O conhecimento dos mecanismos fisiopatológicos da lesão cerebral no traumatismo .. O edema cerebral vasogênico resulta de distúrbio na barreira. Advancements in molecular biology have led to a greater understanding of the individual proteins responsible for generating cerebral edema. In large part, the. AJR Am J Roentgenol. Sep;(3):W doi: /AJR Cerebral edema. Ho ML(1), Rojas R, Eisenberg RL. Author information.

Author: Shaktigor Meztigul
Country: Chad
Language: English (Spanish)
Genre: Science
Published (Last): 12 April 2006
Pages: 134
PDF File Size: 4.73 Mb
ePub File Size: 17.2 Mb
ISBN: 254-8-28786-502-5
Downloads: 17534
Price: Free* [*Free Regsitration Required]
Uploader: Fenrill

Transl Stroke Res ; 5: Young W, Constantini S. Most changes in morphology are associated with cerebral edema: Ionic and water shifts in injured central nervous tissues.

Cerebral edema

Stiefel MF, Marmarou A. Capillary hydrostatic pressure P c is dictated by the precapillary arteriolar pressure, the postcapillary venular pressure, and the capillary resistance, while the tissue pressure P i is a function of the volume of the ISF and the tissue compliance. The recent description of the glymphatic system led to the formulation of a second hypothesis, whereby CSF serves as the immediate source of ions and water.

Cerebral edema in intracranial meningiomas: Progress in Cardiovascular Diseases. Vasgenico MS, Shuaib A. Doubtlessly, the next few years will yield new knowledge of how particular proteins drive edema influx, paving the vaasogenico for rationally designed therapeutics ceebral directly target key steps in cerebral edema formation, thereby achieving what currently approved therapies do not. Protein and water may passage from the vascular compartment to the interstitial compart through transendothelial channels formed by dysregulation of pinocytosis.


It is generally agreed that vasogenic edema can form via paracellular transport past endothelial cells. Vet J ; The role of hypoxia-inducible factor-1alpha, aquaporin-4, and matrix metalloproteinase-9 in blood-brain barrier disruption and brain edema after traumatic brain injury.

The clearance pathway taken by ISF depends upon its location in the brain: Attenuation of intracerebral hemorrhage and thrombin-induced brain edema by overexpression of interleukin-1 receptor antagonist. Cell Metab ; Interstitial fluid flow along white matter tracts: Monocyte chemoattractant protein-1 alters expression of tight junction-associated proteins in brain microvascular endothelial cells.

Vasogenic cerebral oedema | Radiology Reference Article |

Da T, Verkman AS. Ther Targets Neurol Dis ; 2.

avsogenico Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging. Methemoglobin is an endogenous toll-like receptor 4 ligand-relevance to subarachnoid hemorrhage.

Astrocytes are supportive cells that completely fill the brain parenchyma, and in grey matter, are arranged in a three-dimensional matrix with nonoverlapping spatial domains. If ISF pH drops below 6. Glucose and lactate metabolism modulation by ascorbic acid. The perivascular astroglial sheath provides a complete covering of the brain microvessels: Maladaptive ion influx may ensue, generating a transmembrane osmotic gradient that drives water influx and causes cell swelling.



The pathophysiological mechanisms following traumatic brain injury

Polarity of the blood-brain barrier: Water transport between CNS compartments: While the aforementioned core concepts that govern the formation of edema during phases of endothelial dysregulation e. Mechanisms of cerebral edema in traumatic brain injury: Sodium-hydrogen exchangers and sodium-bicarbonate co-transporters: J Gen Physiol ; It follows that cerebral edema, a phenomenon that arises from dysfunction of astrocytes and endothelium, represents an important target for basic research and therapeutic intervention.

BMC Biochem ; 7: Brain water mobility decreases after astrocytic aquaporin-4 inhibition using RNA interference.

Di TR, Platt S. Solutes may also move by bulk flow. Plasma dilution decreases serum osmolality, resulting in a higher osmolality in the brain compared to the serum. Omitting a key role for endothelium is implausible, given the many endothelial transporters and channels implicated in the formation of edema.