Stroke; a journal of cerebral circulation
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The existence in humans of brain tissue at risk for infarction but potentially viable (eg, the penumbra) remains unproven. One retrospective operational definition of such tissue includes its final infarction despite a relatively preserved or even normal cerebral metabolic rate of oxygen (CMRO2) in the early hours after stroke onset. Although previous positron emission tomography (PET) studies identified tissue whose CMRO2 declined from the acute to the subacute stage, in principle compatible with deteriorating penumbra, they all lacked a coregistered CT scan mapping of final infarct and an objective three-dimensional PET data analysis, while many patients were studied in the subacute (up to 48 hours) phase. We have evaluated whether tissue with CMRO2 ranging above a threshold for presumably irreversible damage in the first 18 hours of middle cerebral artery territory stroke, but below it in the chronic stage, could be retrospectively identified within the final infarct volume. ⋯ In a strictly homogeneous sample of prospectively studied patients, we have identified, up to 17 hours after stroke onset, substantial volumes of tissue with CMRO2 well above the assumed threshold for viability that nevertheless spontaneously evolved toward necrosis. This tissue exhibited penumbral ranges of both cerebral blood flow and oxygen extraction fraction and thus could represent the part of penumbra that might be saved with appropriate therapy.
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We know that significant cardiac involvement can occur in patients with acute intracranial hemorrhage, particularly in those with subarachnoid hemorrhage. These patients may present with electrocardiographic abnormalities that were previously thought to be benign. However, many die of cardiovascular sequelae, which suggests more serious cardiac problems. To characterize the cardiac, rhythmic, and myocardial disturbances that occur 2 to 4 hours after subarachnoid hemorrhage, we conducted an experimental study using autologous blood (7.9+/-0.3 mL) injected into the right frontal lobe and subarachnoid space in canines. ⋯ This study demonstrates the high incidence of cardiac involvement, specifically wall motion abnormalities, that occur after subarachnoid hemorrhage and suggests the importance of continuous cardiac monitoring, particularly echocardiographic measurements, in those patients.
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Acute hyperammonemia causes glutamine and water accumulation in astrocytes and loss of the cerebral blood flow response selectively to CO2. We tested whether extraparenchymal pial arterioles not subjected directly to mechanical compression by swollen astrocyte processes also lose hypercapnic reactivity and whether any such loss can be attenuated by inhibiting glutamine synthesis during hyperammonemia. ⋯ Loss of the blood flow response to hypercapnia during acute hyperammonemia is not due simply to swollen astrocyte processes passively impeding blood flow because extraparenchymal resistance arterioles also lose their reactivity selectively to hypercapnia. Lost reactivity depends on glutamine synthesis rather than on ammonium ions per se and may reflect indirect effects of astrocyte dysfunction associated with glutamine accumulation or possibly effects of glutamine on nitric oxide production.