Summary
Extravasated endogenous serum albumin and fibrinogen were identified immunohistochemically in coronal brain sections from normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) after permanent ligation of the right middle cerebral artery. Infarcts were seen in all the SHR but only in 6 out of 14 WKY. Six hours after ligation, extravasated proteins were located primarily within the borders of the infarcts whereas after 24 h and later there was an increasing spread in the white matter. After 7 days, a protein immunoreactivity was seen far outside the infarcted areas, mainly in the white matter and occasionally extending somewhat into the contralateral side. Three weeks after permanent ligation, the immunoreactivity for plasma proteins had a similar extension but was less intense than after 7 days. A gliosis was noted within the protein-positive regions. From 72 h and onwards the immunoreactivity for albumin but not for fibrinogen extended via the white matter into the ipsilateral thalamic nuclei, where marked, mainly cytolytic nerve cell damage and gliosis was found. The close spatial correlation with albumin immunopositivity and the histological features of the thalamic lesions indicate that the propagation of extravasated plasma constituents or degradation products from the infarct may influence the character, timing and extent of remote tissue changes after cerebral infarction.
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Brightmann MW, Klatzo I, Olsson Y, Reese TS (1970) The blood-brain barrier to proteins under normal and pathological conditions. J Neurol Sci 10:215–239
Chui E, Wilmes F, Sotelo JE, Horie R, Fujiwari K, Suzuki R, Klatzo I (1981) Immunocytochemical studies on extravasation of serum proteins in cerebrovascular disorders. In: Cervós-Navarro J, Fritschka E (eds) Cerebral microcirculation and metabolism. Raven Press, New York; pp 121–127
Coyle P (1986) Different susceptibilities to cerebral infarction in spontaneously hypertensive (SHR) and normotensive Sprague-Dawley rats. Stroke 17:520–528
Cragg BG (1970) What is the signal for chromatolysis? Brain Res 23:1–21
Duverger D, MacKenzie ET (1988) The quantification of cerebral infarction following focal ischemia in the rat: influence of strain arterial pressure, blood glucose concentration and age. J Cereb Blood Flow Metab 8:449–461
Fredriksson K, Auer RN, Kalimo H, Nordborg C, Olsson Y, Johansson BB (1985) Cerebrovascular lesions in stroke-prone spontaneously hypertensive rats. Acta Neuropathol (Berl) 68:284–294
Fredriksson K, Kalimo H, Nordborg C, Johansson BB, Olsson Y (1988) Nerve cell injury in the brain of stroke-prone spontaneously hypertensive rats. Acta Neuropathol 76:227–237
Fredriksson K, Kalimo H, Nordborg C, Olsson Y, Johansson BB (1988) Cyst formation and glial response in the brain lesions of stroke-prone spontaneously hypertensive rats. Acta Neuropathol 76:441–450
Fry FJ, Cowan WM (1972) A study of retrograde cell degeneration in the lateral mamillary nucleus of the cat, with special reference to the role of axonal branching in the preservation of the cell. J Comp Neurol 144:1–24
Fujie W, Kirino T, Tomukai N, Iwasawa T, Tamura A (1990) Progressive shrinkage of the thalamus following middle cerebral artery occlusion in rats. Stroke 21:1485–1488
Grabowski M, Nordborg C, Brundin P, Johansson BB (1988) Middle cerebral artery occlusion in the hypertensive and normotensive rat: a study of histopathology and behaviour. J Hypertens 6:405–411
Iizuka H, Sakatani K, Young W (1989) Corticofugal axonal degeneration in rats after middle cerebral artery occlision. Stroke 20:1396–1402
Kalimo H, Fredriksson K, Nordborg C, Auer RN, Olsson Y, Johansson BB (1986) The spread of brain oedema in hypertensive brain injury. Med Biol 64:133–137
Klatzo I, Wisniewski H, Steinwall O, Streicher E (1967) Dynamics of cold injury edema. In: Klatzo I, Seitelberger F (eds) Brain edema. Springer-Verlag, Berlin Heidelberg New York, pp. 554–563
