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Biomedical subjects

M Barletta

Publications and source records attributed to M Barletta.

12 recordsLinked to original sources
PubMed1990

Maternal-fetal electrocardiographic effects and pharmacokinetics after an acute i.v. administration of caffeine to the pregnant rat.

The relationship between fetal exposure and cardiovascular functional effects in the caffeine-treated pregnant rat was investigated. Caffeine (100 mg/kg) was administered intravenously to dams on day 21 of gestation. The transplacental transport of caffeine was studied by obtaining maternal and fetal blood (umbilical vein) samples at designated times after drug administration. Concurrent maternal-fetal electrocardiograms (ECGs) were measured and evaluated for caffeine-induced changes. Maternal and fetal plasma caffeine levels as well as area under the curve values were proportionally related throughout the experiment, indicative of equal exposure to caffeine. The fetal ECG exhibited more extensive changes associated with caffeine than did the dam's, but the effects were not detected in the first 30 min, suggesting a lag period for the action of caffeine on the fetal heart. The frequency of fetal ectopic beats and abnormal T waves were directly related to fetal plasma caffeine levels. Fetal ECG combined with the fetal blood microsampling technique was a practical method of testing for prefunctional effects of caffeine in the rat fetus.

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PubMed1984

The role of the sympathetic nervous system in the cardiovascular effects of systemically administered gamma-aminobutyric acid.

The role of the sympathetic nervous system in the circulatory effects of peripherally administered GABA was investigated in anesthetized dogs. Systemic administration of GABA (10-300 micrograms/kg) decreased blood pressure (BP) by 9-29 mmHg and heart rate (HR) by 15-60 beats/min in anesthetized dogs. Pretreatment with reserpine (1 mg/kg, i.m.) or ganglionic blockade with hexamethonium (10 mg/kg, i.v.) plus atropine (1 mg/kg, i.v.) abolished the GABA-induced hypotension and bradycardia. Intravertebral administration of GABA did not cause greater reduction in BP than by the i.v. route. Bicuculline (1 mg/kg, i.v.) attenuated the BP and HR responses to either intravertebrally or intravenously administered GABA, suggesting peripheral GABA receptors mediate the vasodepressor response to GABA. GABA prevented the bradycardia caused by the preganglionic vagal stimulation, suggesting GABA impairs ganglionic transmission. The depressant effect of GABA on ganglionic transmission was reversed by bicuculline. The depressor and bradycardic effects of i.v. GABA were not mediated by the release of either histamine or prostaglandins, since mepyramine or indomethacin pretreatment failed to alter the BP and HR responses to GABA. Since the doses of GABA used in this investigation probably do not pass the blood brain barrier, it is suggested that systemic administration of GABA decreases BP by a peripheral mechanism that is dependent upon an intact sympathetic nervous system and the ganglionic blocking activity of GABA most likely contributes to its vasodepressor effects upon systemic administration.

Animals↗
PubMed1980

Use of mannitol to obviate propranolol-induced myocardial depression in ischemic canine heart.

To obviate the myocardial depressant action of propranolol, the use of this drug in combination with a positive inotropic agent, mannitol, was studied in the ischemic heart of the dog. Mannitol (25%) administered prior to propranolol augmented myocardial contractility, as shown by an upward shift of the relationship between the pressure change with time and the mean left atrial pressure. Subsequent administration of propranolol did not offset the positive inotropic response to mannitol whereas it markedly reduced the heart rate from a control ischemic value of 127.8 +/- 3.4 to 109 +/- 4.0 beats/min. The myocardial oxygen requirement, as determined by the tension-time index per minute, decreased 26.3 +/- 1.2% below the control ischemic value. These findings suggest that hypertonic mannitol augments contractility in the ischemic failing heart while sustaining the desirable negative chronotropic action of propranolol. This procedure may potentiate the beneficial effects of propranolol on the myocardial oxygen balance and serve as an effective therapeutic modality in the control of acute irreversible ischemia.

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PubMed1977

Small animal model for myocardial infarction.

Myocardial infarctions were produced in rats by electro-cauterization of the left anterior descending artery, and the extent of myocardial damage was measured by serial serum levels of creatine phosphokinase activity utilizing spectrophotometric analysis. All animals were also evaluated for myocardial damage by electrocardiographic wave alterations. A correlation between myocardial infarct size and serum creatine phosphokinase was demonstrated. Significant arrhythmias and death occurred only in experimental groups where myocardial infarction had been produced. This small animal model offers a quick, inexpensive, and simple method for screening therapeutic agents that alter infarct size.

Animals↗
PubMed1975

Method for the production of severe ventricular dysrhythmias in small laboratory animals.

