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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 (Saoo2, Svoo2), 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: Saoo2, –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.

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SYNOPSIS. An immunity to reinfection with E. bovis was demonstrated in 3 experiments involving 60 calves. This immunity develops rapidly, as indicated by resistance to a challenge given 14 days after the immunizing inoculation. In 3 groups of 3 to 6 young calves each, immunity was still present to a moderate degree 2 to 3 months after inoculation; in one group of 5 animals about a year old there was apparently a high degree of immunity about 7 months after the last inoculation. In one experiment an immunizing inoculum of 10,000 oöcysts did not produce as much immunity as 50,000 oöcysts. In 2 experiments there appeared to be little difference in the immunity produced by a single inoculation of 50,000 as compared with 100,000 oöcysts, but inoculation with 100,000 oöcysts, resulted in substantially longer and more severe illness than 50,000 oöcysts. There appeared to be no appreciable difference in clinical symptoms or development of immunity between calves given a single immunizing inoculum and those given the same number of oöcysts in 5 equal inocula on successive days. Treatment with sulfamethazine and sulfamerazine (Merameth) 13 to 15 days after inoculation alleviated the clinical symptoms of coccidiosis without interfering appreciably with the development of immunity. In one experiment with 7 calves, no beneficial effect was noted from 1 or 2 transfusions of 500 ml. of plasma and leucocytes from immune calves into 4 calves 1 and 12 days or 11 days after a challenge inoculation.

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