Summary
Transient global ischemia was produced in cats by interrupting the arterial blood supply to the brain under direct observation of the pial vessels. The pial circulation could be restored only for a brief period after ischemia but intravascular rinsing of the brain during ischemia with various saline solutions considerably improved the postischemic circulation.
The functional status of neuronal activity was assessed by recording the EEG and the pyramidal response (PR) after electrical stimulation of the motor cortex. Perfused and nonperfused cats were compared with regard to the structure and function of the motor cortex in the early postischemic period. The neurophysiological signals recovered after ischemia of much longer duration in the perfused animals than in the nonperfused cats. Severe structural alterations were seen in capillaries, neurons and glial cells when ischemia was long enough to suppress the PR. In the perfused animals these changes were virtually absent even after ischemia up to 30 min duration.
The increased tolerance of the brain to ischemia produced by the intravascular rinsing appears to result from at least two different mechanisms. Elimination of metabolic waste products presumably reduces tissue damage during ischemia and the improved postischemic circulation prevents secondary ischemic lesions.
Zuammenfassung
Passagere Globalischämie wurde an Katzen durch Unterbrechung der Blutversorgung des Gehirns unter direkter Beobachtung der Piagefäße erzeugt. Die piale Zirkulation konnte nur kurzfristig nach der Ischämie wiederhergestellt werden, doch wurde die postischämische Zirkulation durch intravasale Perfusion des Gehirns mittels verschiedener Salzlösungen beträchtlich verbessert.
Der Funktionszustand der neuronalen Aktivität wurde mittels EEG und Pyramidenreaktion (PR) nach elektrischer Reizung des motorischen Cortex geprüft. Perfundierte und nichtperfundierte Katzen wurden im Hinblick auf die Struktur und Funktion des motorischen Cortex in der frühen postischämischen Periode verglichen. Bei perfundierten Tieren kamen die neurophysiologischen Signale nach Ischämie von wesentlich längerer Dauer wieder, als ber nichtperfundierten Katzen. Schwere strukturelle Veränderungen fanden sich an Capillaren, Neuronen und Gliazellen, wenn die Ischämie lange genug anhielt, um die PR zu unterdrücken. Bei perfundierten Tieren fehlten solche Veränderungen selbst nach Ischämie bis zu 30 min Dauer.
Die gesteigerte Toleranz des Gehirns gegenüber Ischämie infolge intravasaler Durchströmung erscheint durch zumindest zwei verschiedene Mechanismen bedingt. Die Eliminierung metabolischer Schlackenstoffe verringert vermutlich die Gewebsschäden während der Ischämie und die verbesserte postischämische Zirkulation verhindert sekundäre ischämische Schäden.
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References
Ames III, A., Wright, R. L., Kowada, M., Thurstone, J. M., Majno, G.: Cerebral ischemia. II. The No-reflow phenomenon. Amer. J. Path.52, 437–454 (1968).
Bakay, L., Lee, J. C.: The effect of acute hypoxia and hypercapnia on the ultrastructure of the central nervous system. Brain91, 697–706 (1968).
Brown, A. W., Brierley, J. B.: The nature, distribution and earliest stages of anoxic-ischemic. nerve cell damage in the rat brain as defined by the optical microscope. Brit. J. exp. Path.49, 87–106 (1968).
Cantu, R. C., Ames III, A.: Distribution of vascular lesions caused by cerebral ischemia. Neurology (Minneap.)19, 128–131 (1968).
Chiang, J., Kowada, M., Ames III, A., Wright, R. L., Majno, G.: Cerebral ischemia. III. Vascular changes. Amer. J. Path.52, 455–476 (1968).
Courville, C. B.: Cerebral anoxia. Los Angeles: San Lucas Press 1953.
Friede, R. L., van Houten, W. H.: Relations between post-mortem alterations and glycolytic metabolism in the brain. Exp. Neurol.4, 197–204 (1961).
Hager, H., Hirschberger, W., Scholz, W.: Electron microscopic changes in the brain tissue of syrian hamsters following acute hypoxia. Aerospace Med.31, 379–387 (1960).
Hills, C. P.: Ultrastructural changes in the capillary bed of the rat cerebral cortex in anoxicischemic brain lesions. Amer. J. Path.44, 531–543 (1964).
Hossmann, K.-A., Olsson, Y.: Suppression and recovery of neuronal function in transient cerebral ischemia. Brain Res.22, 313–325 (1970).
Kabat, H., Dennis, C., Baker, A. B.: Recovery of function following arrest of the brain circulation. Amer. J. Physiol.132, 737–747 (1941).
Karnovsky, M. J.: A formaldehyde-glutaraldehyde fixative of high osmolality for use in electron microscopy. J. Cell Biol.27, 137A (1965).
Kowada, M., Ames III, A., Majno, G., Wright, R. L.: Cerebral ischemia I. An improved experimental method for study; cardiovascular effects; and demonstration of an early vascular lesion in the rabbit. J. Neurosurg.28, 150–157 (1968).
Lindenberg, R.: Morphostatic necrobiosis. Investigations on the nerve cells of the brain. Amer. J. Path.32, 1147–1177 (1956).
—: Patterns of CNS vulnerability in acute hypoxaemia, including anaesthesia accidents. In: J. P. Schadé and W. H. McMenemy (Eds.): Selective vulnerability of the brain in hypoxaemia, p. 189. Oxford: Blackwell Scientific Publ. 1963.
McEwen, L. M.: The effect on the isolated rabbit heart of vagal stimulation and its modification by cocaine, hexamethonium and Quabain. J. Physiol. (Lond.)131, 678–689 (1956).
Patton, H. D., Amassian, W. E.: Single and multiple-unit analysis of cortical stage of pyramidal tract activation. J. Neurophysiol.17, 344–363 (1954).
Venable, J. H., Coggeshall, R.: A simplified lead citrate stain for use in electron microscopy. J. Cell Biol.25, 407–410 (1965)
Webster, H. de F., Ames III, A.: Reversible and irreversible changes in the fine structure of nervous tissue during oxygen and glucose deprivation. J. Cell Biol.26, 885–910 (1965).
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Olsson, Y., Hossmann, K.A. The effect of intravascular saline perfusion on the sequelae of transient cerebral ischemia. Acta Neuropathol 17, 68–79 (1971). https://doi.org/10.1007/BF00684742
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DOI: https://doi.org/10.1007/BF00684742