Hemorrhagic shock causes a reduction in oxygen supply to tissues leading to increased reactive oxygen species resulting in lung injury. Often mechanical ventilation is required as supportive treatment;however, ventila...Hemorrhagic shock causes a reduction in oxygen supply to tissues leading to increased reactive oxygen species resulting in lung injury. Often mechanical ventilation is required as supportive treatment;however, ventilation can also induce lung injury and apoptosis. The purpose of this study was to examine the effects of three modes of controlled mechanical ventilation: volume control, pressure control, and pressure regulated volume control on lung injury as measured by hydrogen peroxide and apoptosis during hemorrhagic shock. Male Sprague-Dawley rats were randomized to the three controlled mechanical ventilation groups. Hemorrhagic shock was elicited by removing approximately 40% of the blood volume over 30 minutes. The rats were treated with one of three modes of mechanical ventilation with 40% oxygen for 60 minutes. The lungs were removed and measured for hydrogen peroxide and apoptosis based on nuclear differential dye uptake. There were no significant differences in hemodynamics, arterial blood values, peak inspiratory pressures, tidal volume, respiratory rates, and intrathoracic pressures across three groups. However, lung hydrogen peroxide production and apoptosis were significantly increased in volume control and pressure control, compared to pressure-regulated volume control. In this study, early signs of ventilator induced lung injury were not detected using commonly employed clinical measurements. However, when examining lung cellular injury (hydrogen peroxide and apoptosis), we were able to measure significant lung damage in volume control and pressure control, but not pressure-regulated volume control. Thus, our results suggest that pressure-regulated volume control is the preferable mode of mechanical ventilation during hemorrhagic shock.展开更多
文摘Hemorrhagic shock causes a reduction in oxygen supply to tissues leading to increased reactive oxygen species resulting in lung injury. Often mechanical ventilation is required as supportive treatment;however, ventilation can also induce lung injury and apoptosis. The purpose of this study was to examine the effects of three modes of controlled mechanical ventilation: volume control, pressure control, and pressure regulated volume control on lung injury as measured by hydrogen peroxide and apoptosis during hemorrhagic shock. Male Sprague-Dawley rats were randomized to the three controlled mechanical ventilation groups. Hemorrhagic shock was elicited by removing approximately 40% of the blood volume over 30 minutes. The rats were treated with one of three modes of mechanical ventilation with 40% oxygen for 60 minutes. The lungs were removed and measured for hydrogen peroxide and apoptosis based on nuclear differential dye uptake. There were no significant differences in hemodynamics, arterial blood values, peak inspiratory pressures, tidal volume, respiratory rates, and intrathoracic pressures across three groups. However, lung hydrogen peroxide production and apoptosis were significantly increased in volume control and pressure control, compared to pressure-regulated volume control. In this study, early signs of ventilator induced lung injury were not detected using commonly employed clinical measurements. However, when examining lung cellular injury (hydrogen peroxide and apoptosis), we were able to measure significant lung damage in volume control and pressure control, but not pressure-regulated volume control. Thus, our results suggest that pressure-regulated volume control is the preferable mode of mechanical ventilation during hemorrhagic shock.
