Mechanical ventilation modulates pro-inflammatory cytokine expression in spinal cord tissue after injury in rats.

RATIONALE: Spinal cord injury (SCI) may induce significant respiratory muscle weakness and paralysis, which in turn may cause a patient to require ventilator support. Central nervous system alterations can also exacerbate local inflammatory responses with immune cell infiltration leading to additional risk of inflammation at the injury site. Although mechanical ventilation is the traditional treatment for respiratory insufficiency, evidence has shown that it may directly affect distant organs through systemic inflammation. OBJECTIVES: This study aimed to better understand the impact of invasive mechanical ventilation on local spinal cord inflammatory responses following cervical or thoracic SCI. METHODS: Five groups of female Sprague-Dawley rats were anesthetised for 24 h. Three groups received mechanical ventilation: seven rats without SCI, seven rats with cervical injury (C4-C5), and seven rats with thoracic injury (T10); whereas, two groups were non-ventilated: six rats without SCI; and six rats with thoracic injury (T10). Changes in inflammatory responses were determined in the spinal cord tissues collected at the local site of injury. Cytokines were measured using ELISA. MAIN RESULTS: SCI induced local pro-inflammatory cytokine IL-6 expression for all groups. Mechanical ventilation also had effects on pro-inflammatory cytokines and independently increased TNF-α and decreased IL-1ß levels in the spinal cords of anesthetized rats. CONCLUSION: These data provide the first evidence that mechanical ventilation contributes to local inflammation after SCI and in the absence of direct tissue injury.

Spinal cord injury modulates the lung inflammatory response in mechanically ventilated rats: a comparative animal study.

Mechanical ventilation (MV) is widely used in spinal injury patients to compensate for respiratory muscle failure. MV is known to induce lung inflammation, while spinal cord injury (SCI) is known to contribute to local inflammatory response. Interaction between MV and SCI was evaluated in order to assess the impact it may have on the pulmonary inflammatory profile. Sprague Dawley rats were anesthetized for 24 h and randomized to receive either MV or not. The MV group included C4-C5 SCI, T10 SCI and uninjured animals. The nonventilated (NV) group included T10 SCI and uninjured animals. Inflammatory cytokine profile, inflammation related to the SCI level, and oxidative stress mediators were measured in the bronchoalveolar lavage (BAL). The cytokine profile in BAL of MV animals showed increased levels of TNF-α, IL-1ß, IL-6 and a decrease in IL-10 (P = 0.007) compared to the NV group. SCI did not modify IL-6 and IL-10 levels either in the MV or the NV groups, but cervical injury induced a decrease in IL-1ß levels in MV animals. Cervical injury also reduced MV-induced pulmonary oxidative stress responses by decreasing isoprostane levels while increasing heme oxygenase-1 level. The thoracic SCI in NV animals increased M-CSF expression and promoted antioxidant pulmonary responses with low isoprostane and high heme oxygenase-1 levels. SCI shows a positive impact on MV-induced pulmonary inflammation, modulating specific lung immune and oxidative stress responses. Inflammation induced by MV and SCI interact closely and may have strong clinical implications since effective treatment of ventilated SCI patients may amplify pulmonary biotrauma.

Placement of the nebulizer before the humidifier during mechanical ventilation: Effect on aerosol delivery.

BACKGROUND: Therapeutic aerosols are commonly used in mechanically ventilated patients. The position of the nebulizer in the ventilator circuit and the humidification of inhaled gases can influence the efficiency of aerosol delivery. We evaluated the effect of nebulizer position on the pulmonary bioavailability of nebulized ipratropium in ventilated patients without known preexisting respiratory disease. METHODS: The study included 38 mechanically ventilated and sedated patients after open heart surgery. Ipratropium (500 microg) was delivered by an ultrasonic nebulizer. Patients were randomized into 2 groups: the nebulizer positioned before the heat humidification system (group 1, n = 19) or at the end of the inspiratory limb before the Y-piece (group 2, n = 19). The amount of ipratropium in the urine collected during the 4 hours after drug administration was measured by mass spectrometry. RESULTS: There were no statistically significant differences in tidal volume or respiratory rate between groups. There were no significant differences between the 2 groups in the amount of drug excreted (group 1 vs 2: 13,237 +/- 2313 pg/mL vs 15,529 +/- 3204 pg/mL) or in pulmonary bioavailability (.9% +/- .1% vs 1.1% +/- .2%). CONCLUSION: The position of the nebulizer in the ventilatory circuit had no effect on the pulmonary bioavailability of ipratropium.