Stroke; a journal of cerebral circulation
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Cross-clamping of the thoracic aorta results in spinal cord ischemia and prominent systemic hypertension. Using a rat model of transient spinal cord ischemia. we examined the effects of manipulation of proximal aortic blood pressure on spinal cord blood flow (SCBF), neurological dysfunction, and changes in spinal histopathology after increasing intervals of aortic occlusion. ⋯ The present study shows that systemic intraischemic hypotension (40 mm Hg) significantly potentiates neurological dysfunction after transient aortic occlusion. The mechanism of the observed effect may include elimination of collateral flow during aortic occlusion and/or consequent potentiation of hypoperfusion during reperfusion. These data indicate that PAP during occlusion should be monitored and/or controlled because it is a critical variable in the determination of outcome in this model of spinal cord ischemia.
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Hematoma volume is an important determinant of outcome and predictor of clinical deterioration in patients with intracerebral hemorrhage. In many cases, worsening results from herniation due to compartmentalized pressure gradients. We used transcranial Doppler sonography (TCD) to assess the impact of hematoma volume on symmetry of intracranial hemodynamics in patients with acute intracerebral hemorrhage. The goal was to evaluate TCD as a noninvasive method for monitoring compartmentalized mass effect. ⋯ Asymmetry of intracranial hemodynamics as assessed by TCD occurs when intracerebral hemorrhage volumes exceed 25 mL. Alterations of pulsatility index reflect intracranial lesion volume more reliably than mean velocity. Although pulsatility is strongly influenced by the presence of intraventricular blood, elevated ratios of ipsilateral-to-contralateral pulsatility correlate primarily with hemispheric lesion volume and may reflect compartmentalized intracranial pressure gradients.
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The sudden death rate from aneurysmal subarachnoid hemorrhage (SAH) is 10%. Since 1989, 26 SAH patients who were witnessed to collapse into coma with respiratory arrest and required cardiopulmonary resuscitation (CPR) at the scene survived to reach the hospital and be diagnosed. Although reports on hospital management of grade V SAH suggest improved outcome, no report has previously addressed the issue of respiratory arrest after acute SAH. We analyze our experience with this unique subgroup of aneurysmal SAH patients. ⋯ Aneurysmal SAH patients that present with respiratory arrest present as grade V patients with elevated ICP. Bystander CPR coupled with early retrieval, diagnosis, and therapy can lead to 20% functional survival in what used to be sudden death from aneurysmal SAH.
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Disturbed cerebral autoregulation has been reported to correlate with an unfavorable outcome after head injury. Using transcranial Doppler ultrasonography, we investigated whether hemodynamic responses to spontaneous variations of cerebral perfusion pressure (CPP) provide reliable information on cerebral autoregulatory reserve. ⋯ Indices derived from spontaneous fluctuations of FV waveform and CPP describe cerebral vascular pressure reactivity. They correlate with outcome after head injury and therefore may be used to guide autoregulation-oriented intensive therapy.
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Recent studies in piglets show that either asphyxia or global cerebral ischemia, which combines effects of hypoxia and hypercapnia, transiently attenuates N-methyl-D-aspartate (NMDA)-induced pial arteriolar dilation. The purpose of this study was to determine individually the effects of hypoxic hypoxia and normoxic hypercapnia on NMDA-dependent cerebrovascular reactivity. In addition, we examined mechanisms involved in reduced cerebral vascular dilation to NMDA. ⋯ Short-term severe hypoxic hypoxia and reventilation impair the NMDA-induced dilatation of pial arterioles. Respiratory acidosis alone does not modify pial arteriolar reactivity to NMDA. The reduced responsiveness of the cerebral blood vessels to NMDA caused by hypoxia appears to be due to action of oxygen radicals.