Granulocytes were collected from the lung lavage fluid of surfactant-depleted rabbits to assess the relationship between granulocyte-related lung injury and ventilatory mode. The number of lavaged granulocytes was determined after 2 and 4 h of conventional mechanical ventilation (2CMV and 4CMV, respectively) or high-frequency oscillatory ventilation (2HFO and 4HFO, respectively). Stimulated respiratory bursts were assayed by luminol-dependent chemiluminescence (LDCL) with N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulation in four groups of rabbits. The number of lavaged granulocytes significantly increased with ventilatory duration in the CMV mode but not in the HFO mode. Meanwhile, peak LDCL response value with FMLP stimulation in 4CMV was substantially lower than values in the other three groups. The decrease in the granulocyte LDCL response in 4CMV suggests oxygen metabolite exhaustion in the cells. CMV increasingly induced the accumulation of granulocytes with activated respiratory bursts in the alveolar spaces with ventilatory duration. HFO did not cause granulocyte accumulation, nor did it impair granulocyte function. The results suggest that HFO is useful for the prevention of lung injury related to activated granulocytes.
Previous studies have indicated that the hypometabolic response to hypoxia depends on ambient temperature (Ta), being more pronounced in the cold. If metabolic rate were an important contributor to the level of ventilation (VE), the magnitude of the hyperpneic response to hypoxia should also depend on Ta. We tested this hypothesis on adult conscious male rats. In normoxia, a drop in Ta from 25 to 10 degrees C increased O2 consumption and CO2 production (VO2 and VCO2, respectively, measured by an open-flow technique) and VE (measured with the barometric method) by 80 and 60%, respectively, with no changes in blood gases. At both Ta, hypoxia (10% inspired O2, 33-35 Torr arterial PO2) induced the same degree of hyperventilation, i.e., the same drop in arterial PCO2 (about -13 Torr). The hyperventilation at 25 degrees C Ta was achieved exclusively by an increase in VE, whereas at 10 degrees C Ta the hyperpnea was minimal (+15%) and accompanied by a drop (-30%) in VO2 and VCO2. Diaphragmatic electromyograms confirmed the VE results. Changes in blood pressure were similar at both Ta. Addition of 3% CO2 to the inspired air further increased VE, indicating that the hypoxic rat was not breathing at its maximal VE at either Ta. We conclude that, in the rat, changes in metabolic rate play an important role in the VE response to hypoxia and that Ta influences the response because of its effect on the degree of hypoxic hypometabolism.
We questioned whether the decrease in O2 consumption (VO2) during hypoxia in newborns is a regulated response or reflects a limitation in O2 availability. Experiments were conducted on previously instrumented conscious newborn dogs. VO2 was measured at a warm ambient temperature (30 degrees C, n = 7) or in the cold (20 degrees C, n = 6), while the animals breathed air or were sequentially exposed to 15 min of fractional inspired O2 (FIO2): 21, 18, 15, 12, 10, 8, and 6%. In normoxia, VO2 averaged 15 +/- 1 (SE) and 25 +/- 1 ml . kg-1 . min-1 in warm and cold conditions, respectively. In the warm condition, hypometabolism (i.e., hypoxic VO2 < normoxic VO2) occurred at FIO2 =10%, whereas in the cold condition, hypometabolism occurred at FIO2 =12%. The same results were obtained in a separate group (n = 14) of noninstrumented puppies. For all levels of FIO2 with hypometabolism, the relationships between measures of O2 availability (arterial O2 saturation or content, venous PO2 or saturation, x-axis) vs. VO2 (y-axis) had lower slopes in warm than in cold conditions. Hence, VO2 during hypometabolism in the warm condition was not the maximal attainable for the level of oxygenation. The results do not support the possibility that the hypoxic drop in VO2 in the newborn reflects a limitation in O2 availability. The results are compatible with the idea that the phenomenon is one of "regulated conformism" to hypoxia.
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