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J Astrup

Publications and source records attributed to J Astrup.

100 records · Page 6Linked to original sources
PubMedDate not supplied

Quantitative MR analysis of glucocorticoid effects on peritumoral edema associated with intracranial meningiomas and metastases.

OBJECTIVE: The purpose of our study was to quantify peritumoral brain edema (PTE) in vivo using NMR relaxation time imaging, as the longitudinal relaxation time T1 is proportional to tissue water content, and to use the method for monitoring the effects of glucocorticoids (GCCs) on PTE in brain tumor patients as a function of time. MATERIALS AND METHODS: Relaxation time imaging (T1 maps) was done on a 1.5 T MR scanner on 23 brain tumor patients [13 cerebral metastases (METs), 10 intracranial meningiomas (MMs), and 9 benign and 1 anaplastic MM] before, and 1, 3, and 7 days after initiation of GCC treatment (dexamethasone 0.26-0.64 mg/kg bw). In addition, 7 patients were studied for 14-63 days of treatment. Imaging analysis included mean T1 of the edema area as a function of time, and an image histogram evaluation technique, which measures 50% of the edema area, where T1 is highest (corresponding to the highest water content of the area), termed the "super-edema." Using a conversion equation, mean T1 in the edema area was recalculated into a percent of tissue water content. RESULTS: After 7 days of GCC treatment total edema area was reduced by 10.3% in the MET patients. The average reduction in mean T1 was 4.6% after 24 h of treatment and 13.5% after 7 days. Expressed in terms of percent tissue water content, the average edema resorption rate in the MET patients was 0.4 +/- 0.1% H2O/day (p < 0.02). Super-edema area was reduced by 64% after 7 days (p < 0.0001). None of the benign MMs responded to GCC treatment, either in edema size or in mean T1, unlike the anaplastic type, in which there was a response comparable to that in the MET patients. The effect of GCCs in up to 63 days of treatment is demonstrated. It is shown that after 40-63 days of GCC treatment, PTE water content is close to the upper normal range for white matter. CONCLUSION: PTE is heterogeneous in terms of the spatial distribution of T1 and, thereby, water content. GCCs reduce T1 in PTE around cerebral metastases significantly after a few days of treatment, possibly through a mechanism that reduces edema production below the level of edema resorption. PTE surrounding benign MM was not affected by GCC treatment, contrary to one anaplastic MM, which leads to the speculation that malignant tumors may produce substances that are affected by GCCs and are prerequisites for a GCC effect. Significant reductions in the highest T1 area (super-edema area) were observed after 24 h of treatment. The anti-edema effect of GCC may last at least 63 days. A lower dose-dependent threshold for the effect seems to exist. The possible mechanisms of actions of the GCCs on PTE are discussed.

Adult↗
PubMedDate not supplied

Biomechanical properties of porcine cerebral bridging veins with reference to the zero-stress state.

Passive mechanical and morphometric properties of porcine cerebral bridging veins were studied. Fifteen cerebral bridging veins were obtained from 7 pigs. The superior sagittal sinus, bridging veins and the meninges were excised and placed in aerated calcium-free Krebs solution. The outflow cuff segment is a narrow region at the junction of the cerebral bridging veins and superior sagittal sinus. The principal direction of collagen fibres was longitudinal in the bridging vein and circumferential in the cuff region. The diameter was smaller in the outflow cuff segment than in the cerebral bridging veins in the pressure range studied (0-23 mm Hg) whereas the thickness was highest in the outflow cuff segment (p < 0.01). The circumferential stress-strain analysis showed that the outflow cuff segment was extensible up to a strain of 0.25. At higher strains the outflow cuff segment was progressively stiffer than the cerebral bridging vein (p < 0.05). The longitudinal stress-strain relation for the cerebral bridging vein was shifted to the left compared to the outflow cuff segment (p < 0.05). When compared to the stress-strain properties in the circumferential direction, the outflow cuff segment was more extensible and the cerebral bridging vein stiffer in longitudinal direction (p < 0.05). The opening angle of the outflow cuff segment and the cerebral bridging vein was 115 +/- 4 and 120 +/- 4 (means +/- SE) without statistical difference between the two regions. In conclusion the difference in biomechanical properties between the outflow cuff segment and the cerebral bridging vein was associated to their difference in histology and fibre arrangement. This indicates that the function of the outflow cuff segment is to act as a flow-limiting resistance to the outflow from the cerebral circulation.

Adaptation, Physiological↗
PubMedDate not supplied

Oxygen and glucose consumption related to Na+-K+ transport in canine brain.

