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Your search keyword '"Respiration, artificial"' showing total 4 results
Start Over Descriptor "Respiration, artificial" Topic respiration Journal experimental lung research
4 results on '"Respiration, artificial"'

1. EXOGENOUS SURFACTANT RESTORES LUNG FUNCTION BUT NOT PERIPHERAL IMMUNOSUPPRESSION IN VENTILATED SURFACTANT-DEFICIENT RATS.

Author

Vreugdenhil, Harriet A., Lachmann, Burkhard, Haitsma, Jack J., Zijlstra, Jitske, Heijnen, Cobi J., Jansen, Nicolaas J., and van Vught, Adrianus J.

Subjects
*ARTIFICIAL respiration, *SURFACE active agents, *PNEUMONIA, *LUNG diseases, *LABORATORY rats
Abstract

The authors have previously shown that mechanical ventilation can result in increased pulmonary inflammation and suppressed peripheral leukocyte function. In the present study the effect of surfactant therapy on pulmonary inflammation and peripheral immune function in ventilated surfactant-deficient rats was assessed. Surfactant deficiency was induced by repeated lung lavage, treated rats with surfactant or left them untreated, and ventilated the rats during 2 hours. Nonventilated rats served as healthy control group. Expression of macrophage inflammatory protein (MIP)-2 was measured in bronchoalveolar lavage (BAL), interleukin (IL)-1β, and heat shock protein 70 (HSP70) were measured in total lung homogenates. Outside the lung phytohemagglutinin (PHA)-induced lymphocyte proliferation, interferon (IFN)-γ and IL-10 production, and natural killer activity were measured in splenocytes. After 2 hours of mechanical ventilation, expression of MIP-2, IL-1β, and HSP70 increased significantly in the lungs of surfactant-deficient rats. Outside the lung, mitogen-induced proliferation and production of IFN-γ and IL-10 reduced significantly. Only natural killer cell activity remained unaffected. Surfactant treatment significantly improved lung function, but could not prevent increased pulmonary expression of MIP-2, IL-1β, and HSP70 and decreased peripheral mitogen-induced lymphocyte proliferation and IFN-γ and IL-10 production in vitro. In conclusion, 2 hours of mechanical ventilation resulted in increased lung inflammation and partial peripheral leukocyte suppression in surfactant-deficient rats. Surfactant therapy ameliorated lung function but could not prevent or restore peripheral immunosuppression. The authors postulate that peripheral immunosuppression may occur in ventilated surfactant deficient patients, which may enhance susceptibility for infections. [ABSTRACT FROM AUTHOR]

Published
2006
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2. Role of nitric oxide in hyperpnea-induced bronchoconstriction and airway microvascular permeability in guinea pigs

Author

Patrícia Pennacchioni-Alves, Fernanda Degobi Tenório Quirino dos Santos Lopes, Celso R. F. Carvalho, Rodolfo de Paula Vieira, Milton A. Martins, Fabia B Pianheri, and Fernanda Magalhães Arantes-Costa

Subjects
Male, Pulmonary and Respiratory Medicine, Bronchoconstriction, Guinea Pigs, Clinical Biochemistry, Hyperpnea, Vascular permeability, Pharmacology, Nitric Oxide, Nitric oxide, Capillary Permeability, Random Allocation, chemistry.chemical_compound, Respiration, medicine, Animals, Respiratory system, Molecular Biology, Evans Blue, business.industry, medicine.disease, Respiration, Artificial, Extravasation, NG-Nitroarginine Methyl Ester, Breath Tests, chemistry, Anesthesia, Nitric Oxide Synthase, medicine.symptom, business
Abstract

The present study aimed to evaluate the role of nitric oxide (NO) on hyperpnea-induced bronchoconstriction (HIB) and airway microvascular hyperpermeability (AMP). Sixty-four guinea pigs were anesthetized, tracheotomized, cannulated, and connected to animal ventilator to obtain pulmonary baseline respiratory system resistance (Rrs). Animals were then submitted to 5 minutes hyperpnea and Rrs was evaluated during 15 minutes after hyperpnea. AMP was evaluated by Evans blue dye (25 mg/kg) extravasation in airway tissues. Constitutive and inductible NO was evaluated by pretreating animals with N(G)-nitro-L-arginine methyl ester (L-NAME) (50 mg/kg), aminoguadinine (AG) (50 mg/kg), and L-arginine (100 mg/kg) and exhaled NO (NOex) was evaluated before and after drug administration and hyperpnea. The results show that L-NAME potentiated (57%) HIB and this effect was totally reversed by L-arginine pretreatment, whereas AG did not have effect on HIB. L-NAME decreased basal AMP (48%), but neither L-NAME nor AG had any effect on hyperpnea-induced AMP. NOex levels were decreased by 50% with L-NAME, effect that was reversed by L-arginine treatment. These results suggest that constitutive but not inducible NO could have a bronchoprotective effect on HIB in guinea pigs. The authors also observed that neither constitutive nor inducible NO seems to have any effect on hyperpnea-induced AMP.

