Stroke; a journal of cerebral circulation
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Transient cerebral ischemia in rats results in selective loss of neuronal viability, eg, hippocampal CA1 neurons. The neurochemical variables responsible for this selective vulnerability to ischemia/reperfusion (IR) appear to involve excitatory amino acids. In brain IR, excitatory amino acid toxicity may be modulated by endogenous nitric oxide (NO.) gas. To investigate NO. in global brain IR, we measured the effects of NO. synthase (NOS) inhibition on interstitial excitatory amino acids in rats. Changes in postischemic cerebral blood flow and blood-brain barrier function also were evaluated. ⋯ NOS inhibition did not attenuate extracellular glutamate accumulation during ischemia and increased its concentration on reperfusion. The elevated glutamate concentration after IR in L-NAME-treated rats did not appear to be due to either a decrease in cerebral blood flow response after ischemia or increases in local blood-brain barrier permeability. For the most part, the blood-brain barrier was spared in the immediate postischemic period by L-NAME treatment. These data suggest that NO. production may oppose synaptic excitatory amino acid accumulation and presumably excitotoxicity during IR.
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Autoregulation of cerebral blood flow is easily disrupted, and loss of this normal physiological reflex may worsen the neurological outcome for patients undergoing intensive care. We studied the response of cerebral blood flow velocity to changes in mean arterial blood pressure. ⋯ Computerized coherent averaging of the cerebral blood flow velocity response to spontaneous blood pressure transients offers a promising new method for noninvasive bedside assessment of autoregulation in patients undergoing intensive care. The time course for autoregulation, when present, is in agreement with that reported in adults.
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Although crossed cerebellar diaschisis is well recognized after stroke, there is controversy concerning its clinical correlations and serial changes, and little is known about its prognostic value. ⋯ This study shows that crossed cerebellar diaschisis is a functional phenomenon that correlates with both stroke severity and infarct hypoperfusion volume and persists despite neurological recovery. Although acute-stage crossed cerebellar diaschisis has no prognostic value independent of acute-stage hypoperfusion volume, it might indicate the proportion of nutritional to nonnutritional perfusion at the infarct site and hence be useful in the evaluation of reperfusion therapies in the acute stage.
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Comparative Study
Assessment of cerebral vasomotor reactivity by transcranial Doppler ultrasound and breath-holding. A comparison with acetazolamide as vasodilatory stimulus.
Evaluating cerebrovascular vasomotor reactivity seems to be of prognostic relevance for patients with occlusive internal carotid artery disease. To evaluate its clinical usefulness, the recently introduced breath-holding maneuver as a carbon dioxide-dependent vasodilatory stimulus was compared with the acetazolamide challenge by means of transcranial Doppler ultrasound and stable xenon-enhanced computed tomography. ⋯ The assessment of vasomotor reactivity by transcranial Doppler ultrasound correlates with cerebral blood flow changes even when different vasodilatory stimuli are used. In cooperative patients the breath-holding maneuver as vasodilatory stimulus seems clinically useful for a first estimation of cerebral vasomotor reactivity.
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Pial arterioles transiently dilate during cortical spreading depression (CSD), although the mechanisms are unclear. We tested the hypothesis that increased production of nitric oxide (NO) promotes arteriolar dilation. ⋯ The reversible inhibition of CSD-induced pial arteriolar dilation by either L-NAME or L-NA suggests that NO contributes to arteriolar dilation observed with CSD.