Abstract
The bronchial circulation supplies nutritive flow to the conducting airways.I studied the local control of blood flow in the bronchial circulation of dogs. The three aims of my study of the bronchial circulation were to determine: 1) distribution of blood flow from the right bronchial artery: 2) the role of autoregulation; and 3) the role of adenosine as a metabolic vasodilator.|I cannulated the right bronchial artery (BA) of chloralose anesthetized, artificially ventilated dogs for constant pressure perfusion and drug infusion. In Aim 1, I measured the distribution of BA flow by infusing 15.1 /vm colored microspheres into the BA of 14 dogs. The results indicate the right main bronchus and right upper lobar bronchi receive most of their blood flow from the BA.|In Aim 2, in 11 dogs, BA perfusion pressure was set at 75, 90, 100, and 115 mmHg, and BA flow was measured with a flow probe to determine whether the bronchial circulation autoregulates. If autoregulation occurred, bronchial vascular conductance (Cbr, calculated as [(flow/perfusion pressure) x 100]) would decrease with increasing perfusion pressure. However, Cbr increased from 1.4±0.7 (SE) to 3.8±0.6 ml/ml/100mmHg (P< 0.0001) as pressure increased. The bronchial circulation has two drainage pathways, one systemic and another anastomotic with the pulmonary circulation. I hypothesized that only the “systemic” pathway supplying the central airways would autoregulate. Therefore, I measured bronchial blood flow to the right central airways with|microspheres and varied pressure from 75-115 mmHg. Central airway vascular conductance increased from 3.8±1.3 to 8.7±1.8 ml/min/100g/100mmHg (P< 0.02), indicating the absence of autoregulation.|In Aim 3, in 7 dogs, I infused an adenosine receptor antagonist, DMPX (1.1/vmol/min), into the BA, to determine if adenosine mediates bronchial vasodilation during airway smooth muscle contraction. DMPX blocked vasodilation to infused adenosine (0.01-0.1/vmol/min). DMPX did not reduce the vasodilation during airway smooth muscle contraction evoked by stimulating airway afferents with hypertonic saline (ACbr = 4.7±1.2 before and 4.2±0.9 ml/min/100mmHg during DMPX) or capsaicin (ACbr = 6.9±1.7 before and 7.7±1.8 ml/min/100mmHg during DMPX). To determine if adenosine is responsible for the reactive hyperemia after lung hyperinflation, I repeated lung inflation before and during DMPX. DMPX did not reduce the vasodilation following lung inflation (ACbr = 1.9±0.4 before and 1.2±0.2 ml/min/100mmHg during DMPX). Therefore, bronchial vasodilation accompanying airway smooth muscle contraction or lung inflation does not require adenosine.