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Introduction: Ventilator-induced lung injury may be caused by overdistension of alveoli during high-pressure ventilation. In this study, we examined the effects of increasing inspiratory time on ventilator-induced lung injury., Methods: Sprague-Dawley rats were divided into four different groups with ten animals per group. Each group was then ventilated for 30 mins with one of four ventilator strategies. All groups were ventilated with an Fio2 of 1.0 and a positive end-expiratory pressure of 0 cm H2O. Group LoP was the negative control group and was ventilated with low pressures (peak inspiratory pressure = 12 cm H2O, rate = 30, and inspiratory time = 0.5 secs). Groups iT = 0.5, iT = 1.0, and iT = 1.5 were the experimental groups and were ventilated with high pressures (peak inspiratory pressure = 45 cm H2O, rate = 10, and inspiratory times = 0.5 secs, iT = 1.0 sec, and iT = 1.5 secs, respectively). Outcome measures included lung compliance, Pao /Fio ratio, wet/dry lung weight, and dry lung/body weight., Results: Final static lung compliance (p =.0002) and Pao2/Fio2 (p =.001) decreased as inspiratory time increased. Wet/dry lung weights (p <.0001) and dry lung/body weights (p <.0001) increased as inspiratory time increased. Light microscopy revealed evidence of intra-alveolar edema and hemorrhage in the iT = 1.0 and iT = 1.5 animals but not the LoP and iT = 0.5 animals., Conclusion: Increasing inspiratory time during high-pressure/high-volume mechanical ventilation is associated with an increase in variables of lung injury.

Cancer can be preferentially damaged and killed at temperatures above 41.0 degrees C. However, the heart and brain malfunction at this temperature, limiting the application of systemic hyperthermia in the treatment of metastatic cancer. We created a hyperthermic perfusion system that maximizes the temperature differential produced and extends the safe hyperthermic time. Mongrel dogs were anesthetized and mechanically ventilated. Temperature probes were placed in the rectum, bladder, peritoneal cavity, proximal aorta, pulmonary artery, and right tympanic canal. Venoarterial perfusion was instituted and the perfusate was warmed to 44 to 45 degrees C. The dogs' rectal temperature was elevated to > or = 42 degrees C for 4 hours. A small amount of venous blood was cooled to 28 to 30 degrees C and reperfused into the right atrium to maintain the pulmonary artery temperature < or = 38 degrees C. At the end of the perfusion, the dogs were decannulated, recovered, and returned to their cages for observation. Ten of 11 dogs survived the operative procedure, and no neurologic deficits were observed. The rectal temperature was successfully elevated to > or = 42 degrees C for 4 hours while maintaining the heart and brain at < or = 38 degrees C. Moderate serum biochemical changes were observed postprocedure. However, only the aspartate transaminase and alkaline phosphatase levels remained elevated above both the baseline and canine reference values by day 7. Lower abdominal and pelvic hyperthermia at 42 degrees C can be safely produced and maintained for 4 hours using an extracorporeal perfusion circuit, while protecting the heart and brain from temperature elevation.