Pulmonary blood flow distribution and hypoxic pulmonary vasoconstriction in pentobarbital-anesthetized horses

by 1968- Lerche, Phillip

Anesthetized horses commonly develop undesirable hypoxemia when dorsally recumbent. The major reason for this is development of ventilation/perfusion (V/Q) mismatching associated with atelectasis of dependent lung tissue. Improving ventilation frequently does not improve oxygenation, suggesting that pulmonary blood flow distribution is abnormal during anesthesia. Perfusion is normally matched to ventilation by hypoxic pulmonary vasoconstriction (HPV). This mechanism causes pulmonary arterioles to constrict in areas where alveolar oxygen (O2) tension is low, redirecting blood flow to better-ventilated alveoli, and is believed to be modulated by nitric oxide (NO). The purpose of this study was to evaluate blood flow distribution in the anesthetized horse and to investigate the role of NO as a regulator of HPV in the anesthetized dorsally recumbent adult horse. Six adult horses anesthetized with pentobarbital were intubated via tracheostomy with a double-lumen tube, which separated gas flow to left and right lungs. Each lung was individually ventilated via a dual-lung ventilator, and 100% O2 was delivered to both lungs. A hypoxic/hyperoxic state was then induced by ventilating the left lung with 100% nitrogen (N2) while 100% O2 was delivered to the right lung. Nitric oxide (NO) production was manipulated by administration of L-arginine (a NO precursor) and L- ii NAME (a NO synthase inhibitor). Each horse was instrumented for collection of pulmonary and arterial blood O2 tensions. Pulmonary blood flow distribution was determined by the pattern of distribution of fluorescent microspheres, which were injected intravenously at strategic time points. Lungs were harvested, dried and sectioned prior to neutron activation and spectrographic analysis of the microspheres. Blood flow was influenced somewhat by gravity, however distribution was mainly heterogeneous in isogravitational planes, and highest in the central lung. Hypoxic pulmonary vasoconstriction was not active in this model, as evidenced by persistent systemic hypoxemia after ventilation of the left lung with 100% N2. Manipulation of NO produced appropriate changes in pulmonary arterial pressure, but had minimal effect on blood flow distribution and systemic arterial oxygenation. Our study suggest that manipulation of NO is unlikely to be helpful in correction of severe hypoxemia due to V/Q mismatching seen during anesthesia in clinical equine patients. iii