John Ludbrook APPS Symposium - Coronary-bronchial blood flow and airway dimensions in exercise-induced syndromes

1. We have an incomplete understanding of integrative cardiopulmonary contr ol during exercise and particularly during the postexercise period, when sy mptoms and signs of myocardial ischaemia and exercise-induced asthma not pr esent during exercise may appear. 2. The hypothesis is advanced that baroreflex de-resetting during exercise recovery is normally associated with (i) a dominant sympathetic vasoconstri ctor effect in the coronary circulation, which, when associated with obstru ctive coronary disease, may initiate a potentially positive-feedback cardio - cardiac sympathetic reflex (variable myocardial ischaemia with symptoms a nd signs); and (ii) a dominant parasympathetic bronchoconstrictor effect in the presence of bronchovascular dilatation, which, when associated with ra ised mediator release in the bronchial wall, reinforces the tendency for ai rway obstruction (variable dyspnoea results). 3. There is a need for new techniques to examine hypotheses concerning auto nomic control, during and after exercise, of the coronary and bronchial cir culations and the dimensions of airways. Accordingly, a new ultrasonic inst rument has been designed named an 'Airways Internal Diameter Assessment (AI DA) Sonomicrometer'. It combines pulsed Doppler flowmetry with transit-time sonomicrometry of airway circumference and single-crystal sonomicrometry o f airway wall thickness. Initial evaluation suggests it is relatively easy to apply during thoracotomy in recovery animals. The component devices are linear and will measure target variables with excellent accuracy. 4. In anaesthetized sheep, intubated with controlled ventilation, intraveno us isoproterenol causes large increases in bronchial blood flow, a fall in arterial pressure and a reduction in airway circumference. This may reflect the dominant action of reflex vagal activity over direct beta -adrenocepto r inhibition of bronchial smooth muscle, the reflex source being baroreflex secondary to the fall in arterial pressure. These findings provide insight into the integrative mechanisms underlying the paradoxical negative effect s sometimes observed when beta -adrenoceptor agonists are used in asthma.