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(Stroke. 2003;34:1396.)
© 2003 American Heart Association, Inc.
Original Contributions |
Neurosciences Critical Care/Cerebrovascular Center, University Hospitals of Cleveland, Department of Neurology/Neurosurgery, Case Western Reserve University, Cleveland, Ohio
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertonic saline solutions (HSs) have been used in various concentrations in patients with intracranial pathologies to treat cerebral edema and elevated intracranial pressure (ICP).1 Since the first animal experiments by Weed and McKibben2 in 1919, many data have been published on the use of HSs in both animal models and human patients with hemorrhagic shock with and without elevated ICP and with isolated intracranial processes. All these studies have shown that HS effectively reduces ICP and cerebral edema with subsequent enhancement of cerebral perfusion pressure. Another beneficial effect of HS is an increase in intravascular volume and therefore maintenance of adequate cardiac output and blood pressure. Several possible mechanisms of action of HS have been reported: reduction in brain water by creation of an osmotic effect to draw water from the brain to the intravascular space; improvement of cerebral blood flow (CBF), presumably by exertion of a dehydrating effect of cerebrovascular endothelium and erythrocytes; restoration of normal membrane resting potential; and reduction in adhesion of polymorphonuclear cells to cerebral microvasculature with attenuation of pial vessel dilatation. Taken together, all these effects may reduce cerebral ischemia and improve cerebral oxygen delivery.
Subarachnoid hemorrhage (SAH) is a devastating condition that carries high morbidity and mortality. A major cause of poor outcome after SAH is the development of cerebral vasospasm with subsequent infarction. Because of the CBF-enhancing properties noted in animal models and its maintenance of adequate intravascular volume, HS may be a good candidate for fluid resuscitation in SAH patients. Despite this
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