarizations (VPDs) in 27 patients completing a 37 day protocol. Although both drugs significantly reduced VPDs relative to placebo, ethmozine was a superior antiarrhythmic drug in ach9eving near-total abolition of VPDs (30% of patients), which was never observed during disopyramide dosing (p less than .05). At the 80% VPD reduction level, ethmozine was effective in 56% of all patients compared with an effectiveness in only 22% of patients during disopyramide therapy (p less than .05). The mean peak plasma level of ethmozine was 0.66 +/- 0.8 micrograms/ml, which significantly fell to a trough level of 0.1 +/- 0.08 micrograms/ml (p less than .001). Mean peak and trough plasma levels of disopyramide exhibited less fluctuation (2.6 +/- 0.9 micrograms/ml vs 2.2 +/- 0.9 micrograms/ml). Ethmozine had no effect on the QT interval, whereas disopyramide prolonged it significantly. Importantly, while disopyramide produced serious side effects in 30% of patients, ethmozine was well tolerated with no statistically significant side effects compared with placebo.

Adult↗

PubMed1984

Investigational antiarrhythmic drugs for the treatment of ventricular rhythm disturbances.

Currently available antiarrhythmic drugs possess very poor therapeutic-to-toxic ratios, and therefore, there is a great deal of interest in the development of new investigational agents to suppress ventricular rhythm disturbances. This article includes most of the investigational ventricular antiarrhythmic drugs in which there has been a great deal of recent active investigation and interest. It stresses the different patient populations that have been tested with each of these antiarrhythmic drugs, pointing out those drugs that have been documented to be effective in nonsustained ventricular tachycardia or sustained ventricular tachycardia and sudden cardiac death.

Amiodarone↗

PubMed1983

Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli.

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.

Adult↗

PubMed1981

Comparative teratogenicity of cortisone and phenytoin in mice.

Single administrations of cortisone or phenytoin to pregnant mice on Days 11--14 of gestation caused similar skeletal and dissimilar soft tissue fetal anomalies. Cortisone reduced both maternal and fetal weight, whereas phenytoin only reduced fetal weight without adversely affecting maternal weight. A correlation between fetal weight reduction and cleft palate incidence was evident for each drug. Because probit analysis of dose--response regression lines did not deviate from parallelism after drug challenge, it was concluded that cortisone and phenytoin may produce palatal anomalies in the mouse fetus by a similar mechanism.

Animals↗

PubMed1980

Teratogenic potential of cocaine hydrochloride in CF-1 mice.

This investigation revealed that cocaine hydrochloride was teratogenic when administered in nontoxic doses to gravid CF-1 mice on Days 7-12 of gestation. The teratogenic susceptibility of the CF-1 mouse fetus to cocaine hydrochloride was evident throughout this portion of the gestation period. The early appearance of eye defects and the occurrence of skeletal defects later in gestation after cocaine hydrochloride challenge paralleled the sequence of ontogenesis.

Abnormalities, Drug-Induced↗

PubMed1978

Influence of cobalt (dietary), cobalamins, and inorganic cobalt salts on phenytoin- and cortisone-induced teratogenesis in mice.

Various cobalt-containing agents (cyanocobalamin, sodium cobaltinitrite, and cobaltous chloride), which formerly had been shown to prevent the onset of cleft palate in CF-1 mice injected with cortisone, were studied to determine whether they would afford similar protection against phenytoin. Phenytoin, however, failed to cause cleft palate in the mouse fetus when given to pregnant animals alone; and cortisone, on the contrary, induced this anomaly in the presence of the so-called cobalt antagonists as well as when administered in their absence. It is suggested from these results that high dietary intake of cobalt prevents cleft palate caused by phenytoin challenge and also negates the protective effects associated with the acute administration of cobalt compounds. Therefore, it is concluded that these well-known teratogens inhibit palatal closure in mice by different mechanisms.

Animals↗

PubMed1978

Effects of 1,10-phenanthroline and a zinc complex of 1,10-phenanthroline on nucleic acid synthesis in mouse liver and spleen.

The effects of 1,10-phenanthroline and a zinc complex of 1,10-phenanthroline on nucleic acid synthesis were examined by noting the capcity of these agents to incorporate [methyl-3H]thymidine, or [5-3H]uridine into hepatic and splenic DNA and RNA. Within 32 hours after the intraperitoneal injection of 1,10-phenanthroline in mice, a decrease of [methyl-3H]thymidine incorporation into hepatic DNA was observed. The administration of the zinc complex of 1,10-phenanthroline decreased the incorporation of [5-3H] uridine into hepatic RNA within 24 hours and decreased the formation of [3H]DNA from [methyl-3H]thymidine in the liver within 24 and 32 hours. An increase of the isotopic incorporation into hepatic RNA and of the pool size of ATP within 2 hours after the administration of the complex was also noted. In the splenic studies, the zinc complex significantly inhibited the formation of labeled DNA and RNA at 2, 8, 24, and 32 and 2, 8 and 24 hours postinjection, respectively. A relationship exists between the results obtained from sequential treatment (zinc chloride after 1,10-phenanthroline) and those derived from the zinc complex of 1,10-phenanthroline pertaining to an inhibition of isotopic incorporation into hepatic and splenic nucleic acid.

Adenine Nucleotides↗

PubMed1977

Teratogenicity of zinc chloride, 1,10-phenanthroline, and a zinc-1,10-phenanthroline complex in mice.

Zinc chloride, in single doses of 12.5, 20.5 and 25 mg/kg ip on Day 8,9,10, or 11 of gestation in CF-1 albino mice, produced skeletal anomalies without accompanying soft tissue defects. Ripple ribs, the most unusual anomaly, first appeared when the zinc salt was given on Day 9 of gestation in a dose of 20.5 mg/kg, becoming more prevalent when 25 mg/kg of the drug was administered on Day 11.1,10-Phenanthroline, in single doses of 30 mg/kg ip on Day 8,9,10, or 11 of gestation elicited skeletal defects comparable to those caused by zinc chloride as well as soft tissue anomalies, but a significant incidence of the former occurred with this agent only following its injection on Day 8 of gestation. A zinc-1,10-phenanthroline complex in single doses of 50 mg/kg on Day 8,9,10, or 11 of gestation yielded significant incidences of skeletal and soft tissue anomalies only when the complex was administered on Day 8 or 9 of gestation. This dosage level was toxic to both the mother and fetus when given on Day 10 of gestation. However, when the complex was given on Day 8,9,10, or 11 in a dose of 25 mg/kg, neither toxic nor teratogenic effects were observed in the mother or fetus, respectively.

Animals↗

PubMed1976