To investigate changes in cerebral circulation and oxygen metabolism during aging, regional cerebral blood flow (rCBF), regional oxygen extraction fraction (rOEF), regional cerebral metabolic rate of oxygen (rCMRO2) and regional cerebral blood volume (rCBV) were measured using the 15O labelled gas inhalation technique and a multi-slice positron emission tomograph (PET) in 22 healthy volunteers, aged from 26 to 64 years old. The measurements were performed with subjects at rest, without sensory deprivation. The values of rCBF, rOEF, rCMRO2 and rCBV in more than 40 anatomical structures of the brain were evaluated by studying a large series of scans in each region of interest after the functional PET image had been anatomically identified using x-ray computed tomographic images corresponding to the PET. In mean gray values, only CMRO2 showed significant reduction with age. rCMRO2 significantly decreased with age only in the supratentrium, and much more in the left hemisphere. Especially remarkable was rCMRO2 reduction in the left caudate region. Both CBF and OEF were variable and less age-dependent. It was concluded that CMRO2 could be reflecting healthy brain aging most properly.

Background: Acute blood pressure (BP) elevation and cardiac abnormalities are known to follow ischemic stroke. Brain natriuretic peptide (BNP), which is produced in response to such cardiovascular alterations, is expected to play a hemodynamic role. We measured plasma BNP concentrations in patients with cerebral infarction (CI) to determine the implications of BNP in acute ischemic stroke. Methods: Eighty-eight patients with CI, 59 with essential hypertension, 44 with spontaneous intracerebral hemorrhage, 22 with asymptomatic atrial fibrillation (Af), and 20 age- and sex-matched healthy volunteers were recruited in the study. CI patients were divided into 2 subgroups either having Af (27 patients) or not (61 patients). BNP levels were repeatedly measured in 58 patients with CI. BNP levels were compared between ischemic subgroups categorized by size of infarction. Correlation was investigated between BNP levels and hemodynamic parameters. Results: BNP levels in CI patients were significantly higher, but they decreased in the subacute period. BNP levels in CI patients without Af were correlated with mean arterial blood pressure (MAP) on admission or the degree of reduction in MAP at day 1, while in CI patients with Af BNP levels showed negative correlation with MAP on admission. Follow-up serum sodium levels in CI patients with Af were negatively correlated with BNP levels on admission. Conclusions: This study suggests the hemodynamic implications of BNP in acute ischemic patients.

Spontaneous neuronal activity was recorded in the cerebral cortex and the CA1 sector of the hippocampus in gerbils during and after 5-min ischemia, produced by bilateral clamping of the common carotid arteries. It was found that spontaneous activity in both cortical and CA1 neurons ceased within 60s after the onset of ischemia and that it began to reappear 10-20 min after the recirculation. During the next 24 h most CA1 neurons which were recorded showed hyperactivity. This was evident primarily by an increase in spike discharges, whereas recordings from the cerebral cortex were within the preocclusion ranges. On the 2nd day after ischemia, functioning CA1 neurons could not be found, as if they were in a state of functional death, although histological sections showed a general preservation of their cellular structure at that time.

Changes in morphology, behavior of the blood-brain barrier (BBB), regional cerebral blood flow (rCBF), and local cerebral glucose utilization (LCGU) were assessed and correlated in Mongolian gerbils following 5 min cerebral ischemia, produced by bilateral clamping of the common carotid arteries. The morphological changes were confined to the hippocampus and revealed a conspicuously delayed destruction of the CA1 neurons, occurring after 3 days. Following release of carotid occlusions, there were two separate openings of the BBB. One, occurring shortly after recirculation, was associated with focal hyperemia in the cerebral cortex, hippocampus and basal ganglia; the second opening was observed after several days and was associated with severe neuronal destruction in the CA1 sector. Correlation of quantitative and qualitative rCBF assays with 14C-deoxyglucose autoradiographic observations indicated an uncoupling between blood flow and glucose metabolism, observed in the hippocampus at 10 min after recirculation. The described changes provide a further insight into the post-ischemic events which determine the outcome of ischemic injury.

Micro-blood vessels (MBVs), located in the area of edema, were studied in cat brain at various time intervals (1 h, 24 h, 7 days) after cold-lesion injury. Both cold-injured and adjacent gyri were examined for blood-brain barrier (BBB) permeability to i. v. injected horseradish peroxidase (HRP) with circulation times of 40 min and 24 h. Evans blue (EB) was used as a tracer for gross evaluation of the extension of brain edema. Localization of alkaline phosphatase (AP) and binding of cationized ferritin (CF), considered as a marker of anionic sites, were also studied ultrastructurally. Twenty-four hours after cold injury, the extravasated edema fluid, outlined by EB tracer, was observed to be spreading through the white matter (WM) into the adjacent gyrus. At this time, numerous, larger than capillary MBVs, presumably arterioles and venules located in the edematous WM, showed accumulations of HRP injected at the time of the operation, in the basement membrane, in abluminal pits, and in numerous pinocytotic vesicles and vacuoles of endothelial cells (ECs). The animals killed after 24 h with 40 min HRP circulation showed extravasation of HRP tracer in a zone underlying the necrotic cold injury lesion. On the other hand, there was no evidence of an abnormal HRP leakage in the further removed areas of edema in the WM, particularly in the adjacent gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)