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Structural changes at cell junction
j Mol Cell Cardiol 18 (Supplement 1) (1986)
4SSTRUCTURAL
CHANGES AT CELL JUNCTIONS. G.R. Bullock. Ciba-Geigy Pharmaceuticals, Horsham, West Sussex, U.K. The response of the cell junction to ischaemia appears to be a gradual process compared with the withdrawal of ions such as calcium. Short periods of ischaemia produce few ultrastruetural changes other than a widening of the free intercellular spaces which may be due to loss of cell water (1). As the ischaemie process develops, then different components of the cell junction become involved but the desmosome seems to be remarkably resistant (2). Using freeze fracture techniques, it is possible to evaluate these changes in more detail and it has been demonstrated that changes in the arrangement of the inter-membranous particles takes place (3). Clumping of particles in the sarcolemma away from this area suggest possible phase transition changes and hence altered membrane fluidity. By maintaining the integrity of the junction, the heart has a way of combating at least moderate ischaemie conditions. (I)-Bullock G.R. In 'Protection of Tissues Against Hypoxia' Ecls Wauqier, Borgers and Amery 1982. Elsevier Biomedical Press. (2) Kawamura K. and James T . N . J . Mol. Cell Cardiol. 3:31-60 1971. (3) Green C.R. and Severs N . J . , J . Cell Biol. 99:453-463 1984.
5SEFFECTS OF ISCHAEMIA ON VASCULATURE. T. Nevalainen. Department of Pathology, University of Turku, Turku, Finland The effects of ischaemia on the structure and function of coronary vessels have been evaluated most thoroughly in the open-chest anesthesized dog. In the beating heart the flow into the capillary bed is controlled by precapillary sphincters in the terminal arterioles. Short periods (up to 20 min) of ischaemia result during reperfusion in vasodilatation which is mediated through increased tissue adenosine levels. Longer periods of ischaemia (60 and more min) result in degenerative vascular changes and no-reflow during reperfusion. Endothelial cells swell and lose their pinocytotic vesicles and form spherical cytoplasmic protrusion in the capillary lumina. Prolonged isehaemia (over 3 hours) causes ruptures in microvaseular walls. Such vessels become permeable to large tracers, e.g. carbon particles, end reperfusion results in haemorrhage. Capillaries in ischaemic myocardium collapse and become occluded by compression caused by intra- and extracellular oedema and contracture of myoeytes. Erythrocytes plug collapsed mierovessels. However, in vitro observations have shown that no-fellow may result from isehaemia even without erythrocyte plugging. Capillary compression is the main determinant of no-reflow after ischaemia. Degenerative ischaemie changes in vascular walls further contribute to vascular incompetence in vivo.
6S STRUCTURAL ALTERATIONS IN
CARDIAC CONDUCTING CELLS IN OXYGEN DEFICIENCY. L.C. Armiger, C.M. Knell. Department of Pathology, University of Auckland School of Medicine, Auckland, New Zealand. The fine structural effects of oxygen deficiency on the cardiac conduction system were studied in the dog and the rat, using various in vitro and in vivo models. Observations did not support the concept that conducting cells are inherently more resistant to ischaemia and anoxia than contractile myocardial cells. Nodal cells altered more rapicUy than His-Purkinje cells in the dog, but not in the rat, which has less clearly-defined cell differences in these regions and a greater glycogen content in the atrioventricular node. Cellular alteration was uniform in global ischaemia in the isolated rat heart, but focal in high-flow, glucose-free ano~da. Comparisonof in vitro and in vivo observations in the dog indicated that better collateral blood flow is chiefly responsible for preservation of conducting elements in the context of myocardial infarction. (Supported by the Medical Research Council and the National Heart Foundation of New Zealand. )
4SSTRUCTURAL
CHANGES AT CELL JUNCTIONS. G.R. Bullock. Ciba-Geigy Pharmaceuticals, Horsham, West Sussex, U.K. The response of the cell junction to ischaemia appears to be a gradual process compared with the withdrawal of ions such as calcium. Short periods of ischaemia produce few ultrastruetural changes other than a widening of the free intercellular spaces which may be due to loss of cell water (1). As the ischaemie process develops, then different components of the cell junction become involved but the desmosome seems to be remarkably resistant (2). Using freeze fracture techniques, it is possible to evaluate these changes in more detail and it has been demonstrated that changes in the arrangement of the inter-membranous particles takes place (3). Clumping of particles in the sarcolemma away from this area suggest possible phase transition changes and hence altered membrane fluidity. By maintaining the integrity of the junction, the heart has a way of combating at least moderate ischaemie conditions. (I)-Bullock G.R. In 'Protection of Tissues Against Hypoxia' Ecls Wauqier, Borgers and Amery 1982. Elsevier Biomedical Press. (2) Kawamura K. and James T . N . J . Mol. Cell Cardiol. 3:31-60 1971. (3) Green C.R. and Severs N . J . , J . Cell Biol. 99:453-463 1984.
5SEFFECTS OF ISCHAEMIA ON VASCULATURE. T. Nevalainen. Department of Pathology, University of Turku, Turku, Finland The effects of ischaemia on the structure and function of coronary vessels have been evaluated most thoroughly in the open-chest anesthesized dog. In the beating heart the flow into the capillary bed is controlled by precapillary sphincters in the terminal arterioles. Short periods (up to 20 min) of ischaemia result during reperfusion in vasodilatation which is mediated through increased tissue adenosine levels. Longer periods of ischaemia (60 and more min) result in degenerative vascular changes and no-reflow during reperfusion. Endothelial cells swell and lose their pinocytotic vesicles and form spherical cytoplasmic protrusion in the capillary lumina. Prolonged isehaemia (over 3 hours) causes ruptures in microvaseular walls. Such vessels become permeable to large tracers, e.g. carbon particles, end reperfusion results in haemorrhage. Capillaries in ischaemic myocardium collapse and become occluded by compression caused by intra- and extracellular oedema and contracture of myoeytes. Erythrocytes plug collapsed mierovessels. However, in vitro observations have shown that no-fellow may result from isehaemia even without erythrocyte plugging. Capillary compression is the main determinant of no-reflow after ischaemia. Degenerative ischaemie changes in vascular walls further contribute to vascular incompetence in vivo.
6S STRUCTURAL ALTERATIONS IN
CARDIAC CONDUCTING CELLS IN OXYGEN DEFICIENCY. L.C. Armiger, C.M. Knell. Department of Pathology, University of Auckland School of Medicine, Auckland, New Zealand. The fine structural effects of oxygen deficiency on the cardiac conduction system were studied in the dog and the rat, using various in vitro and in vivo models. Observations did not support the concept that conducting cells are inherently more resistant to ischaemia and anoxia than contractile myocardial cells. Nodal cells altered more rapicUy than His-Purkinje cells in the dog, but not in the rat, which has less clearly-defined cell differences in these regions and a greater glycogen content in the atrioventricular node. Cellular alteration was uniform in global ischaemia in the isolated rat heart, but focal in high-flow, glucose-free ano~da. Comparisonof in vitro and in vivo observations in the dog indicated that better collateral blood flow is chiefly responsible for preservation of conducting elements in the context of myocardial infarction. (Supported by the Medical Research Council and the National Heart Foundation of New Zealand. )