Published in:
01-01-2009 | Year in Review 2008
Year in review in Intensive Care Medicine, 2008: I. Brain injury and neurology, renal failure and endocrinology, metabolism and nutrition, sepsis, infections and pneumonia
Authors:
Massimo Antonelli, Elie Azoulay, Marc Bonten, Jean Chastre, Giuseppe Citerio, Giorgio Conti, Daniel De Backer, François Lemaire, Herwig Gerlach, Johan Groeneveld, Goran Hedenstierna, Duncan Macrae, Jordi Mancebo, Salvatore M. Maggiore, Alexandre Mebazaa, Philipp Metnitz, Jerôme Pugin, Jan Wernerman, Haibo Zhang
Published in:
Intensive Care Medicine
|
Issue 1/2009
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Excerpt
Recent experimental evidence suggests that matrix metalloproteinases (MMPs) are implicated in the pathophysiology of traumatic brain injury (TBI) by increasing blood–brain barrier permeability and exacerbating post-traumatic edema. MMPs are zinc-dependent and cell surface-associated endopeptidases that cleave all extracellular matrix (ECM) components, including collagen, laminin, and proteoglycans. The MMPs and their potential deleterious effects are tightly regulated at transcriptional and post-transcriptional levels through proform activation and by MMP tissue inhibitors (TIMPs) Two members of this family have a very specific and marked activity against gelatin and are termed gelatinases. In vitro studies have demonstrated that the secretion of gelatinases is significantly increased in cortical cultures when mechanical injury is simulated. In human TBI, data about the presence of gelatinases in the brain extracellular fluid (ECF) and their temporal profile, both in plasma and ECF, are still lacking. Sahuquillo’s group [
1] examined the acute profile of MMP-2 and MMP-9 in the plasma of patients with moderate or severe TBI and, more interestingly, in the brain extracellular fluid (ECF). High levels of gelatinases were found in plasma and brain ECF in the early phase of TBI, indicating that both local and systemic trauma-induced upregulation of gelatinases in the acute phase might play an important role in the pathophysiology of TBI and could be a future therapeutic target. …