In earlier reports from this laboratory, it was shown that 3 weeks' pretreatment with desoxycorticosterone acetate (DCA) pellet implantation and saline as drinking fluid caused a nearly 20,000-fold potentiation of the acute cardiotoxicity of isoproterenol. In such animals, the beta-receptor stimulant consistently elicited severe ventricular dysrhythmias, usually leading to ventricular fibrillation (VF) and death. In the present study, a similar enhancement of isoproterenol arrhythmogenic activity after DCA-saline pretreatment was demonstrated also in the guinea pig and albino mouse. It was found, further, that isoproterenol consistently caused an alteration of the total myocardial electrolyte content in DCA-saline-treated rats, consisting of a decrease of magnesium (Mg) and potassium (K) levels and elevation of sodium (Na). In control rats, on the other hand, isoproterenol did not alter the myocardial Mg content and increased K. The emertence of cardiac irregularities and VF could be inhibited by pretreatment with antiarrhythmic drugs. On a molar basis, these agents decreased the incidence of VF in the following descending order: dl-propranolol (100), practolol (39), d-propranolol (34), sotalol (20), quinidine (8), and lidocaine (5). In the presence of any of the listed drugs, except for lidocaine, isoproterenol did not lower Mg levels and had variable effects on those of Na and K. Pretreatment with Mg gluconate was likewise effective in preventing isoproterenol-induced dysrhythmias and death. These findings demonstrate that: a) sensitization of the myocardium by DCA-saline treatment is not species-specific for the rat; b) this phenomenon can be a useful method for the screening of antiarrhythmic drugs; and c) isoproterenol-induced dysrhythmias may be associated with myocardial electrolyte alterations involving especially Mg depletion.

Animals↗
PubMedDate not supplied

A method to obtain maternal-fetal plasma samples using a microsampling technique in the rat: transplacental passage of cefoxitin.

A microsampling technique that allows taking blood samples from the umbilical vein of the pregnant rat is described. Such techniques are needed in order to allow pharmacokinetic and embryo exposure to be correlated with teratogenic endpoints. Cefoxitin was administered intravenously (300 mg/kg) into tracheotomized, pentobarbital anesthetized dams on day 21 in gestation. Blood samples were collected via the carotid artery from the dam and the umbilical vein of the fetus at designated times. Up to three samples of 20 to 30 microliters each, were taken from individual fetuses at 20-min intervals. With few exceptions, fetal cefoxitin concentrations were homogeneous at each sampling period. Fetal concentrations were low compared to maternal concentrations as seen by the small fetal/maternal area under the curve ratio (0.053 +/- 0.006).

Animals↗
PubMedDate not supplied

An investigation of the toxic effects of combustion products--analysis of smoke components.

A comprehensive experimental design was developed to study the effects of thermal degradation products formed by the combustion of building materials on the behavior of rats. Three materials were studied. They were Douglas fir, wool, and polyvinyl chloride. Each material was tested under both flaming and nonflaming modes of combustion. The smoke and gases produced by each material were analyzed by specific gas detector tubes, gas chromatography/mass spectrometry, and infrared spectroscopy. Products measured during combustion included oxygen, carbon monoxide, carbon dioxide, hydrogen cyanide, and hydrocarbons. Part of a much larger study, this paper will deal with the analytical aspects of the experimental design.

Animals↗
PubMedDate not supplied

Comparative kinetics of serum and vitreous humor digoxin concentrations in a guinea pig model. Part I: Intravenous administration of digoxin.

The pharmacokinetics of a single intravenous dose of digoxin in the guinea pig was investigated with emphasis on the penetration of digoxin into the vitreous humor. A controlled study was undertaken and data was collected which indicated that digoxin follows an open, two-compartment pharmacokinetic model with a terminal half-life of 318 minutes. The data indicated that the ratio of vitreous concentrations to serum concentrations were determined to be equal following an initial tissue distribution phase.

Animals↗
PubMedDate not supplied

Use of cerebellar cGMP in the measurement and characterization of the diazepam/ethanol interaction.

The characterization and measurement of the benzodiazepine and ethanol interaction has been of major interest for many years. Various pharmacological and biochemical studies have been employed to investigate this interaction, which is believed to occur predominantly in the CNS, but localization of one particular brain area has not been investigated. This research employed the rat cerebellum as a site to study the diazepam/ethanol interaction. The measurement of cerebellar ethanol and diazepam, by gas chromatography, demonstrated an enhancement of diazepam levels by ethanol. Ethanol and diazepam, alone and in combination, displayed a significant depression of cerebellar 3',5'-Guanosine Cyclic Monophosphate (cGMP). The depression seen by the combination was significantly greater than the simple algebraic sum, but insignificantly different from the corrected algebraic sum. The double reciprocal plot of the data demonstrated a common ordinate intercept for the diazepam line and the diazepam/ethanol (2 g/kg) line, thus indicating a competitive mechanism of action.

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