hypercapnia/inflammation

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Effects of acute hypercapnia with and without acidosis on lung inflammation and apoptosis in experimental acute lung injury.

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We investigated the effects of acute hypercapnic acidosis and buffered hypercapnia on lung inflammation and apoptosis in experimental acute lung injury (ALI). Twenty-four hours after paraquat injection, 28 Wistar rats were randomized into four groups (n=7/group): (1) normocapnia (NC, PaCO2=35-45

Autonomic dysregulation as a basis of cardiovascular, endocrine, and inflammatory disturbances associated with obstructive sleep apnea and other conditions of chronic hypoxia, hypercapnia, and acidosis.

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Obstructive sleep apnea has traditionally been viewed as a structural disease. A multitude of systemic endocrine and cardiovascular abnormalities have been previously attributed to the prevalence of obesity in these patients. A growing body of clinical evidence, however, points to a relationship

Brainstem serotonergic, catecholaminergic, and inflammatory adaptations during chronic hypercapnia in goats.

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Despite the prevalence of CO₂ retention in human disease, little is known about the adaptive neurobiological effects of chronic hypercapnia. We have recently shown 30-d exposure to increased inspired CO₂ (InCO₂) leads to a steady-state ventilation that exceeds the

Midbrain and cerebral inflammatory and glutamatergic adaptations during chronic hypercapnia in goats.

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Cognitive impairment is associated with multiple human diseases that have in common chronic hypercapnia. However, the mechanisms leading to chronic hypercapnia-induced cognitive decline are not known. We have previously shown chronic hypercapnia through exposure to increased inspired CO₂

Modulatory effects of hypercapnia on in vitro and in vivo pulmonary endothelial-neutrophil adhesive responses during inflammation.

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Reducing tidal volume as a part of a protective ventilation strategy may result in hypercapnia. In this study, we focused on the influence of hypercapnia on endothelial-neutrophil responses in models of inflammatory-stimulated human pulmonary microvascular endothelial cells (HMVEC) and in an animal

Therapeutic hypercapnia enhances the inflammatory response to endotoxin in the lung of spontaneously breathing rats.

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OBJECTIVE To test the hypothesis that therapeutic hypercapnia enhances the proinflammatory responses to endotoxemia in the lung and spleen of rats. METHODS Prospective randomized study. METHODS Hospital research institute. METHODS Forty-eight adult male rats. METHODS Rats were randomly assigned for

Inflammatory Mediators in Tracheal Aspirates of Preterm Infants Participating in a Randomized Trial of Permissive Hypercapnia.

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UNASSIGNED Ventilator-induced lung injury is considered to be a main factor in the pathogenesis of bronchopulmonary dysplasia (BPD). Optimizing ventilator strategies may reduce respiratory morbidities in preterm infants. Permissive hypercapnia has been suggested to attenuate lung injury. We aimed to

A role for heat shock factor 1 in hypercapnia-induced inhibition of inflammatory cytokine expression.

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Hypercapnia, elevated levels of CO2 in the blood, is a known marker for poor clinical prognosis and is associated with increased mortality in patients hospitalized with both bacterial and viral pneumonias. Although studies have established a connection between elevated CO2 levels and poor pneumonia

Effect of Therapeutic Hypercapnia on Inflammatory Responses to One-lung Ventilation in Lobectomy Patients.

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BACKGROUND One-lung ventilation (OLV) can result in local and systemic inflammation. This prospective, randomized trial was to evaluate the effect of therapeutic hypercapnia on lung injury after OLV. METHODS Fifty patients aged 20 to 60 yr undergoing lobectomy were randomly provided with air or

Effects of therapeutic hypercapnia on inflammation and apoptosis after hepatic ischemia-reperfusion injury in rats.

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BACKGROUND Therapeutic hypercapnia (TH) has been demonstrated to protect several organs ischemia-reperfusion injury. The study aimed to investigate the effects of therapeutic hypercapnia on hepatic ischemia-reperfusion injury (HIRI). METHODS Thirty adult male Wistar rats weighing (250+/-20) g were

[Permissive and non-permissive hypercapnia: mechanisms of action and consequences of high carbon dioxide levels].

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Acute lung injury is a disease with high incidence of mortality and its treatment is still controversial. Increasing the levels of CO2 beyond the physiological range has been proposed as a potential protective strategy for patients on mechanical ventilation, as it could moderate the inflammatory

[External respiratory function in children with bilateral, chronic, nonspecific inflammatory disease of the lungs after surgical treatment].

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The results of operative treatment of children with bilateral chronic unspecific inflammatory diseases of the lungs were studied in follow-up periods of up to 17 years. Among the 73 patients studied, 19 had a history of bilateral and the remaining a history of unilateral resections. According to the

Permissive hypercapnia, instituted via reduction of pressure amplitude on pulmonary tissue protection during high frequency oscillatory ventilation, is not protective in a rat model of acid-induced lung injury.

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BACKGROUND Assuming that HFOV (high frequency oscillatory ventilation) with hypercapnia could be more protective than normocapnia, in a rat model of lung injury, we evaluated the effect of hypercapnic acidosis during HFOV. METHODS After inducing lung injury by intratracheal instillation of

[Effect of hypercapnia on the clinical prognosis and severity of infection in patients with severe community-acquired pneumonia]

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Objective: To investigate the effect of hypercapnia at admission on the clinical prognosis and the severity of infection in patients with severe community-acquired pneumonia (SCAP). Methods:

Chronic inflammatory demyelinating polyneuropathy and respiratory failure.
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Neuromuscular respiratory failure is not considered to be a clinical feature of chronic inflammatory demyelinating polyneuropathy (CIDP). We present 4 patients with CIDP who required respiratory assistance and mechanical ventilation. Two patients needed emergent intubation and one patient lapsed in

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