Biomedical subjects
E Byrne-Quinn
Publications and source records attributed to E Byrne-Quinn.
Aminorex (Menocil) and amphetamine: acute and chronic effects on pulmonary and systemic haemodynamics in the calf.
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Hypoxic and hypercapnic ventilatory drives in children native to high altitude.
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Augmentation of chemosensitivity during mild exercise in normal man.
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Ventilatory control in normal man: effects of acute exercise, chronic physical conditioning and chronic hypoxia.
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Forearm circulation in man at high altitude.
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Ventilatory control in the athlete.
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Acquired attenuation of chemoreceptor function in chronically hypoxic man at high altitude.
To determine whether chronic exposure to hypoxia during adulthood produces alterations in the control of ventilation, measurements of the resting ventilatory response to hypoxia and hypercapnia, as well as ventilatory response to hypoxia during exercise, were carried out in a group of 10 long-term (3-39 yr) non-native residents of Leadville, Colo. (elevation 3100 m). A group of 8 subjects native to Leadville was also studied and 10 low altitude subjects of Denver, Colo. (elevation 1600 m) served as controls. Hypoxic ventilatory drive was measured as the shape parameter A of isocapnic VE-PA(o2) curves. In the non-native high altitude resident this parameter averaged 43% of the value for low altitude controls (P<0.05) denoting a diminished ventilatory response to hypoxia. The degree of attenuation was related to the length of time spent at high altitude. In the high altitude natives the parameter A averaged 9.6% of control (P<0.01). Similarly hypercapnic ventilatory drive as measured by the slope of the isoxic VE-PA(co2) lines was reduced in the non-native residents to 65% of control (P<0.05) and in the natives averaged 54% of control (P<0.01). In contrast with these findings at rest induction of hypoxia during exercise produced an increase in ventilation comparable to that in the controls in both groups of highlanders. Hence chronic exposure to hypoxia during adulthood in man results in marked attenuation of the ventilatory response to hypoxia at rest and this is a function of the length of exposure to hypoxia. This attenuation of the ventilatory response to hypoxia was associated with a decrease in hypercapnic ventilatory drive. The fact that hypoxic ventilatory drive was almost completely absent while hypercapnic drive was only partially reduced parallels closely the more important role of the peripheral chemoreceptors in mediating ventilatory responses to hypoxia than to hypercapnia. This suggests that the alterations in ventilatory control at altitude are due to failure of peripheral chemoreceptor function.
Maintenance of sinus rhythm after DC reversion of atrial fibrilllation. A double-blind controlled trial of long-acting quinidine bisulphate.
Ninety-two patients were entered in a double-blind controlled trial of long-acting quinidine bisulphate for the maintenance of sinus rhythm following DC reversion of atrial fibrillation. By random selection two statistically comparable groups of patients were obtained, a control group being given a placebo and a treated group quinidine bisulphate 1.5 g. per day in two 12-hourly doses. Thirty-seven patients were followed up in the control group and twenty-eight patients in the treated group. The maintenance of sinus rhythm in the treated group was significantly longer than in the control group, especially during the first three months. The mean serum quinidine level in the treated group was 2.2+/-0.3 (SEM) mg. per litre. There was one death among the patients treated with quinidine, which may have been due to quinidine toxicity caused by a high serum quinidine level.
Hypoxic ventilatory drive in normal man.
A technique is described which permits the inscription of the ventilatory response to isocapnic hypoxia in man as a continuous curve relating alveolar oxygen tension and minute ventilation. The adjustment of ventilation to changes in alveolar oxygen tension is complete in 18-23 sec and this is sufficiently rapid to justify the use of a non-steady-state method. Changes in alveolar carbon dioxide tension are prevented by addition of carbon dioxide to the inspired gas. The resulting [unk]V(E)-P(Ao2) curves are hyperbolic such that falling P(Ao2) produces only slight rises in [unk]V(E) until a critical P(Ao2) range of 50-60 mm Hg is reached. With further fall in P(Ao2), [unk]V(E) increases steeply and the slope of the curve approaches infinity at a tension of 30-40 mm Hg. For purposes of quantitation these curves are approximated by a simple hyperbolic function, the parameters of which are evaluated by a least squares fit of the data. The parameter A denotes curve shape such that the higher the value of A. the greater the increase in ventilation for a given decrease in P(Ao2) and hence the greater the hypoxic drive. Curves are highly reproducible for each subject and curves from different subjects are similar. In 10 normal subjects at resting P(ACo2), A = 180.2 +/-14.5 (SEM). When P(ACo2) is adjusted to levels 5 mm Hg above and below control in six subjects A = 453.4 +/-103 and 30.2 +/-6.8 respectively. These latter values differed significantly from control (P < 0.05). These changes in curve shape provide a clear graphic description of interaction between hypercapnic and hypoxic ventilatory stimuli. At normal P(ACo2) the [unk]V(E)-P(Ao2) curve has an inflection zone located over the same P(o2) range as the inflection in the oxygen-hemoglobin dissociation curve. This indicated that ventilation might be a linear function of arterial oxygen saturation or content. Studies in four subjects have demonstrated that ventilation is indeed related to arterial oxygen content in a linear fashion. These data suggest, but do not prove, that oxygen tension in chemoreceptor tissue as in part determined by circulatory oxygen delivery may be an important factor in controlling the ventilatory response to hypoxia.
Beriberi heart disease in London.
Haemodynamic measurements before and after treatment are described in two patients with beriberi heart disease. The first patient had severe disease with a cardiac output of 17.3 litres per minute, which had returned to normal a month later. The second patient had moderate disease with a cardiac output of 7.4 litres per minute; a fall in this and a rise in systemic vascular resistance was found one and two hours after the intravenous injection of aneurine hydrochloride. The plasma pyruvate concentration was raised in the first patient but only slightly so in the second, in whom the pyruvate metabolism test was abnormal. The haemodynamic studies in both cases were of considerable help in making the diagnosis. The diagnosis of beriberi should be considered in any patient with heart disease who has a history of alcoholism, especially as prompt vitamin treatment is curative.