Effects of an iodinated water supply.
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Disinfectants↗
Biomedical subjects
M H Malagodi
Publications and source records attributed to M H Malagodi.
Relation of etidocaine and bupivacaine toxicity to rate of infusion in rhesus monkeys.
The relationship between infusion rate of etidocaine and bupivacaine and central nervous system toxicity was studied in three rhesus monkeys. Increasing the infusion rate from 0.5 to 2.0 mg/kg.min-1 decreased the seizure dosage of etidocaine but had no effect on that of bupivacaine. Arterial plasma concentrations of etidocaine and bupivacaine that induced electrical seizure activity increased as the infusion rate was increased from 0.5 to 1.0 mg/kg. min-1. A plasma decay study in a fourth animal demonstrated that etidocaine decayed more rapidly than did bupivacaine. These results suggest that the rate of administration of these agents is important in determining central nervous system toxicity.
Acetanilides↗
Diazepam in the prophylaxis of lignocaine seizures.
Diazepam 0.05-0.25 mg/kg increased the dose of lignocaine required to cause seizures in Rhesus monkeys by 24-34%. Spontaneous ventilation was maintained adequately during lignocaine administration following diazepam treatment and no adverse cardiovascular effects occurred. Before the onset of lignocaine-induced seizures in non-treated animals, the animals appeared to be drowsy. However, prior to administration of diazepam masked this effect. Convulsions were controlled by smaller doses of diazepam in non-treated animals than in diazepam-treated animals. Also, the animals that were pretreated with diazepam had a greater duration of depression after seizure.
Acid-Base Equilibrium↗
Effects of calcium antagonist, 6-(N, N-diethylamino) hexyl-3, 4, 5-trimethoxybenzoate, on digitalis-induced arrhythmias and cardiac contractions.
6-(N, N-Diethylamino) hexyl-3, 4, 5-trimethylbenzoate (TMB-6) and lidocaine were equipotent (1 mg/kg) in the conversion of ectopic rhythms to normal rhythms in digoxin-toxic dogs. However, TMB-6 had fewer side effects on heart rates and dp/dt than lidocaine. TMB-6 inhibited the contractile force of electrically stimulated dog and guinea-pig atria and ventricles at concentrations ranging from 2.5 X 10(-5) to 1.7 X 10(-4) M. Elevation of extracellular Ca++ concentrations from 2.7 to 5.4 mM produced a significant increase in the ID50 of TMB-6 in atria (from 2.5 X 10(-5) to 5.0 X 10(-5) M in dogs and from 7.2 X 10(-5) to 1.0 X 10(-4) M in guinea pigs). TMB-6 (7.3 X 10(-5) to 2.4 X 10(-4) M) depressed the amplitude of Ca++-dependent action potentials in depolarized dog cardiac Purkinje fibers. These results are discussed with regard to the antagonism of TMB-6 on Ca++ availability in the myocardium which leads to the conversion of cardiac arrhythmias.
Action Potentials↗
Fluroxene toxicity induced by phenobarbital.
Because of reports of fluroxene toxicity in man, the effect of phenobarbital treatment on the toxicity and metabolism of fluroxene was studied in 9 rhesus monkeys. Six monkeys that were exposed to a mean calculated alveolar fluroxene concentration of 5.8% for 4-hr periods up to a total of 16 hr showed no evidence of toxicity. Two animals were sacrificed after a single 4-hr exposure to obtain control measures of fluroxene metabolites in tissues. Four monkeys that had previously survived received exposures to fluroxene and 3 monkeys that had no exposure to fluroxene died during fluroxene anesthesia after treatment with phenobarbital (mean time, 3 hr). Toxicity was manifested by arterial hypotension, pulmonary edema, and arterial hypoxemia. Phenobarbital treatment enhanced production of fluroxene metabolites, including the highly toxic trifluoroethanol. Concentrations of trifluoroethanol in mixed-expired gas, blood, and urine, and of total nonvolatile fluorine in blood, urine, and tissues of animals treated with phenobarbital were 2 to 10 times as in control animals. The results suggest that the rhesus monkey is a valuable model for the study of fluroxene pharmacology and that inclusion of an enzyme-inducing challenge in the evaluation of potential toxicity of other anesthetics seems warranted.
Anesthesia↗
Etidocaine, bupivacaine, and lidocaine seizure thresholds in monkeys.
The central nervous system toxicities of etidocaine, bupivacaine, and lidocaine were studied during constant-rate intravenous infusions in rhesus monkeys. Comparison of drug effects was achieved by determining the drug dosages and arterial plasma concentrations that induced electrical seizure activity. The central nervous system toxicity of etidocaine was similar to that of bupivacaine. The toxicity of each was four times greater than that of lidocaine. Since the drug infusion rates were proportional to anesthetic potencies in clinical usage, the therapeutic-toxic ratios of these three drugs are similar.
Acetanilides↗
Studies on the mechanism of action of a new Ca-2+ antagonist, 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride in smooth and skeletal muscles.
1. The rabbit aortic strip, guinea-pig ileum and rabbit skeletal muscle sarcoplasmic reticulum preparations were used to determine at which sites and in what manner 8-(N,N-diethylamino)-octyl 3,4,5,-trimethoxybenzoate (TMB-8) interferes with Ca2+ availability in smooth and skeletal muscles. 2. TMB-8 (50 muM) significantly inhibited equivalent responses of the rabbit aortic strip to KCl and noradrenaline. 3. TMB-8 (65 muM) produced no significant alteration in the extracellular space of the guinea-pig ileum as measured with [3H]-sorbitol. 4. The resting cellular Ca2+ influx as well as the resting 45Ca2+ efflux in the guinea-pig ileum preparation were significantly inhibited by TMB-8 (65 muM). 5. TMB-8 (5 muM and 50 muM) had no significant effect on the uptake of 45Ca2+ by the sarcoplasmic reticulum preparation of skeletal muscle; however, TMB-8 (5 muM) did significantly inhibit the caffeine (20 mM)-induced release of 45Ca2+ from this preparation. 6. It is concluded that TMB-8 reduces Ca2+ availability in smooth and skeletal muscles by stabilizing Ca2+ binding to cellular Ca2+ stores and thereby inhibits the release of this Ca2+ by contractile stimuli.
Animals↗
Letter: Allergy and febrile seizures.
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Child↗
Venous air embolism prophylaxis with a surface-active agent.
The protective effect of a nonionic surface-active polyol agent (Pluronic F-68) against bolus injection and constant-rate IV infusion of air was studied in 21 dogs anesthetized with pentobarbital. Aortic, pulmonary artery and right ventricular pressures, cardiac output, end-tidal CO2 concentration, wasted ventilation, and blood surface tensions were measured before and after the IV administration of this surfactant. The magnitudes of change in the cardiorespiratory responses measured after venous air embolism were significant (p less than 0.05) reduced in the treated animals. This agent may be advantageous for surgical patients when an increased risk of venous air embolism exists.
Animals↗
Effect of vitamin D in fluoride-treated rats.
Fluoridated drinking water (30 mg and 100 mg F per liter) was used to induce rachitic changes in rats fed a vitamin D free diet containing calcium and phosphorus in a ratio of 1 : 1. Supplements of vitamin D3 (70 IU of cholecalciferol per week) completely prevented the rachitogenic effects of fluoride. This protective effect occurred despite evidence that vitamin D enhanced the intestinal absorption of fluoride.
Animals↗