Kuroiwa T, Ting P, Martinez H, Klatzo I (1985) The biphasic opening of the blood-brain barrier to proteins following temporary middle cerebral artery occlusion. Acta Neuropathol (Berl) 68:122–129
Lieberman AR (1971) The axon reaction: a review of the principal features of perikaryal responses to axon injury. Int Rev Neurobiol 14:49–124
Martin JJ (1969) Thalamic syndromes. Handb Clin Neurol 2:469–496
Matthews MA (1973) Death of the central neuron: an electron microscopic study of thalamic retrograde degeneration following cortical ablation. J Neurocytol 2:265–288
Mesulam MM (1982) Tracing neuronal connections with horseradish peroxidase. Ibro handbook series: methods in neurosciences. Wiley and Sons, New York, pp 3–135
Nag S (1984) Cerebral changes in chronic hypertension: combined permeability and immunohistochemical studies. Acta Neuropathol (Berl) 62:178–184
21.Ogata J, Fujishima M, Tamaki K, Nakatomi Y, Ishitsuka T, Omae T (1980) Stroke-prone spontaneously hypertensive rats as an experimental model of malignant hypertension. 1. A light- and electron-microscopic study of the brain. Acta Neuropathol (Berl) 51:179–184
Ogata J, Fujishima M, Tamaki K, Nakatomi Y, Ishitsuka T, Omae T (1981) Vascular changes underlying cerebral lesions in stroke-prone spontaneously hypertensive rats. A serial section study. Acta Neuropathol (Berl) 54:183–188
Robertson RT (1977) Bidirectional movement of horseradish peroxidase and the demonstration of reciprocal thalamocortical connections. Brain Res 129:538–544
Salahuddin TS, Kalimo H, Johansson BB, Olsson Y (1988) Observations on exsudation of fibronectin, fibrinogen and albumin in the brain after carotid infusion of hyperosmolar solutions. Acta Neuropathol 76:1–10
Salahuddin TS, Johansson BB, Kalimo H, Olsson Y (1988) Structural changes in the rat brain after carotid infusions of hyperosmolar solutions. An electron microscopic study. Acta Neuropathol 77:5–13
Sokrab T-EO, Johansson BB, Tengvar C, Kalimo H, Olsson Y (1988) Adrenaline-induced hypertension: morphological consequences of the blood-brain barrier disturbance. Acta Neurol Scand 77:387–396
Sokrab T-EO, Johansson BB, Kalimo H, Olsson Y (1988) A transient hypertensive opening of the blood-brain barrier can lead to brain damage. Extravasation of serum proteins and cellular changes in rats subjected to aortic compression. Acta Neuropathol (Berl) 75:557–565
Sokrab T-EO, Kalimo H, Johansson BB (1990) Parenchymal changes related to plasma protein extravasation in experimental seizures. Epilepsia 31:1–8
Tamura A, Graham DI, McCulloch J, Teasdale GM (1981) Focal cerebral ischemia in the rat. 1. Description of technique and early neuropathological consequences following middle cerebral artery occlusion. J Cereb Blood Flow Metab 1:53–60
Tamura A, Graham DI, McCulloch J, Teasdale GM (1981) Focal cerebral ischemia in the rat. 2. Regional cerebral blood flow determined by [14C]iodoantipyrine autoradiography following middle cerebral artery occlusion. J Cereb Blood Flow Metab 1:61–69
Tengvar C (1986) Extensive intraneuronal spread of horseradish peroxidase from a focus of vasogenic edema into remote areas of the central nervous system. Acta Neuropathol (Berl) 71:177–189
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Supported by grants from the Swedish Medical Research Council (Project 14X-4968), the Swedish Heart Lung Foundation, King Gustaf V and Queen Victoria Foundation and from the 1987 Foundation for Stroke Research
Reported in part at the XIVth International Joint Conference on Stroke and Cerebral Circulation, San Antonio, Texas, February 9–11, 1989. Published as an abstract in Stroke 20:146 (1989)
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Nordborg, C., Sokrab, T.E.O. & Johansson, B.B. The relationship between plasma protein extravasation and remote tissue changes after experimental brain infarction. Acta Neuropathol 82, 118–126 (1991). https://doi.org/10.1007/BF00293954
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DOI: https://doi.org/10.1007/BF00293954