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Biomedical subjects

D M Aviado

Publications and source records attributed to D M Aviado.

At least 37 records · Page 2Linked to original sources
PubMed1975

Five fluorocarbons for administration of aerosol bronchodilators.

The exposure of the upper respiratory tract to aerosol propellants produces apnea, bradycardia, and biphasic fall and rise in aortic blood pressure in anesthetized dogs. This response represents the irritation of sensory receptors in the nasal and nasopharyngeal mucosa and is not elicited with aerosol propellants administered via a tracheal cannula bypassing the upper respiratory tract. When this is done, a different reflex is elicited, consisting of tachycardia that is mediated by the thoracic sympathetic nerves. There is either bronchodilation or bronchoconstriction depending on the type of propellant. The three propellants (11, 12, and 114) widely used in aerosols, when inspired in large doses, elicit both bradycardia and tachycardia and induce bronchoconstriction or bronchodilation. Two additional propellants (115 and C318), which are not ordinarily used to dispense bronchodilator drugs, do not elicit any change in heart rate and produce only bronchodilation. It is suggested that these two propellants merit further investigation and may replace the three widely used ones if these prove the use and abuse of aerosols.

Aerosol Propellants↗
PubMed1975

Toxicity of aerosol propellants in the respiratory and circulatory systems. IX. Summary of the most toxic: trichlorofluormethane (FC 11).

The acute inhalational toxicity of trichlorofluoromethane (FC 11) is summarized in this paper. There is a striking similarity in threshold concentrations between the mouse and the rat on one hand and the dog and the monkey on the other. The mouse and rat require lower levels of concentration, i.e. (1 to 2.5%) to influence the respiratory system but higher levels (2.5 to 5.0%) to affect the circulatory system. The respiratory systems of the monkey and the dog have about the same sensitivity as those of the other two species in that the threshold level of FC 11 is 2.5 to 5%. The circulatory systems of the monkey and the dog can be influenced by a concentration of 0.5%.

Aerosol Propellants↗
PubMed1975

Toxicity of aerosol propellants in the respiratory and circulatory systems. VI. Influence of cardiac and pulmonary vascular lesions in the rat.

Three propellants were selected for investigation in rats because of their non-uniform effect in mice and monkeys. Trichlorofluoromethane (FC 11) provoked arrhythmia in all three animal species, dichlorodifluoromethane (FC 12) in monkeys and rats but not in mice, and difluoroethane (FC 152a) only in rats. In rats the alterations in heart rate and electrocardiographic pattern during inhalation of these propellants are largely brought about by release of catecholamines from the adrenal gland, because adrenalectomy or prior injection of beta-adrenergic blocking drugs decreased the incidence of cardiac effects. Rats that have pulmonary vascular thrombosis or cardiac necrosis become more sensitive to proarrhythmic activity of these propellants.

Adrenal Glands↗
PubMed1975

Toxicity of aerosol propellants in the respiratory and circulatory systems. VII. Influence of pulmonary emphysema and anesthesia in the rat.

Experimental induction of pulmonary emphysema caused an increase in sensitivity of the rat to toxicity from inhalation of propellants. The emphysematous rat showed an exaggerated reduction in pulmonary compliance in response to inhalation of trichlorofluoromethane (FC 11). In emphysematous and non emphysematous rats without anesthesia the inhalation of FC 11 caused tachycardia, arrhythmias and other abnormalities in the electrocardiogram. The tachycardiac response was eliminated by induction of barbiturate anesthesia, which increased the sensitivity of the heart to occurrence of abnormalities in the electrocardiogram in response to inhalation of FC 11 as well as of dichlorodifluoromethane (FC 12) and difluoroethane (FC 152a). The acceleration in heart rate in response to inhalation of FC 11, hypoxia or hypercapnea was prevented by prior treatment with a beta-blocking drug.

Adrenergic beta-Antagonists↗
PubMed1975

Toxicity of aerosol propellants in the respiratory and circulatory systems. VIII. Respiration and circulation in primates.

