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Biomedical subjects

A Bush

Publications and source records attributed to A Bush.

At least 235 records · Page 13Linked to original sources
PubMed1989

Multiple pulmonary arteriovenous fistulas in childhood.

Three cases of multiple pulmonary arteriovenous fistulas are described in children who presented at five months, two and nine years of age. Mass spectrometry was used to measure pulmonary blood flow and, in two cases, the intrapulmonary right-to-left shunt. The shunt fractions were 51% and 35%, with no significant change on breathing 100% oxygen. In one case, effective pulmonary blood flow was measured during cardiac catheterisation by the argon-freon rebreathing method and agreed closely with that found from the Fick, principle with measured oxygen consumption. Treatment consisted of surgical ligation of a lower lobe pulmonary artery in the youngest child, balloon embolisation in the second, and initial surgical oversewing of a single large fistula followed twenty months later by steel coil embolisation in the third. The last and oldest child is well and no longer cyanosed. The first two children died seven months after treatment with evidence of progression of their pulmonary arteriovenous fistulas. The first of these, who also had an atrial septal defect and discordant thoraco-abdominal arrangement, died of heart failure. Autopsies on both children confirmed extensive involvement of both lungs by arteriovenous fistulas. In one case who had a diffuse, telangiectatic form of pulmonary arteriovenous fistulas, microscopic serial reconstructions of lung tissue revealed that anastomoses occurred between arteries accompanying terminal bronchioles and intra-acinar arteries and adjacent veins. Occlusion of the pulmonary arteries supplying the fistulas led to extensive fibrosis within them, and was associated with enlargement of the corresponding bronchial arterial circulation.

Arteriovenous Fistula↗
PubMed1989

Effects of infusion of prostacyclin on anatomical intrapulmonary right to left shunt: a useful model of human hypoxic vasoconstriction?

1. Eleven infants and children (mean age 4.3 years, range 0.2-12 years) with pulmonary vascular disease secondary to congenital cardiac anomalies (n = 6) or bronchopulmonary dysplasia (n = 5), were studied during cardiac catheterization while ventilated on 100% oxygen. 2. All had a raised pulmonary vascular resistance (mean 11.8 units, range 4.1-26.0 units, normal value less than 3 units) and a raised anatomical intrapulmonary right to left shunt (mean 22%, range 8-50%, normal value less than 5%). The elevated shunt was attributed to the effects of 100% oxygen and general anaesthesia causing alveolar collapse, with only partial compensation for impairment of gas exchange by compensatory local hypoxic vasoconstriction. 3. When prostacyclin was infused, pulmonary vascular resistance fell by 3.2 +/- 1.8 units (mmHg litre-1 min m2), and pulmonary blood flow rose by 1.0 +/- 0.7 litre min-1 m-2 (mean +/- 95% confidence intervals). 4. Intrapulmonary right to left shunt fraction increased in eight of 11 patients, with a maximal rise for the group of 5.9 +/- 4.6% (mean +/- 95% confidence intervals). However, even at doses of prostacyclin sufficient to cause systemic vasodilatation and tachycardia, there was no evidence for a selective increase in shunt fraction. 5. We suggest that studying the effects of therapeutic interventions on intrapulmonary shunt fraction may be a useful model in vivo of human hypoxic pulmonary vasoconstriction.

Blood Pressure↗
PubMed1989

Effect of infused adenosine on cardiac output and systemic resistance in normal subjects.

1. The purine nucleoside adenosine relaxes smooth muscle in vitro and is a vasodilator in animals, but its effects on cardiac output and systemic vascular resistance have not been measured in normal conscious human subjects. 2. We have studied the effects of infused adenosine in doses of 0.005, 0.03 and 0.07 mg kg-1 min-1 on pulmonary blood flow and systemic vascular resistance in eight healthy volunteers, using a non-invasive, inert gas method and mass spectrometry. 3. At a dose of 0.07 mg kg-1 min-1, there was a rise in effective pulmonary blood flow (which is approximately equivalent to cardiac output) of 0.52 +/- 0.08 l min-1 m-2 (mean +/- s.e. mean) and a fall in estimated systemic vascular resistance of 357 +/- 44 dyn s cm-5. Despite this marked systemic vasodilation, there was no significant change in mean heart rate. 4. The effects of this dose of adenosine were maximal 2 min after starting the infusion, and had disappeared within 5 min of stopping it. 5. Adenosine may be therapeutically useful in the reduction of left ventricular afterload, where the absence of reflex tachycardia may be advantageous. We suggest that adenosine in doses of 0.03 mg kg-1 min-1 should be evaluated as a selective pulmonary vasodilator.

