PubMed · 9046324
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M D Heifetz. 1997. Split dura for revascularization.. https://doi.org/10.3171/jns.1997.86.3.0575a
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Despite the completion of several multi-center clinical trials comparing medical management and carotid endarterectomy, there is still controversy as to when carotid endarterectomy is appropriate. The volume of this surgery appears to be increasing. However, available performance data indicate that the surgical proficiency required for the clinical trials is not achieved uniformly in actual practice. Therefore, benefits of carotid endarterectomy, when considered from a public health perspective, are limited by the following: (1) endarterectomy is an expensive stroke prevention modality; (2) endarterectomy addresses the needs of only a relatively small subset of stroke patients, and (3) endarterectomy for asymptomatic patients, without clearer evidence that these individuals benefit, may decrease the cost-effectiveness of this surgical procedure.
Increased levels of endothelin-1 (Et-1), a potent vasoconstrictor, have been correlated with hypertension and neuronal damage in ischemic/reperfusion injury. The presence of polymorphonuclear cells (PMNs) in the brain has been shown to be directly responsible for this observed pathology. To address the question of whether Et-1 plays a role in this process, human brain-derived endothelial cells (CNS-ECs) were cultured with Et-1. The results demonstrate that Et-1 induces production of the neutrophil chemoattractant interleukin-8 (IL-8) twofold to threefold after 72 hours; mRNA was maximal after 1 hour of stimulation. Conditioned culture medium derived from Et-1-stimulated CNS-ECs induced a chemotactic response in the PMN migration assay. The inflammatory cytokines tumor necrosis factor-alpha (TNF) and IL-1beta functioned additively with Et-1 in increasing IL-8 production. In contrast, transforming growth factor-beta (TGF-beta), but not IL-10, completely abolished the effect of Et-1 on IL-8 production. However, Et-1 did not modulate intercellular adhesion molecule-1 (ICAM-1) expression. These data demonstrate that Et-1 may be a risk factor in ischemic/reperfusion injury by inducing increased levels of the neutrophil chemoattractant IL-8.
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