| 1. |
- Auer, R. N., et al.
(författare)
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The distribution of hypoglycemic brain damage
- 1984
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Ingår i: Acta Neuropathologica. - 0001-6322. ; 64:3, s. 177-191
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Tidskriftsartikel (refereegranskat)abstract
- Rats were exposed to insulin-induced hypoglycemia resulting in periods of cerebral isoelectricity ranging from 10 to 60 min. After recovery with glucose, they were allowed to wake up and survive for 1 week. Control rats were recovered at the stage of EEG slowing. After sub-serial sectioning, the number and distribution of dying neurons was assessed in each brain region. Acid fuchsin was found to stain moribund neurons a brilliant red. Brains from control rats showed no dying neurons. From 10 to 60 min of cerebral isoelectricity, the number of dying neurons per brain correlated positively with the number of minutes of cerebral isoelectricity up to the maximum examined period of 60 min. Neuronal necrosis was found in the major brain regions vulnerable to several different insults. However, within each region the damage was not distributed as observed in ischemia. A superficial to deep gradient in the density of neuronal necrosis was seen in the cerebral cortex. More severe damage revealed a gradient in relation to the subjacent white matter as well. The caudatoputamen was involved more heavily near the white matter, and in more severely affected animals near the angle of the lateral ventricle. The hippocampus showed dense neuronal necrosis at the crest of the dentate gyrus and a gradient of increasing selective neuronal necrosis medially in CA1. The CA3 zone, while relatively resistant, showed neuronal necrosis in relation to the lateral ventricle in animals with hydrocephalus. Sharp demarcations between normal and damaged neuropil were found in the hippocampus. The periventricular amygdaloid nuclei showed damage closest to the lateral ventricles. The cerebellum was affected first near the foramina of Luschka, with damage occurring over the hemispheres in more severely affected animals. Purkinje cells were affected first, but basket cells were damaged as well. Rare necrotic neurons were seen in brain stem nuclei. The spinal cord showed necrosis of neurons in all areas of the gray matter. Infarction was not seen in this study. The possibility is discussed that a neurotoxic substance borne in the tissue fluid and cerebrospinal fluid (CSF) contributes to the pathogenesis of neuronal necrosis in hypoglycemic brain damage.
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| 4. |
- Blomström-Lundqvist, C, et al.
(författare)
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A long term follow up of 15 patients with arrhythmogenic right ventricular dysplasia
- 1987
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Ingår i: British Heart Journal. - 0007-0769. ; 58:5, s. 477-488
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Tidskriftsartikel (refereegranskat)abstract
- The clinical course in 15 patients with features consistent with arrhythmogenic right ventricular dysplasia is described. At referral seven patients had abnormal physical findings, nine had abnormal electrocardiograms with non-specific right-sided abnormalities, and seven patients had increased heart size or prominent right ventricles on chest x ray. During long term follow up (mean 8.8 years, range 1.5 to 28 years) 11 patients had abnormal physical findings, 11 had electrocardiographic changes, and nine had increased heart size. Recurrent sustained right ventricular tachycardia was the most common arrhythmia (10 patients). Two patients experienced ventricular fibrillation. Seven patients suffered from over 10 episodes of ventricular tachycardia, nine required cardioversions, and 10 patients had associated serious symptoms such as syncope, severe hypotension, or cardiac arrest. Four patients required operation to correct the arrhythmia and three patients developed right heart failure. Two out of three deaths were sudden. These data suggest that in arrhythmogenic right ventricular dysplasia right ventricular abnormalities may be progressive and that the condition may affect the left ventricle. The course of the ventricular arrhythmias was highly variable and could not be predicted in individual patients. The potential for lethal ventricular arrhythmias is evident and warrants intensive diagnostic efforts to identify patients with adverse prognostic features.
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| 5. |
- Blomström-Lundqvist, C, et al.
(författare)
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Cardioangiographic findings in patients with arrhythmogenic right ventricular dysplasia
- 1988
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Ingår i: British Heart Journal. - 0007-0769. ; 59:5, s. 556-563
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Tidskriftsartikel (refereegranskat)abstract
- The dimension, contractility, and regional wall motion of the right and left ventricles were scored on the angiograms of 13 patients with arrhythmogenic right ventricular dysplasia. In 10 patients the right ventricle was enlarged, in eight the contractility of the right ventricle was reduced, and in all but one patient there were regional wall motion abnormalities of the right ventricle. The most common abnormality of regional wall motion was mild hypokinesia. There were bulging or dyskinetic areas in seven patients. Regional wall motion abnormalities of the left ventricle were found in five patients, two of whom also had bulging or dyskinetic areas. The reproducibility of right ventricular dimension, contractility, and regional wall motion scores was generally fair but varied unexpectedly both within and between two observers (Kendall's Tau 0.38-0.92). The score values of regional wall motion for some of the segments differed considerably within and between observers. One of the observers consistently gave higher scores than the other. These data suggest that a more objective approach is needed for evaluating angiographic changes in arrhythmogenic right ventricular dysplasia.
