Effects of prone and supine position on oxygenation and inflammatory mediator in a hydrochloric acid-induced lung dysfunction in rats (original) (raw)
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Effects of Pentoxifylline on TNF-Alpha and Lung Histopathology in HCl-Induced Lung Injury
Clinics, 2008
OBJECTIVE: To evaluate the effects of pentoxifylline on hydrochloric acid-induced lung lesions in rats subjected to mechanical ventilation. METHODS: Twenty male, adult Wistar-EPM-1 rats were anesthetized and randomly grouped (n=5 animals per group) as follows: control-MV (mechanical ventilation, MV group); bilateral instillation of HCl (HCl group); bilateral instillation of HCl followed by pentoxifylline (50 mg/kg bw) infusion (HCl+PTX group) and pentoxifylline infusion followed by bilateral instillation of HCl (PTX+HCl group). At 20, 30, 90 and 180 min after treatments, the blood partial pressures of CO 2 and O 2 were measured. The animals were euthanized, and bronchoalveolar lavages were taken to determine the contents of total proteins, corticosteroid and TNF-α. Samples of lung tissue were used for histomorphometric studies and determining the wet-to-dry (W/D) lung weight ratio. RESULTS: In the MV group, rats had alveolar septal congestion, and, in the HCl group, a remarkable recruitment of neutrophils and macrophages into the alveoli was noticed; these events were reduced in the animals with PTX+HCl. The partial pressure of oxygen increased in PTX+HCl animals (121±5 mmHg) as compared with the HCl (62±6 mmHg) and HCl+PTX (67±3 mmHg) groups within 30 minutes. TNF-α levels in bronchoalveolar lavage were significantly higher in the HCl group (458±50 pg/mL), reduced in the HCl+PTX group (329±45 pg/mL) and lowest in the PTX+HCl group (229±41 pg/mL). The levels of corticosteroid in bronchoalveolar lavage were significantly lower in the HCl (8±1.3 ng/mL) and HCl+PTX group (16±2 ng/mL) and were highest in the PTX+HCl (27±1.9 ng/mL). CONCLUSION: Pretreatment with PTX improves oxygenation, reduces TNF-α concentration and increases the concentration of corticosteroid in bronchoalveolar lavage upon lung lesion induced by HCl.
American Journal of Translational Research, 2021
Background: Acute respiratory distress syndrome (ARDS) is a severe form of respiratory failure characterized by altered lung mechanics and poor oxygenation. Bronchial hyperresponsiveness has been reported in ARDS survivors and animal models of acute lung injury. Whether this hyperreactivity occurs at the small airways or not is unknown. Objective: To determine ex-vivo small airway reactivity in a rat model of acute lung injury (ALI) by hydrochloric acid (HCl) instillation. Methods: Twelve anesthetized rats were connected to mechanical ventilation for 4-hour, and randomly allocated to either ALI group (HCl intratracheal instillation; n=6) or Sham (intratracheal instillation of 0.9% NaCl; n=6). Oxygenation was assessed by arterial blood gases. After euthanasia, tissue samples from the right lung were harvested for histologic analysis and wet-dry weight ratio assessment. Precision cut lung slice technique (100-200 μm diameter) was applied in the left lung to evaluate ex vivo small airway constriction in response to histamine and carbachol stimulation, using phase-contrast video microscopy. Results: Rats from the ALI group exhibited hypoxemia, worse histologic lung injury, and increased lung wet-dry weight ratio as compared with the sham group. The bronchoconstrictor responsiveness was significantly higher in the ALI group, both for carbachol (maximal contraction of 84.5±2.5% versus 61.4±4.2% in the Sham group, P<0.05), and for histamine (maximal contraction of 78.6±5.3% versus 49.6±5.3% in the Sham group, P<0.05). Conclusion: In an animal model of acute lung injury secondary to HCL instillation, small airway hyperresponsiveness to carbachol and histamine is present. These results may provide further insight into the pathophysiology of ARDS.
Jornal Brasileiro de Pneumologia, 2012
OBJETIVO: A ventilação mecânica (VM) por si própria pode contribuir diretamente para a lesão pulmonar. Assim, o objetivo do presente estudo foi investigar biomarcadores precoces relacionados ao equilíbrio oxidantes/antioxidantes, estresse oxidativo e inflamação causados por VM de curta duração em pulmões de camundongos saudáveis. MÉTODOS: Vinte camundongos C57BL/6 machos foram randomicamente divididos em dois grupos: VM, submetidos a VM com baixo volume corrente (V T, 6 mL/kg) por 30 min; e respiração espontânea (RE), utilizados como controles. Amostras de homogeneizados de pulmão foram testados quanto à atividade de enzimas antioxidantes, peroxidação lipídica e expressão de TNF-α. RESULTADOS: Comparados ao grupo RE, houve uma redução significativa na atividade de superóxido dismutase (≈35%; p < 0,05) e aumento da atividade de catalase (40%; p < 0,01), glutationa peroxidase (500%; p < 0,001) e mieloperoxidase (260%; p < 0,001), ao passo que a razão glutationa reduzida/gl...