Published
2010

3. LUNG MECHANICS IN THE TIMP3 NULL MOUSE AND ITS RESPONSE TO MECHANICAL VENTILATION

Author

Lynda McCaig, Erica L. Martin, Ruud A. W. Veldhuizen, James F. Lewis, Timothy C. Bailey, Emily A. Truscott, and Kevin J. Leco

Subjects
Lung Diseases, Pulmonary and Respiratory Medicine, medicine.medical_specialty, Pathology, Pulmonary Surfactant-Associated Proteins, medicine.medical_treatment, Clinical Biochemistry, Respiratory physiology, Pulmonary compliance, Mice, Airway resistance, Internal medicine, Respiration, Animals, Medicine, Gene Silencing, Lung Compliance, Molecular Biology, Mice, Knockout, Tissue Inhibitor of Metalloproteinase-3, Mechanical ventilation, business.industry, Airway Resistance, Null (mathematics), Respiration, Artificial, Compliance (physiology), Respiratory Mechanics, Cardiology, Breathing, business, Bronchoalveolar Lavage Fluid
Abstract

Tissue inhibitor of metalloproteinase-3 (TIMP3) null mice develop emphysema-like airspace enlargement due to an enzymatic imbalance. This study investigates how these abnormalities alter lung mechanics and the response to 2 different mechanical ventilation strategies. Phenotypically, TIMP3 null mice had increased compliance, and decreased resistance, tissue damping, and tissue elastance over wild-type controls. Decreased compliance and increased resistance were observed following the injurious ventilation strategy; however, the TIMP3 null response to both ventilation strategies was similar to wild-type mice. In conclusion, TIMP3 null mice have significant alterations in lung mechanics; however, this does not affect their response to ventilation.

Published
2007

4. Effectiveness of nitric oxide during spontaneous breathing in experimental lung injury

Author

Rolf Rossaint, Frederik Stadermann, Sandra Terbeck, Nadine Hochhausen, Johannes Bickenbach, Ralf Kuhlen, and Rolf Dembinski

Subjects
Pulmonary and Respiratory Medicine, ARDS, Swine, medicine.medical_treatment, Clinical Biochemistry, Acute Lung Injury, Respiratory physiology, Lung injury, Nitric Oxide, Nitric oxide, Biphasic Positive Airway Pressure, Positive-Pressure Respiration, chemistry.chemical_compound, Administration, Inhalation, Medicine, Animals, Hypoxia, Molecular Biology, Mechanical ventilation, Lung, business.industry, Pulmonary Gas Exchange, Respiration, Hemodynamics, medicine.disease, Respiration, Artificial, Disease Models, Animal, medicine.anatomical_structure, chemistry, Anesthesia, Breathing, Respiratory Mechanics, Female, business
Abstract

Inhaled nitric oxide (iNO) improves gas exchange in about 60% of patients with acute respiratory distress syndrome (ARDS). Recruitment of atelectatic lung areas may improve responsiveness and preservation of spontaneous breathing (SB) may cause recruitment. Accordingly, preservation of SB may improve effectiveness of iNO. To test this hypothesis, iNO was evaluated in experimental acute lung injury (ALI) during SB. In 24 pigs with ALI, effects of 10 ppm iNO were evaluated during controlled mechanical ventilation (CMV) and SB in random order. Preservation of SB was provided by 4 different modes: Unassisted SB was enabled by biphasic positive airway pressure (BIPAP), moderate inspiratory assist was provided by pressure support (PS) and volume-assured pressure support (VAPS), maximum assist was ensured by assist control (A/C). Statistical analysis did not reveal gas exchange improvements due to SB alone. Significant gas exchange improvements due to iNO were only achieved during unassisted SB with BIPAP (P

Published
2010

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