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Biomedical subjects

I G Town

Publications and source records attributed to I G Town.

5 recordsLinked to original sources
PubMed1998

Extreme hypoventilation reduces ventilator-induced lung injury during ventilation with low positive end-expiratory pressure in saline-lavaged rabbits.

OBJECTIVE: To compare the degrees of ventilator-induced lung injury caused by two ventilation protocols. DESIGN: Randomized trial. SETTING: University animal laboratory. SUBJECTS: Sixteen New Zealand white rabbits. INTERVENTIONS: After five sequential saline lung lavages, eight pairs of anesthetized rabbits were allocated randomly to receive either of two ventilation protocols for 4 hrs during neuromuscular blockade. Both groups received 3 cm H2O of positive end-expiratory pressure and 100% oxygen. Control group animals received an estimated tidal volume of 12 mL/kg, an inspiratory time of 0.7 sec, and a ventilatory rate adjusted for a PaCO2 of 35 to 45 torr (4.7 to 6 kPa). Study group animals were ventilated through an intratracheal catheter, with inspiratory time of 1.5 secs, ventilatory rate of 20 breaths/min, and peak inspiratory pressure of 4 to 8 cm H2O, adjusted to maintain PaCO2 at 150 to 250 torr (20 to 33 kPa). MEASUREMENTS AND MAIN RESULTS: Arterial blood gases were measured every 30 mins. After 4 hrs, a final lung lavage was performed. Physiologic parameters, cell counts and protein concentration in the final lavage, and lung histology were compared between groups. The alveolar-arterial oxygen tension gradient was higher in the study group over the first 1.5 hrs, but the time profile showed significantly (p = .001) greater improvement in the study group. After 4 hrs, the mean alveolar-arterial oxygen tension gradient was lower in the study group (94 torr [12.5 kPa] vs. 201 torr [26.8 kPa]). The increase in neutrophil count from the initial to the final lung lavage was lower in the study group (0.27 x 10(7) cells/L vs. 2.01 x 10(7) cells/L, p = .037), as was the absolute value of the neutrophil count in the final lavage (1.33 x 10(7) cells/L vs. 3.02 x 10(7) cells/L, p = .04). The median hyaline membrane score was lower in the study group (0.5 vs. 3.0) but the difference was not statistically significant. CONCLUSION: These findings suggest that a very low tidal volume reduces ventilator-induced lung injury in saline-lavaged rabbits during ventilation at low lung volume.

Animals↗
PubMed1996

Pressure-limited ventilation with permissive hypercapnia and minimum PEEP in saline-lavaged rabbits allows progressive improvement in oxygenation, but does not avoid ventilator-induced lung injury.

OBJECTIVE: To determine whether pressure-limited intermittent mandatory ventilation with permissive hypercapnia and positive end-expiratory pressure (PEEP) titrated to arterial oxygen tension (PaO2) prevents or reduces acute lung injury, compared to conventional ventilation, in saline-lavaged rabbits. DESIGN: Prospective randomised trial. SETTING: University animal laboratory. SUBJECTS: 18 New Zealand White rabbits. INTERVENTIONS: Following five sequential saline lung lavages, anaesthetised rabbits were randomly allocated in pairs to receive either of two ventilation protocols using intermittent mandatory ventilation. The study group had peak inspiratory pressure limited to 15 cm H2O and arterial partial pressure of carbon dioxide (PaCO2) was allowed to rise. The control group received 12 ml/kg tidal volume with rate adjusted for normocarbia. PEEP and fractional inspired oxygen (FIO2) were adjusted to maintain, PaO2 between 8 and 13.3 kPa (60 and 100 mm Hg) using a predetermined protocol. At 10 h or following death, lung lavage was repeated and lung histology evaluated. MEASUREMENTS AND MAIN RESULTS: The mean increase in lavage cell counts and protein concentration and hyaline membrane scores were not significantly different between the groups. Oxygenation progressively improved more in the study group (p = 0.01 vs control for PaO2/FIO2 ratio and alveolar-arterial oxygen tension gradient (AaDO2)). PEEP was similar and the mean airway pressure higher in the control group, suggesting that this probably resulted from less ventilator-induced injury in the study group. Four deaths occurred in the control group (three due to pneumothorax and one to hypoxaemia) and none in the study group (p = 0.08). CONCLUSIONS: This ventilatory protocol may have failed to prevent lung overdistension or it may have provided insufficient PEEP to prevent injury in this model; PEEP greater than the lower inflection point of the pressure-volume curve has been shown to prevent injury almost entirely.

Animals↗
PubMed1993

Temporal association between pulmonary inflammation and antioxidant induction following hyperoxic exposure of the preterm guinea pig.

The time course and nature of the pulmonary inflammatory and antioxidant responses, both during and after hyperoxic-induced acute lung injury were studied in the preterm guinea pig. Three-day preterm (65 days gestation) guinea pigs were randomly exposed to either 21% O2 (control) or 95% O2 (hyperoxia) for 72 hours. All pups were then maintained in ambient conditions for up to a further 11 days, during which time lung damage was monitored. In animals exposed to hyperoxia, evidence of acute lung injury and inflammation was characterized by a marked increase in microvascular permeability and elevated numbers of neutrophils in bronchoalveolar lavage fluid. Protein concentration, elastase-like activity and elastase-inhibitory capacity in lavage fluid were at a maximum at the end of the 72 hours hyperoxic exposure. Four days later, all values had returned to control levels. In contrast, increased numbers of neutrophils, macrophages and lymphocytes were recovered in the lavage fluid during this early recovery period. Coinciding with the influx of inflammatory cells, there was a significant increase in glutathione peroxidase, manganese superoxide dismutase and catalase activities in immature lung. Lung copper/zinc superoxide dismutase activity remained unchanged during both experimental periods. The strong temporal relationship between the influx of inflammatory cells to the lung and the induction of pulmonary antioxidant enzyme defences suggests that a common mechanism underlies both responses. These findings have led us to regard inflammation in the hyperoxic-injured immature lung as a beneficial event and not, as previously suggested, as part of the injurious process.

Animals↗