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| 6. |
- Blomström-Lundqvist, C, et al.
(författare)
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Electrocardiographic findings and frequency of arrhythmias in Bartter's syndrome
- 1989
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Ingår i: British Heart Journal. - 0007-0769. ; 61:3, s. 274-279
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Tidskriftsartikel (refereegranskat)abstract
- Twenty four hour electrocardiograms in 20 patients with Bartter's syndrome, a disorder associated with chronic potassium deficiency, were analysed for atrial and ventricular extrasystoles, pauses (RR interval greater than 2 s), and heart rate. The 12 lead resting electrocardiogram was also evaluated. There were slight electrocardiographic changes with ST segment depression (greater than or equal to - 0.5 mm) in seven patients, flat or low amplitude T waves in seven, and U waves (greater than or equal to + 1.0 mm) in three patients. The QT interval was prolonged in 18 patients. Nine patients had one or more ventricular extrasystoles in 24 hours. Only two patients had more than 200 ventricular extrasystoles in 24 hours. No patient had ventricular tachycardia. A total of nine patients had one or more atrial extrasystoles in 24 hours, but only one patient had more than 200 in 24 hours. One patient had an attack of non-sustained supraventricular tachycardia. No patient had pauses. Dangerous tachycardia was rare in these patients with chronic potassium deficiency caused by Bartter's syndrome. The general pattern of slight electrocardiographic changes may reflect an adaptation of the myocardium to hypokalaemia. Further studies are, however, needed to determine whether these findings are relevant to long term prognosis.
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| 7. |
- Boström, Anders E, 1951, et al.
(författare)
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Elastodynamic scattering from inclusions with thin interface layers
- 1988
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Ingår i: Wave Propagation in Structural Composites AMD Vol. 90; Proceedings of the Joint ASME/SES Applied Mechanics and Engineering Sciences Conference, June 20-22, 1988. ; , s. 109-116
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Konferensbidrag (refereegranskat)
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| 8. |
- Boström, Anders E, 1951, et al.
(författare)
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Ground motion amplification on alluvial valleys
- 1989
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Ingår i: Applied Mathematics and Mechanics 35; Proceedings of the Second I.U.T.A.M.-I.U.P.A.P. Symposium on Elastic Wave Propagation.
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Konferensbidrag (refereegranskat)
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| 10. |
- Fredriksson, K, et al.
(författare)
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Cerebral microangiopathy in stroke-prone spontaneously hypertensive rats. An immunohistochemical and ultrastructural study
- 1988
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Ingår i: Acta Neuropathologica. - 1432-0533. ; 75:3, s. 241-252
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Tidskriftsartikel (refereegranskat)abstract
- The morphology of cerebral microvessels was studied immunohistochemically and ultrastructurally in 6- to 9-month-old normotensive Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone SHR (SHRSP) with a systolic blood pressure of 138 +/- 15 mm Hg, 189 +/- 9 mm Hg, and 258 +/- 30 mm Hg respectively. Regions with major opening of the blood-brain barrier (BBB) were revealed by an i.v. injection of Evans Blue. Multifocal BBB opening with massive leakage of plasma constituents rich in fibrinogen-fibrin-related antigen occurred in SHRSP with a blood pressure above 210-220 mm Hg. BBB-leakage sites were found in the cerebral cortex and the basal ganglia, most frequently in the arterial border zones. The perivascular tissue spaces were dilated within the BBB-leakage sites, in particular around arterioles. Damaged endothelial and smooth muscle cells were replaced by fibrin-like material, multiple layers of basement membranes and bundles of collagen fibrils surrounded by proliferated fibroblasts. The degenerative-infiltrative-proliferative disease process transformed short segments of single arterioles into severely thickened, tortuous and stenotic vessels. Fibrinoid degeneration, formation of microaneurysms and fibrin-rich vascular occlusions were observed. In contrast, only minor or no vascular alterations were seen in regions with preserved BBB in SHRSP and SHR. A severely increased intraluminal pressure load appears to be of major pathogenetic importance for breakdown of the BBB and initiation of the vascular disease process in SHRSP. However, since only short segments of a limited number of widely separated vessels are severely affected, and the number of affected vessels increase towards arterial end and border zones, additional predisposing and aggravating factors may play significant roles in the development of fibrinoid vascular lesions in arterial hypertension.
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