Adenosine↗
PubMed1989

Comparison of the cardiovascular and pulmonary effects of oral celiprolol, propranolol and placebo in normal volunteers.

1. The effects on heart rate, blood pressure and pulmonary function of single oral doses of celiprolol hydrochloride (400 mg), and propranolol (40 mg) were compared with placebo in 12 healthy volunteers, in a double-blind three-period crossover study. 2. Celiprolol had no effect on heart rate while propranolol caused a significant reduction compared with placebo. Systolic blood pressure was reduced by propranolol but not celiprolol, whereas standing diastolic blood pressure was lowered by both drugs. 3. The maximal expiratory flow at 50% vital capacity (MEF.50), was significantly lower after propranolol compared with placebo and celiprolol. Celiprolol had no effect on the flow-volume loop parameters. 4. Effective pulmonary blood flow was significantly increased by celiprolol, but reduced by propranolol. 5. A high incidence of subjective side-effects were experienced on celiprolol (10/12; particularly unpleasant in 5). Side-effects were experienced to a lesser extent on placebo (8/12). Only one volunteer experienced a side-effect on propranolol. 6. Oral celiprolol exerts its hypotensive effect by vasodilatation without reflex tachycardia. It does not cause airways obstruction in healthy subjects.

Adrenergic beta-Antagonists↗
PubMed1988

Time course of the effects of epoprostenol on effective pulmonary blood flow in normal volunteers.

1. Epoprostenol (prostacyclin) has been widely used as a vasodilator, but its effects on cardiac output are controversial and the time course of its effects little studied. 2. We report its cardiovascular effects in doses of 5 and 10 ng kg-1 min-1 in six healthy volunteers. 3. Each of the two doses caused a mean 20% rise in effective pulmonary blood flow and a 15% rise in heart rate. These effects appeared to reach a maximum within 10 min of starting or increasing the rate of infusion, with no evidence of a rebound effect. 4. When the dose was reduced, heart rate and effective pulmonary blood flow appeared to reach a new steady state within 5 min of reducing or stopping the infusion. Only minor side-effects were encountered, and they were rapidly reversed on stopping the drug. 5. These results should be applied to the therapeutic use of epoprostenol as a vasodilator, particularly when titrating the optimum dose for a given individual.

Adult↗
PubMed1988

Correlations of lung morphology, pulmonary vascular resistance, and outcome in children with congenital heart disease.

Pulmonary vascular resistance was measured in air, oxygen, and after administration of vasodilators in 14 children with pulmonary hypertension and congenital heart disease. Lung morphology was examined by light microscopy and assessed quantitatively. In this selected group of patients (a) medial muscle thickness of greater than 20% in the intra-acinar arteries and Heath-Edwards changes of I or II were significantly associated with perioperative death from pulmonary complications after cardiac surgery; (b) children with lower percentage medial muscle thickness had a higher baseline resistance (r = -0.84) associated with Heath-Edwards grade III or higher changes (most of these patients were not offered corrective surgery); (c) when the lowest pulmonary vascular resistance was less than 3 units, Heath-Edwards grading was I or II (n = 4). When the pulmonary vascular resistance was greater than 6 units, however, there was no direct correlation with Heath-Edwards grading (n = 9). Four patients with a resistance of greater than 6 units had only grade I or II changes. Three had a medial muscle thickness above 20%, and were among those who died at or soon after operation. It is concluded that (a) patients with a lowest pulmonary vascular resistance of greater than 6 units have a bad prognosis whatever their lung morphology; and (b) some patients with Heath-Edwards grade I or II will have a high resistance (this group has a high medial muscle mass and a poor prognosis and would not be detected by Heath-Edwards grading alone).

Adult↗
PubMed1988

Comparison of the haemodynamic effects of epoprostenol (prostacyclin) and tolazoline.

The haemodynamic effects of infusion of epoprostenol (prostacyclin) and bolus injection of tolazoline were compared in a crossover study in 11 children with pulmonary hypertension caused by pulmonary vascular disease. The children were studied during cardiac catheterisation, while they were anaesthetised, paralysed, and ventilated with 100% oxygen. The order of drug administration was not randomised because tolazoline has a half life of hours whereas epoprostenol has a half life of a few minutes. Both drugs caused pulmonary and systemic vasodilatation, and there were no significant differences between the two. The 95% confidence intervals suggest that tolazoline did not have a clinically important haemodynamic advantage over epoprostenol. Previous reports suggest that serious side effects are common when tolazoline is used in repeated doses; epoprostenol has only a few minor side effects that are rapidly reversible when the infusion is stopped. Epoprostenol is more expensive than tolazoline but this study suggests that epoprostenol is a more suitable pulmonary vasodilator if more than a single dose is required.

