Pulmonary vascular response to acute hypoxia in normal, unanesthetized calves

¹ Department of Internal Medicine, University of Utah College of Medicine, Salt Lake City, Utah

The natural occurrence of altitude-dependent pulmonary hypertensive heart disease in cattle stimulated an investigation of the effect of experimentally induced acute hypoxia on the pulmonary vascular resistance of normal unanesthetized calves. Gas mixtures of 10–16% O₂ in N₂ were administered through an endotracheal tube, for periods averaging 7 min, 22 times during 19 studies in 15 animals. Cardiac catheterization and dye dilution techniques were used to measure arterial and mixed venous blood gas composition (Sa_oo2, Sv_oo2), pulmonary (PAP) and carotid arterial (CAP) pressures, and cardiac output (CI) before, during, and occasionally after hypoxia. Pulmonary artery wedge pressure was measured in some animals and did not change. Changes in calculated pulmonary vascular resistance (PVRI) were assessed to infer alterations in vascular tone. Mean changes ±se of various parameters were as follows: Sa_oo2, –30 ± 4%; CI, +1.57 ± 0.5 liters/min/m²; PAP, +12.7 ± 2 mm Hg; PVRI, +0.7 ± 0.3 mm Hg/liter/min/m². All were statistically significant at the 5% level. The relative increment in PAP was three times greater than in CI. It is concluded that hypoxia produces pulmonary vasoconstriction in these animals. The magnitude of the response is greater than has been observed in previous studies on intact unanesthetized animals of other species.

Note:
With the Technical Assistance of Filimon Ukradyha, Robert P. Carlisle, and Arthur S. Ruby