C M Busst
6 Papers
157 Citations
C M Busst is an academic researcher. The author has contributed to research in topics: Pulmonary hypertension & Vascular resistance. The author has an hindex of 5, co-authored 6 publications.
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Papers
Correlations of lung morphology, pulmonary vascular resistance, and outcome in children with congenital heart disease.
Andrew Bush,C M Busst,Sheila G. Haworth,Alison A. Hislop,W B Knight,B Corrin,Elliot A. Shinebourne +6 more
TL;DR: Patients with a lowest pulmonary vascular resistance of greater than 6 units have a bad prognosis whatever their lung morphology; and 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).
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Does prostacyclin enhance the selective pulmonary vasodilator effect of oxygen in children with congenital heart disease
TL;DR: It is suggested 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.
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Cardiovascular effects of tolazoline and ranitidine.
TL;DR: It is concluded that there may be H2 receptors within the pulmonary and systemic circulations and that tolazoline may mediate some of its effects through these H2 receptor rather than by alpha adrenergic receptor blockade.
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Comparison of the haemodynamic effects of epoprostenol (prostacyclin) and tolazoline.
TL;DR: 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, and it is suggested that epop Frostenol is a more suitable pulmonary vasodilator if more than a single dose is required.
Effects of infusion of prostacyclin on anatomical intrapulmonary right to left shunt: a useful model of human hypoxic vasoconstriction?
TL;DR: It is suggested that studying the effects of therapeutic interventions on intrapulmonary shunt fraction may be a useful model in vivo of human hypoxic pulmonary vasoconstriction in infants and children with pulmonary vascular disease secondary to congenital cardiac anomalies.
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