This study examines the relation between Na+-K+ transport and metabolism in the canine brain. Cerebral oxygen and glucose consumption was measured by the sagittal sinus outflow technique. Synaptic transmission and related metabolism was blocked by pentobarbital 40 mg/kg (EEG flat). Lidocaine blocked an additional 15-20%, presumable by restricting Na+-K+ leak fluxes and reducing the demand for Na+-K+ transport. Ouabain blocked an additional 20-25% of metabolism. Ouabain also inhibited the Na+-K+ sensitive ATPase associated transport and caused a net efflux of K+ from the cellular compartment as evidenced by an increasing extracellular K+ concentration in the cortex. Accordingly, a total of 40% of metabolism in te EEG-arrested barbiturate inhibited brain could be related to Na+-K+ leak fluxes and associated transport. The remaining 60% are related to processes unidentified by this study. It is concluded that cerebral metabolism may be reduced below the hitherto described barbiturate minimum.

Animals↗
PubMedDate not supplied

Cell density and cortex thickness in the border zone surrounding old infarcts in the human brain.

Six cases of completed ischemic stroke in the middle cerebral artery territory of more than two months' duration were selected for this study of neuropathology. Coronal brain slices of the entire brain were cut for histology and stained with Klüver-Barrera's stain. Neuronal and glial cell density, and cortex thickness were measured at various distances from the border of the infarct. Corresponding counting points in the contralateral hemisphere served as control in all cases. The density of histologically intact neurons was in all cases normal at a distance of 0.5 cm or more from the border of the infarcts. In one half of the cases the border zone between infarcted and normal tissue was less than a few cells in thickness. This study of old brain infarcts confirms the commonly held view that there is an abrupt transition between infarcted and normal tissue. This observation suggests that the wide zone of low blood flow and metabolism surrounding cerebral infarcts is not caused by selective loss of neurons. Instead, we hypothesize that such change in blood flow and metabolism is the result of neuronal disconnection and cortical deactivation.

Aged↗
PubMedDate not supplied

Cell density in the border zone around old small human brain infarcts.

Nine brain autopsy cases of small old cerebral infarcts were selected for neuropathological studies. Eight of the patients had cortical infarcts, in two cases with extension into the striate body. In one case the infarct involved the striate body only. The density of neurons and glial cells was measured in the coronal and the horizontal planes at various distances from the margin of the infarct. Corresponding counting points in the contralateral hemisphere served as control. On light microscopy, the infarcted cortex was irregularly shaped, but on serial sections the bulging parts appeared to be cut off from the infarcted tissue ("pseudo-infarct islands"). The zone of transition from infarcted to normal brain tissue was less than a few mm wide. In one patient, tomographic measurements of the cerebral blood flow (CBF) and a CT scan could be compared with the neuropathological findings. In this patient, CBF in the surroundings of the infarct was decreased despite a normal neuronal density. The study supports the traditional view held by pathologists that a sharp transition exists between infarcted and normal brain tissue and suggests that the hypoperfusion zone surrounding the region of complete infarction may be due to mechanisms other than selective loss of neurons.

Brain↗
PubMedDate not supplied

Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia.

As shown previously, the electrical function of the brain is critically dependent on cerebral blood flow in the sense that reduction beyond an ischemic threshold of approximately 15 ml/100 gm per minute (approximately 35% of control) in the baboon leads to complete failure of the somatosensory evoked response. This study tests the hypothesis that electrical failure in ischemia may be directly associated with a massive release of intracellular K+ or with a critical degree of extracellular acidosis. By microelectrode techniques, measurements of blood flow, extracellular activity of K+ and H+ as well as evoked potential were made in the baboon neocortex. Reductions in blood flow were obtained by occlusion of the middle cerebral artery and depression beyond the ischemic threshold of electrical function achieved by a reduction of systemic blood pressure which, in the ischemic zones, changed local cerebral blood flow proportionally. Abolition of evoked response could not be explained by depolarization by release of intracellular K+, nor was it critically dependent on cortical pH. However, the massive release of intracellular K+ was by itself critically dependent on cortical blood flow and occurred at 18 greater than 6 greater than 2 ml/100 gm per minute (median with 5% confidence limits). Thus a dual threshold in ischemia for neuronal function is described, the threshold for release of K+ being clearly lower than the threshold for complete electrical failure. Further, the findings support the concept of an ischemic penumbra during which the neurons remain structurally intact but functionally inactive. That neurons can survive for some time in this state of lethargy is evidenced by the observations that an increase in rCBF, if sufficient, can restore evoked potential and normalize extracellular K+ activity as well as pH.

Animals↗