Liquid ventilation.

M Davies

doi:10.1046/j.1440-1754.1999.355404.x

Home/Archive/PubMed

PubMed · 10571753

Liquid ventilation.

M Davies

View original source ↗Export metadata ↓

Abstract

Research on using liquid ventilation to provide artificial respiration in mammals has been ongoing since the 1960s. The development of inert perfluorocarbon (PFC) liquids with high oxygen and carbon dioxide solubility has made gas exchange with liquid ventilation possible. In 1991 the technique of partial liquid ventilation was introduced where PFC are instilled into the lungs whilst continuing with conventional mechanical ventilation. Partial liquid ventilation has been shown to improve gas exchange and lung function with decreased secondary lung injury, in animal models of acute lung injury and surfactant deficiency. It has been used in uncontrolled trials in preterm neonates, and preliminary results are available from a randomized controlled trial of partial liquid ventilation in paediatric acute respiratory distress syndrome. Perfluorocarbons can also be used to deliver drugs to the lungs, to lavage inflammatory exudate and debris from the lungs, and as an intrapulmonary X-ray contrast medium. Many questions about partial liquid ventilation remain unanswered particularly with regard to the dose of PFC required, its ideal method of administration and the long-term effects. Partial liquid ventilation promises to be an exciting new therapy for infants and children with a variety of respiratory problems. The technique requires ongoing research and experimentation.

Explore related subjects

Acute Disease Bronchoalveolar Lavage Child, Preschool Fluorocarbons Humans Infant Infant, Newborn Respiratory Distress Syndrome, Newborn Respiratory Insufficiency Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

M Davies. 1999. Liquid ventilation.. https://doi.org/10.1046/j.1440-1754.1999.355404.x

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

Loss of noradrenaline transporter sites in frontal cortex of rats with acute (ischemic) liver failure.

There is increasing evidence that central noradrenaline (NA) transport mechanisms are implicated in the central nervous system complications of acute liver failure. In order to assess this possibility, binding sites for the high affinity NA transporter ligand [3H]-nisoxetine were measured by quantitative receptor autoradiography in the brains of rats with acute liver failure resulting from hepatic devascularization and in appropriate controls. In vivo microdialysis was used to measure extracellular brain concentrations of NA. Severe encephalopathy resulted in a significant loss of [3H]-nisoxetine sites in frontal cortex and a concomitant increase in extracellular brain concentrations of NA in rats with acute liver failure. A loss of transporter sites was also observed in thalamus of rats with acute liver failure. This loss of NA transporter sites could result from depletion of central NA stores due to a reserpine-like effect of ammonia which is known to accumulate to millimolar concentrations in brain in ischemic liver failure. Impaired NA transport and the consequent increase in synaptic concentrations and increased stimulation of neuronal and astrocytic noradrenergic receptors could be implicated in the pathogenesis of the encephalopathy and brain edema characteristic of acute liver failure.

Acute Disease↗

PubMed2000

Modeling axonal injury in vitro: injury and regeneration following acute neuritic trauma.

Traumatic injury to axons was modeled in vitro using sympathetic principal neurons from the rat superior cervical ganglion. Neurons were grown as a pure culture on collagen in parallel tracks, with cell somata confined to the center, and neurites occupying the periphery of the culture dish. Growing as fascicles on tracks, the neurites demonstrated periodic varicosities. Neuritic transection was reliably and reproducibly achieved with a motor driven rubber impactor injury device. During a period lasting at least 1 h, dieback involving the proximal neurites averaged 105 +/- 10 microm. This was followed by neurite regeneration, with the injured segment being traversed within 36 h at an average rate of regeneration of 595 +/- 15 microm/day. The distal neurite segments showed degenerative changes within 1 h following transection, with initial receding of neurites progressing to vacuolation, beading, blebbing, and eventual detachment from the underlying matrix. This in vitro model of axonal injury allows neuritic injury to be studied at the cellular and molecular levels, and also provides a unique opportunity to test potential neuromodulatory and neuroprotective strategies.

Acute Disease↗

PubMed2000

A hematopoietic cell L-selectin ligand that is distinct from PSGL-1 and displays N-glycan-dependent binding activity.

Human hematopoietic progenitor cells express L-selectin and also express PSGL-1, a ligand for all selectins. Using a shear-based adhesion assay, a hematopoietic cell L-selectin ligand (HCLL) that is expressed on the hematopoietic cell line KG1a and on normal human hematopoietic progenitors was previously identified. To characterize the structural biology of HCLL and to define its relationship to PSGL-1, the effects of chemical and enzymatic treatments on HCLL activity of KG1a cells and membrane preparations were analyzed. Protease digestions and chemical treatments of KG1a cells and membranes indicated that HCLL is an integral membrane glycoprotein. Glycosidase digestions of membrane protein preparations and metabolic treatments of KG1a cells with glycosylation processing modifiers revealed that L-selectin binding determinants on HCLL are sialofucosylated structures presented on complex-type N-glycans. Adhesion assays and biochemical studies showed that this glycoprotein is also expressed on circulating blasts in native acute leukemias. HCLL is distinguishable from PSGL-1: (1) KG1a cells sorted for PSGL-1 expression had equivalent HCLL activity; (2) anti-PSGL-1 blocking antibodies and proteases known to eliminate L-selectin binding to PSGL-1 had no effect on HCLL binding activity of KG1a cells; (3) blasts from native leukemias with low expression of PSGL-1 and CD34 display high HCLL activity; and (4) despite high level expression of PSGL-1, HCLL activity was absent on HL60 cells. These data provide first evidence of a naturally expressed membrane L-selectin ligand expressing binding determinant(s) on an N-linked glycoconjugate. This novel ligand may help mediate L-selectin-dependent cell-cell adhesive interactions within the cytoarchitecture of the bone marrow microenvironment. (Blood. 2000;96:2765-2774)

Acute Disease↗