We studied the effect of systemic hypoxia on the bronchial vascular pressure-flow relationship in anesthetized ventilated sheep. The bronchial artery, a branch of the bronchoesophageal artery, was cannulated and perfused with a pump with blood from a femoral artery. Bronchial blood flow was set so bronchial arterial pressure approximated systemic arterial pressure. For the group of 25 sheep, control bronchial blood flow was 22 ml/min or 0.7 ml·min-1·kg-1. During the hypoxic exposure, animals were ventilated with a mixture of N2 and air to achieve an arterial PO2 (Pa(O)(2)) or 30 or 45 Torr. For the more severe hypoxic challenge, bronchial vascular resistance (BVR), as determined by the slope of the linearized pressure-flow curve, decreased acutely from 3.8 ± 0.4 mmHg·ml-1·min to 2.9 ± 0.3 mmHg·ml-1·min after 5 min of hypoxia. However, this vasodilation was not sustained, and BVR measured at 30 min of hypoxia was 4.2 ± 0.8 mmHg·ml-1·min. The zero flow intercept, an index of downstream pressure, remained unaltered during the hypoxic exposure. Under conditions of moderate hypoxia (Pa(O)(2) = 45 Torr), BVR decreased from 4.6 ± 0.3 to 3.8 ± 0.4 mmHg·ml-1·min at 5 min and remained dilated at 30 min (3.6 ± 0.5 mmHg·ml-1·min). To determine whether dilator prostaglandins were responsible for the initial bronchial vascular dilation under conditions of severe hypoxia (Pa(O)(2) ≃ 30 Torr), we studied an additional group of animals with pretreatment with the cyclooxygenase inhibitors indomethacin (2 mg/kg) and ibuprofen (12.5 mg/kg). Neither of these inhibitors blocked the acute bronchial hypoxic vasodilation. Thus the acute bronchial artery dilation observed with hypoxia is probably not due to release of dilator prostaglandins, and it is likely a direct effect of hypoxic blood on bronchial vascular smooth muscle, similar to the response of other systemic arteries.
ASJC Scopus subject areas
- Physiology (medical)