The low-pressure propellants influence predominantly the circulation, whereas the high pressure propellants affect the respiration in anesthetized monkeys. There are four groups according to the level of toxicity: Class 1, low-pressure propellants of high toxicity that cause tachycardia and hypotension; Class 2, low-pressure propellants of intermediate toxicity that influence either circulation or respiration or both; Class 3, high-pressure propellants of intermediate toxicity that cause bronchoconstriction; and Class 4, high-pressure propellants of low toxicity that do not influence respiration or circulation even when inhaled at levels of up to 20 percent concentration.

Aerosol Propellants↗
PubMed1975

Hemodynamic effects of aerosol propellants. I. Cardiac depression in the dog.

The inhalation of fluorocarbons caused a depression of myocardial contractility, aortic hypotension, a decrease in cardiac output and an increase in pulmonary vascular resistance. The minimal concentrations that elicited these changes are as follows: 1% trichlorofluoromethane (FC11); 2.5% dichlorotetrafluoroethane (FC114); and 10% dichlorodifluoromethane (FC12). Inhalation of 20% octafluorocyclobutane (FC318) and difluoroethane (FC152a) did not influence these hemodynamic parameters. As in previous comparisons, the most widely used aerosol propellants are potentially cardiotoxic in the anesthetized dog.

Aerosol Propellants↗
PubMed1975

Hemodynamic effects of aerosol propellants. II. Pulmonary circulation in the dog.

The inhalation of trichlorofluoromethane (FC11), dichlorotetrafluoroethane (FC114) and dichlorodifluoromethane (FC12) caused a reduction in mean aortic blood pressure but only FC11 and FC114 caused a reduction in mean pulmonary arterial pressure. The primary cause of the fall is a decrease in pulmonary blood flow. When blood flow to a lobe is kept constant and the adrenergic alpha receptors are blocked by injection of phentolamine, the inhalation of FC11 caused vasodilation. In the intact circulation, the vasodilation is masked by release of catecholamines which constrict the pulmonary blood vessels.

Adrenergic alpha-Antagonists↗
PubMed1975

Cardiac effects of sodium selenite.

The classical idea that selenium is toxic to the heart at levels higher than available in a balanced diet is not supported by experimental work. In mice, treatment with sodium selenite increased the LD50 of ouabain and 2,4-dinitrophenol, and increased the tolerance to nitrogen inhalation. Although sodium selenite had no effect on the dog heart with circulation intact, there was a reduction in coronary vascular resistance in the heart-lung preparation. In the isolated ventricular segment perfused with blood, the administration of sodium selenite caused a positive inotropic effect which appeared even after blockade of beta-adrenergic receptors and in segments perfused with a Krebs-bicarbonate solution that was deficient in oxygen. These results cannot be explained merely as the correction of a selenium deficiency but rather as a positive influence of sodium selenite on the heart that has been acutely stressed by oxygen lack, ouabain, or 2,4-dinitrophenol.

Animals↗
PubMed1975

Antitussive drugs. I. Cardiopulmonary effects of codeine.

In the anesthetized dog, codeine causes a combination of pulmonary vasoconstriction and systemic vasodilation. Pulmonary blood flow is either increased or decreased, relating to a primary stimulation or depression of myocardial contractility. The overall effect is an elevation in pulmonary arterial pressure largely due to vasoconstriction of the pulmonary blood vessels.

Animals↗
PubMed1975

Antitussive drugs. II. Bronchopulmonary effects of dextromethorphan and doxylamine.

Unlike codeine, dextromethorphan does not cause pulmonary vasoconstiction in the anesthetized dog. The other effects of dextromethorphan are as follwos: a rise in pulmonary resistance indicating bronchoconstriction, and increase in pulmonary blood flow relating to a positive inotropic action, and a decrease in aortic blood pressure resulting from systemic vasodilation. These effects are blocked by previous injections of doxylamine, an antihistaminic drug. This interaction suggests a rationale for the combined use of dextromethorphan and doxylamine in the treatment of upper respiratory infection.

Airway Resistance↗