hypercapnia/atrophy

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Papilloedema and optic atrophy in chronic hypercapnia.

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Two patients are described with hypercapnia of 10 and 13 years duration. Both patients had papilloedema at different stages of their illness and one patient developed optic atrophy. Whether such changes are due to local retinal vascular changes, general change in cerebral vasculature or the result

Neuromuscular electrical stimulation improves muscle atrophy induced by chronic hypoxia-hypercapnia through the MicroRNA-486/PTEN/FoxO1 pathway.

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Previous work has confirmed that the chronic hypoxia-hypercapnia (CHH) associated with chronic obstructive pulmonary disease contributes to the development of skeletal muscle atrophy. Neuromuscular Electrical Stimulation (NMES) has shown some efficacy when used as a treatment to reduce skeletal

Sustained hypercapnia induces cerebral microvascular degeneration in the immature brain through induction of nitrative stress.

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Hypercapnia is regularly observed in chronic lung disease, such as bronchopulmonary dysplasia in preterm infants. Hypercapnia results in increased nitric oxide synthase activity and in vitro formation of nitrates. Neural vasculature of the immature subject is particularly sensitive to nitrative

Ventilatory and cardiovascular responses to hypercapnia and hypoxia in multiple-system atrophy.

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BACKGROUND Loss of medullary sympathoexcitatory neurons may contribute to baroreflex failure, leading to orthostatic hypotension in multiple-system atrophy (MSA). The cardiovascular responses to chemoreflex activation in MSA have not been explored to date. OBJECTIVE To determine whether ventilatory

Hypercapnia attenuates ventilator-induced diaphragm atrophy and modulates dysfunction.

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BACKGROUND Diaphragm weakness induced by prolonged mechanical ventilation may contribute to difficult weaning from the ventilator. Hypercapnia is an accepted side effect of low tidal volume mechanical ventilation, but the effects of hypercapnia on respiratory muscle function are largely unknown. The

[Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity].

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High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence also suggest a significant role for high levels of carbon dioxide (CO(2)). Hypercapnia is a facilitator of nitration in vitro, and nitrative stress is known to have

Hypercapnia- and trans-arachidonic acid-induced retinal microvascular degeneration: implications in the genesis of retinopathy of prematurity.

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High oxygen tension is a major factor in the genesis of retinopathy of prematurity (ROP). However, clinical and experimental evidence suggests a significant role for high carbon dioxide (CO(2)) tension as well. Along these lines, although ischemia is often considered to be synonymous with an oxygen

Blood flow magnetic resonance imaging of retinal degeneration.

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OBJECTIVE This study aims to investigate quantitative basal blood flow as well as hypercapnia- and hyperoxia-induced blood flow changes in the retinas of the Royal College of Surgeons (RCS) rats with spontaneous retinal degeneration, and to compare with those of normal rat

Hypercapnia: is there a cause for concern?

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Concern that barotrauma may lead to further deterioration in pulmonary function in patients with ARDS has stimulated interest in developing methods of reducing it. These new modalities have had limited acceptance. The reasons for this include technical difficulties, associated complications, and the

Effect of mild hypercapnia on outcome and histological injury in a porcine post cardiac arrest model.

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To evaluate in an established porcine post cardiac arrest model the effect of a mild hypercapnic ventilatory strategy on outcome.

METHODS

The left anterior descending coronary artery was occluded in 14 pigs and ventricular fibrillation induced and left

Acute, short-term hypercapnia improves microvascular oxygenation of the colon in an animal model of sepsis.

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BACKGROUND The deterioration of microcirculatory oxygenation of the gut plays a vital role in the development of sepsis. Acute hypercapnia enhances the microcirculatory oxygenation of the splanchnic region under physiological conditions, while the effect of hypercapnia under sepsis is unknown. The

Ventilatory and integrated physiological responses to chronic hypercapnia in goats.

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CONCLUSIONS Chronic hypercapnia per se has distinct effects on the mechanisms regulating steady-state ventilation and the CO2 /H+ chemoreflex. Chronic hypercapnia leads to sustained hyperpnoea that exceeds predicted ventilation based upon the CO2 /H+ chemoreflex. There is an integrative ventilatory,

Accuracy of Defining Characteristics for Nursing Diagnoses Related to Patients with Respiratory Deterioration.

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To evaluate accuracy of defining characteristics (DCs) for impaired gas exchange (IGE), impaired spontaneous ventilation (ISV), and ineffective breathing pattern (IBP) in respiratory deterioration.This study is a retrospective analysis of medical records.

Brainstem respiratory control: substrates of respiratory failure of multiple system atrophy.

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Multiple system atrophy may manifest with severe respiratory disorders, including sleep apnea and laryngeal stridor, which reflect a failure of automatic control of respiration. This function depends on a pontomedullary network of interconnected neurons located in the parabrachial/Kölliker Fuse

Purkinje cell degeneration elevates eupneic and hypercapnic ventilation in rats.

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Previous studies have demonstrated that among cerebellar nuclei, the fastigial nucleus (FN) plays a major role in facilitation of respiration, especially during hypercapnia. Since the FN primarily receives inhibitory afferents from Purkinje cells (PCs), we hypothesized that degeneration of PCs would

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