Blood Pressure↗
PubMed1988

Diagnosis of pulmonary hypertension from radiographic estimates of pulmonary arterial size.

The reported accuracy of radiographic measurements in predicting pulmonary hypertension is very variable. Measurements of right and left descending pulmonary artery diameter have been reported to provide a correct diagnosis in as many as 98% of patients. A study was carried out to determine the predictive value of measurements made from the chest radiographs of 50 normal subjects and of 27 patients undergoing right heart catheterisation for cardiac or pulmonary vascular disease, taking account of radiographic magnification. After such corrections a right descending pulmonary artery diameter over 16.7 mm or a left descending pulmonary artery diameter of over 16.9 mm distinguished 12 of 23 pulmonary hypertensive subjects, with no false positive results. The diameter was then arbitrarily squared (any differences between patients and control subjects being exaggerated) and the product was divided by either predicted or actual lung volume in an attempt to correct for body size. The new index distinguished 19 of 23 patients with pulmonary hypertension, with one false positive, when the divisor was actual lung volume; when predicted lung volume was used 18 of 23 patients were distinguished, again with one false positive result.

Adult↗
PubMed1988

Rebreathing method for the simultaneous measurement of oxygen consumption and effective pulmonary blood flow during exercise.

This paper describes a rebreathing method for the simultaneous measurement of oxygen consumption (VO2) and effective pulmonary blood flow (QP. eff) at rest and during exercise. Subjects rebreathed a test gas consisting of 35% oxygen, 3.5% chlorodifluoromethane (freon-22), and 10% argon in nitrogen for 30 seconds or until the respired oxygen tension fell to below 13.3 kPa. Sixty normal subjects were studied on a motorized treadmill, the Bruce protocol being used. The rebreathing manoeuvre was performed at three minute intervals, and was initially practised sitting down. Measurements were then made with the subjects standing at rest, and subsequently during the last minute of each stage of the Bruce exercise protocol until the subjects were exhausted. Heart rate was recorded from the electrocardiogram. Oxygen uptake plotted against calculated power (watts) showed a discontinuity between resting and exercise values, probably because power output during treadmill exercise is underestimated. The arbitrary addition of 30 watts to the exercise power output abolished this discontinuity. There was good agreement between rebreathing estimates of oxygen consumption and values measured during a second exercise test by the conventional open circuit argon dilution method. Coefficients of variation of oxygen consumption and effective pulmonary blood flow measured by rebreathing were usually less than 10% even during maximal exertion. At rest mean (SD) effective pulmonary blood flow corrected for body surface area was 2.2 (0.46) l/min/m2. Effective pulmonary blood flow rose linearly with oxygen consumption. At rest the arteriovenous oxygen content difference for pulmonary blood (VO2/QP eff) was 9.1 (1.6) ml/dl, rising to a maximum of 16.4 (1.8) ml/dl. The stroke volume index was 27.5 (6.8) ml/m2, rising to a maximum of 46.5 (7.1) ml/m2 during exertion.

Adult↗
PubMed1988

Cardiovascular function at rest and on exercise in patients with cryptogenic fibrosing alveolitis.

Cardiovascular complications are common in fibrosing alveolitis, but there have been few physiological studies of the pulmonary circulation in this condition, and those that have been carried out have usually depended on right heart catheterisation. This paper reports non-invasive measurements of effective pulmonary blood flow, oxygen uptake, pulmonary arteriovenous oxygen content differences, and estimates of mixed venous oxygen saturation in 20 patients with histologically proved cryptogenic fibrosing alveolitis at rest and while exercising on a motorized treadmill. Results were compared with those of 20 age and sex matched normal subjects, at rest and at an arbitrarily chosen oxygen uptake of 0.75 l/min. The latter results were obtained by linear interpolation. Effective pulmonary blood flow was normal at rest, but oxygen dispatch to the tissues (blood flow x blood oxygen content) was significantly reduced at rest (mean reduction 190 (SD 68) ml/l/min; p less than 0.01) and at an oxygen uptake of 0.75 l/min (mean reduction 128 (50) ml/l/min; p less than 0.02), reflecting the presence of systemic arterial hypoxaemia. Pulmonary arteriovenous oxygen content differences were similar in patients and normal subjects, but mixed venous saturation was lower in the patients at rest (mean % reduction 6.8 (2.6); p less than 0.02) and at an oxygen uptake of 0.75 l/min (mean % reduction 9.6 (2.9); p less than 0.002). It is concluded that the supply of oxygen potentially available to the tissues is reduced at rest and during exercise in patients with fibrosing alveolitis and hence, by analogy with normal people exercising under hypoxic conditions, that pulmonary blood flow is inappropriately low in this condition. The low mixed venous oxygen saturation may contribute to the development of pulmonary hypertension in some patients. The rebreathing technique used in this study may be of use in monitoring treatment; it could be applied many times to the same patient, and might be a suitable way of following the response to pulmonary vasodilators.

