Surfactant depletion is most often used to study acute respiratory failure in animal models. Because model stability is often criticized, the authors tested the following hypotheses: Repeated pulmonary lavage with normal saline provides stable experimental conditions for 24 hours with a PaO2/FiO2 ratio < 300 mm Hg. Lung injury was induced by bilateral pulmonary lavages in 8 female pigs (51.5 +/- 4.8 kg). The animals were ventilated for 24 hours (PEEP: 5 cm H2O; tidal volume: 6 mL/kg; respiratory rate: 30/min). After 24 hours the animals were euthanized. For histopathology slides from all pulmonary lobes were obtained. Supernatant of the bronchoalveolar fluid collected before induction of acute respiratory distress syndrome (ARDS) and after 24 hours was analyzed. A total of 19 +/- 6 lavages were needed to induce ARDS. PaO2/FiO2 ratio and pulmonary shunt fraction remained significantly deteriorated compared to baseline values after 24 hours (P < .01). Slight to moderate histopathologic changes were detected. Significant increases of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 were observed after 24 hours (P < .01). The presented surfactant depletion-based lung injury model was associated with increased pulmonary inflammation and fulfilled the criteria of acute ling injury (ALI) for 24 hours.
OBJECTIVE: Systemic PaO2 oscillations occur during cyclic recruitment and derecruitment of atelectasis in acute respiratory failure and might harm brain tissue integrity. DESIGN: Controlled animal study. SETTING: University research laboratory. SUBJECTS: Adult anesthetized pigs. INTER-VENTIONS: Pigs were randomized to a control group (anesthesia and extracorporeal circulation for 20 hr with constant PaO2, n = 10) or an oscillation group (anesthesia and extracorporeal circulation for 20 hr with artificial PaO2 oscillations [3 cycles min¹], n = 10). Five additional animals served as native group (n = 5). MEASUREMENTS AND MAIN RESULTS: Outcome following exposure to artificial PaO2 oscillations compared with constant PaO2 levels was measured using 1) immunohistochemistry, 2) real-time polymerase chain reaction for inflammatory markers, 3) receptor autoradiography, and 4) transcriptome analysis in the hippocampus. Our study shows that PaO2 oscillations are transmitted to brain tissue as detected by novel ultrarapid oxygen sensing technology. PaO2 oscillations cause significant decrease in NISSL-stained neurons (p < 0.05) and induce inflammation (p < 0.05) in the hippocampus and a shift of the balance of hippocampal neurotransmitter receptor densities toward inhibition (p < 0.05). A pathway analysis suggests that cerebral immune and acute-phase response may play a role in mediating PaO2 oscillation-induced brain injury. CONCLUSIONS: Artificial PaO2 oscillations cause mild brain injury mediated by inflammatory pathways. Although artificial PaO2 oscillations and endogenous PaO2 oscillations in lung-diseased patients have different origins, it is likely that they share the same noxious effect on the brain. Therefore, PaO2 oscillations might represent a newly detected pathway potentially contributing to the crosstalk between acute lung and remote brain injury.
SummaryBackgroundIntra-vesical pressure measurement as the reference standard for assessing intra-abdominal pressures is mainly indirect and discontinuous. We therefore evaluated a motility capsule for continuous intra-abdominal pressure measurement in an animal model with a high probability for capillary leakage and intestinal edema.Material/MethodsMotility capsules were inserted into the stomachs of 8 anesthetized and ventilated pigs. Stomach pH, pressure, and temperature data were wirelessly transmitted to a recorder attached to each animal’s abdomen. Intra-gastric pressures measured by the capsule were compared to intra-vesical pressures measured by a pressure transducer system.ResultsThe intra-abdominal pressures ranged from 3 to 15 mmHg (7.8±2.4 mmHg [mean ±SD]) measured via the bladder. The capsule pressure recordings ranged from 1 to 3 mmHg (1.7±0.5 mmHg [mean ±SD]). Bland-Altman analysis revealed an unacceptable bias between the 2 methods. The test bias was 6.2 (±1.4) mmHg and the limits of agreement were from 3.3 to 8.9 mmHg.ConclusionsPressures in the stomach as measured by motility capsule underestimated the intra-vesical pressures. Discrepancies between gastric and intra-vesical pressures could be caused by gastric dilatation or different position of the 2 devices to the zero reference point.
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