Can we prevent coronary disease in Rhode Island?
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Biomedical subjects
Publications and source records attributed to R A Carleton.
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The mechanisms and potential mediator of hypercapneic pulmonary hypertension are incompletely understood. We studied 18 dogs, anaesthetised and spontaneously breathing both room air and after the inhalation of a gas mixture containing 10% CO2, 20.9% O2, and 69.1% N2, to determine the role of histamine, serotonin, and acidaemia in pulmonary hypertension produced by hypercapnia. Hypercapnia increased the mean pulmonary artery pressure by 0.33 kPa (2.5 mmHg) while wedge pressure and pulmonary arteriolar resistance did not change. Cardiac output significantly increased, indicating that the pulmonary hypertensive effect of hypercapnia is mainly flow related. Neither chlorpheniramine nor methysergide had significant effects on hypercapneic pulmonary hypertension. The infusion of sodium bicarbonate corrected the pH; pulmonary artery pressure and cardiac output increased while pulmonary arteriolar resistance dropped, suggesting that the increased cardiac output masked the effect of pH on pulmonary arteriolar resistance. The lack of effect of chlorpheniramine or methysergide on pulmonary resistances indicates that the vasoconstrictive effect of increased hydrogen ion concentration which accompanies hypercapnia is attributable neither to histamine nor to serotonin release.
Electrocardiographic excerpts from three patients demonstrate bigeminy, concealed bigeminy, trigeminy, concealed trigeminy, and Wenckebach's pattern of variation in the coupling interval from sinus beat to ventricular ectopic beat. These diverse manifestations of ventricular ectopy support the hypothesis that reentry in man reflects conduction of an initial impulse, with delay, to cause the coupled reentrant beat.
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An unusual electrocardiogram (ECG) is presented which demonstrates two mechanisms of communication between the atria and the ventricles. The first appears to reflect ordinary atrio-ventricular impulse propagation. The second appears likely to represent stimulation of the ventricles by mechanical atrial systole.
A well documented case of combined hypertrophic subaortic stenosis and calcific aortic stenosis is reported. Detection of multilevel involvement in cases of left ventricular outflow obstruction requires a high index of suspicion and precise hemodynamic and angiographic documentation. Careful analysis of the total data base is necessary for proper management of the patient. The pathogenesis of this combined lesion is unclear: Asymmetrical septal hypertrophy may occur as a consequence of the valvular stenosis, or it may be that abnormal leaflet motion in patients with hypertrophic obstruction produces leaflet thickening, calcification, deformity and stenosis.
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