2002
Purpose: To describe the epidemiology of the acute respiratory distress syndrome (ARDS) in a Brazilian ICU. Methods: This prospective observational, non-interventional study, included all consecutive patients with ARDS criteria [1] admitted in the ICU of a Brazilian tertiary hospital, between January 1997 and September 2001. Were collected in a prospective fashion the following variables: age, gender, APACHE II score at ICU admission and at ARDS diagnosis, cause of ARDS, presence of AIDS, cancer and immunosuppression, occurrence of barotrauma, performance of traqueostomy, mortality, duration of mechanical ventilation (MV), length of stay (LOS) in ICU and in hospital. The lung injury score (LIS) [2] was used to quantify the degree of pulmonary injury in the first week of ARDS. Results: There was 2182 patients (P) admitted in ICU during the study period, of whom 141 (6.46%) had ARDS criteria. Seventy-six (54%) were men, the mean age was 46 ± 18 years, APACHE II 18 ± 7 and 19 ± 7 at admission and at ARDS diagnosis, respectively. Septic shock accounted for 42% (60 P) of the ARDS causes, sepsis 22% (31 P), diffuse pulmonary infection 16% (23 P), aspiration pneumonia 11% (15 P), non-septic shock 5% (7 P) and others 4% (5 P). Ten percent (14 P) had AIDS, 30% (43 P) cancer and 25% (36 P) immunosuppression. All patients were mechanically ventilated with Tidal Volume between 4 and 8 ml/kg. Only 3.5% (5 P) had barotrauma and 10% (14 P) performed traqueostomy. Mortality rate was 79% in the ICU. The patients required 12 ± 10 days on MV, ranging from 1 to 55 days. The LOS in ICU and hospital was 14 ± 13 (1-69) days and 28 ± 32 (1-325) days, respectively. There was a time delay of 3.7 ± 4.5 days between admission in ICU and the onset of ARDS. The Murray score (mean ± SD) was 3.2 ± 0.4, 3 ± 0.5, 3 ± 0.5, 2.9 ± 0.6, 2.8 ± 0.7, 2.7 ± 0.7 and 2.6 ± 0.8 in the first 7 days, respectively. Conclusions: ARDS in our hospital has a similar incidence of reports in the USA and Europe. There was a higher mortality, which could be explained by a high incidence of infection causes of ARDS, mainly septic shock, and elevated combined occurrence of AIDS, cancer and immunosuppression, along the degree of LIS. The incidence of barotrauma was low, as a consequence of the current mechanical ventilation strategies.
BACKGROUND: Mechanical ventilation and administration of a high oxygen concentration are simultaneously used in the management of respiratory failure. We conducted this study to evaluate the effect of a high inspired oxygen concentration on ventilator-induced lung injury. METHODS: Forty sets of isolated/perfused rabbit lungs were randomized for 60 min of pressure-control ventilation at a plateau inspiratory pressure of 25 or 15 cm H 2 O and positive end-expiratory pressure of 3 cm H 2 O while receiving 100% or 21% O 2 . The temperature, pH, and partial pressure of CO 2 in the perfusate were maintained the same in all groups (n ϭ 10 for each group). The outcome measures used to assess lung injury included: the change in weight gain and ultrafiltration coefficient, the frequency of vascular failure, the histological lesions and the concentration of tumor necrosis factor-␣ and malondialdehyde in the bronchoalveolar lavage fluid. RESULTS: The two groups ventilated at the higher inspiratory pressure/tidal volume experienced greater weight gain and increases in the ultrafiltration coefficient, more frequently suffered vascular failure, and presented higher composite scores of histological damage than the two groups ventilated at the lower inspiratory pressure/tidal volume. Hyperoxia was not found to further increase any of the monitored markers of lung injury. No difference was noticed among the four experimental groups in the alveolar lavage fluid levels of tumor necrosis factor-␣ or malondialdehyde. CONCLUSIONS: These findings suggest that short-term administration of a high oxygen concentration is not a major determinant of ventilator-induced lung injury in this experimental model.
Clinics, 2015
OBJECTIVES: Hypertonic saline has been proposed to modulate the inflammatory cascade in certain experimental conditions, including pulmonary inflammation caused by inhaled gastric contents. The present study aimed to assess the potential anti-inflammatory effects of administering a single intravenous dose of 7.5% hypertonic saline in an experimental model of acute lung injury induced by hydrochloric acid. METHODS: Thirty-two pigs were anesthetized and randomly allocated into the following four groups: Sham, which received anesthesia and were observed; HS, which received intravenous 7.5% hypertonic saline solution (4 ml/kg); acute lung injury, which were subjected to acute lung injury with intratracheal hydrochloric acid; and acute lung injury + hypertonic saline, which were subjected to acute lung injury with hydrochloric acid and treated with hypertonic saline. Hemodynamic and ventilatory parameters were recorded over four hours. Subsequently, bronchoalveolar lavage samples were collected at the end of the observation period to measure cytokine levels using an oxidative burst analysis, and lung tissue was collected for a histological analysis. RESULTS: Hydrochloric acid instillation caused marked changes in respiratory mechanics as well as blood gas and lung parenchyma parameters. Despite the absence of a significant difference between the acute lung injury and acute lung injury + hypertonic saline groups, the acute lung injury animals presented higher neutrophil and tumor necrosis factor alpha (TNF-a), interleukin (IL)-6 and IL-8 levels in the bronchoalveolar lavage analysis. The histopathological analysis revealed pulmonary edema, congestion and alveolar collapse in both groups; however, the differences between groups were not significant. Despite the lower cytokine and neutrophil levels observed in the acute lung injury + hypertonic saline group, significant differences were not observed among the treated and non-treated groups. CONCLUSIONS: Hypertonic saline infusion after intratracheal hydrochloric acid instillation does not have an effect on inflammatory biomarkers or respiratory gas exchange.
Release of ANP and its physiological role in pulmonary injury due to HCl
The American journal of physiology
NARUSE, AND OSAHIKO ABE. Release of AAP and its physiological role in pulmonary injury due to HCl. Am. J. Physiol. 258 (Regulatory Integrative Comp. Physiol. '27): R690-R696, 1990.-The effect of pulmonary injury induced by aspiration of HCl on plasma atria1 natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration.