Respiratory care with oxygen inhalation is often a necessity to maintain life, and it is one of the important therapeutic adjuncts in respiratory disease and in intensive care after surgery. However, it has been reported that oxygen toxicity occurs after prolonged exposure to 100% 0, [Smith, 1899; Kistler et al. 1967; Schaffner et al. 1967; Rowland and Newman, 1969. Subjective symptoms of oxygen toxicity include tracheal irritation, frequent cough, some burning sensation in the trachea, tachypnea, severe dyspnea, etc. [Welch, 1963; Fisher et al, 1968; Milier et al, 1970; Clark and Lambertsen, 1971; Sackner, 1975]. Pathologic findings are atelectasis, injuries to the pulmonary capillaries and hemorrhage in the alveoli in gross specimens. There can be inflammation, proliferation of fibrin, thickening of alveolar membranes, degeneration of collagen fibers and interstitial edema in the microscopic findings. [Penrod, 1956; Cedergren, 1959; Bean, 1965; Schaffner, 1967]. Dubois and colleagues [1961] found that the amount of pulmonary surfactant was decreased in oxygen toxicity and atelectasis followed by the decreased pulmonary surfactant. Many authors reported that vital capacity, inspiratory force, pulmonary compliance, pulmonary capillary blood flow and pulmonary elasticity were deceased and arteriovenous shunting increased. [Comroe et al, 1945; Fuson et al, 1965; Kistler et al, 1966; Knowles and Blenner-hassett, 1967; Barber et al, 1978]. Many human volunteers were examined after prolonged exposure in a high oxygenated chamber and there were a few reports on animals with oxygen toxicity, subjects including rabbits. Gas partial pressures of alveoli and arteries were measured in rabbits exposed to 100% 0, and the alveolar-arterial gas gradients were analyzed, which is the basis for the study of oxygen toxicity. These rabbits were divided into two groups; rabbits under natural respiration, and second group under artificial respiration with a respirator. The alveolar PO2 [PAO2] and PCO2 [PACO2], and the arterial PO2 [PaO2] were measured under varying 02 pressures; 15% 02, 21% 02 and 100% 02 The results obtained are as follows: 1. There are no significant changes in PaO2 and increases in PaCO2 resulting in an increase in [A-a] DO2 and [a-A] -DCO2 when subjects breath normal air after more than 65 hours exposures to 100% 02 2. Inhalations with 100% 02 or 15% 02 after the exposure to 100% 02 show the same trend of change in PaO2, PaCO2, [A-a] DO2 and [a-A] DCO2 as above. 3. The use of a respirator after exposure to 100% 02 does not show a significant difference in results compared to the natural respiration. 4. [A-a] DO2 was present in quite a few in less than 65 hours of exposure to 100% 02 and the value rapidly increased after 65 hours of exposure to 100% 02. These imply that there are [A-V] shunt in normal rabbits and also that the [A-V] sh