Adult↗
PubMed1987

Primary biliary cirrhosis and ulcerative colitis.

Four patients with ulcerative colitis also had primary biliary cirrhosis, as judged by compatible liver histology, positive serum mitochondrial antibody tests, and normal cholangiography (in the 3 patients in whom it was performed). Primary biliary cirrhosis may be another hepatobiliary association of ulcerative colitis, and although less common than primary sclerosing cholangitis should be considered as a cause of cholestasis in these patients.

Adult↗
PubMed1987

Cardiovascular effects of tolazoline and ranitidine.

The cardiovascular effects of ranitidine were studied in 12 children with congenital heart disease who had been given tolazoline as a pulmonary vasodilator. Ranitidine was given as prophylaxis against gastrointestinal haemorrhage induced by tolazoline. Tolazoline 1-2 mg/kg caused significant falls in pulmonary and systemic vascular resistances and a rise in heart rate. After intravenous administration of ranitidine 3 mg/kg both resistances rose again and neither resistance then differed significantly from baseline levels. Heart rate also fell and the final heart rate was significantly below baseline levels. We conclude that there may be H2 receptors within the pulmonary and systemic circulations and that tolazoline may mediate some of its effects through these H2 receptors rather than by alpha adrenergic receptor blockade. The safety of H2 blockade in children, particularly those with pulmonary hypertension, needs further investigation.

Blood Circulation↗
PubMed1987

Modification of pulmonary hypertension secondary to congenital heart disease by prostacyclin therapy.

We have shown that PGI2 is a powerful but not selective pulmonary vasodilator, and we believe that there is a role for PGI2 in pulmonary vascular disease secondary to congenital heart disease, but much work remains to be done, including comparisons of PGI2 with other vasodilators. The role of PGI2 in altering the cellular and chemical events producing pulmonary vascular disease secondary to congenital heart disease, and any role in long-term treatment, is largely unexplored.

Child↗
PubMed1986

Use of different magnification factors to calculate radiological lung volumes.

In previous papers from this laboratory, Pierce et al described a method of measuring lung volumes from routine chest radiographs. The images on the film are magnified, and this was taken into account in their calculations. Their findings have recently been confirmed by Rodenstein et al. It is important to measure magnification accurately because errors in linear dimensions are cubed when volume is calculated. This paper describes two simple methods of improving the accuracy of the calculation of magnification.

Humans↗
PubMed1986

Does prostacyclin enhance the selective pulmonary vasodilator effect of oxygen in children with congenital heart disease?

We have obtained dose-response curves for the effects of prostacyclin on the pulmonary and systemic circulations in 20 children (median age 3 years) with pulmonary hypertension complicating congenital heart disease. Results were obtained with the children breathing both air and 100% oxygen. Under both sets of conditions, remote respiratory mass spectrometry was used to measure oxygen consumption and hence cardiac output by the direct Fick principle. When the subjects breathed air, prostacyclin caused a dose-dependent fall in pulmonary vascular resistance (measured in mm Hg . liter-1 . min . m2) (11.12 to 8.07, standard error of difference [SED] = 0.5, p less than .01). The level of the pulmonary vascular resistance when the subjects breathed air during the infusion of 20 ng/kg/min prostacyclin was not significantly different from that found when they breathed 100% oxygen and did not receive the drug (8.67 vs 8.93, SED = 0.55, p = NS). When infused while the subjects breathed 100% oxygen, prostacyclin caused additional dose-dependent pulmonary vasodilation (pulmonary vascular resistance 8.93 to 7.23, SED = 0.3, p less than .01). Unlike 100% oxygen, prostacyclin was not selective, and caused tachycardia and systemic hypotension at the higher doses. These results suggest that in children with congenital heart disease 100% oxygen does not maximally vasodilate the pulmonary circulation, and further pulmonary vasodilatation can be obtained with a blood-borne agent.

Adolescent↗