Temporal profile of ischemic tissue damage, neutrophil response, and vascular plugging following permanent and transient (2H) middle cerebral artery occlusion in the rat

We investigated the temporal profile of ischemic tissue damage, neutrophil response, and vascular occlusion after permanent and transient middle cerebral artery occlusion in the rat. Focal cerebral ischemia was induced by advancing a nylon monofilament to occlude middle cerebral artery (MCA). Two groups of rats were investigated: (1) those with permanent MCA occlusion (n = 29), and (2) and those having the arterial occlusion released after 2 h (n = 34). Experiments were terminated at 6, 12, 24, 48, 72, 96 and 168 h after the onset of ischemia, and brain sections were stained with hematoxylin and eosin for histological evaluation. Initially, the cortical lesion was smaller in rats subjected to transient MCA occlusion than in rats subjected to permanent MCA occlusion (p < 0.02). The surface area of the lesion was identical in both groups at 48 h after the onset of ischemia. Neutrophil infiltration into tissue and the time of peak neutrophil infiltration occurred earlier after transient MCA occlusion than after permanent MCA occlusion (6 h, 48 h in transient; 12 h, 72 h in permanent). Within the lesions, the number of occluded vessels was significantly lower in the transient ischemia group than in the permanent ischemia group during the time interval between 12-48 h (p < 0.01). Our data suggest that the temporal evolution of the lesion, the pattern of neutrophil infiltration and the chronology of microvascular occlusion differs depending on whether the MCA occlusion is transient (2 h) or permanent; however, significant differences in the size of the brain lesion disappeared 48 h after onset of ischemia.

[1]  R. Morawetz,et al.  Regional cerebral blood flow thresholds during cerebral ischemia. , 1979, Federation proceedings.

[2]  B. Siesjö,et al.  Focal and Perifocal Changes in Tissue Energy State during Middle Cerebral Artery Occlusion in Normo- and Hyperglycemic Rats , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[3]  P. Kochanek,et al.  Polymorphonuclear leukocyte accumulation in brain regions with low blood flow during the early postischemic period. , 1986, Stroke.

[4]  M. Kowada,et al.  Cerebral ischemia. II. The no-reflow phenomenon. , 1968, The American journal of pathology.

[5]  J. Ryu,et al.  Reevaluation of transient ischemic attacks as a risk factor for early mortality. , 1991, Stroke.

[6]  K. Madden,et al.  Tissue Plasminogen Activator Cerebrovascular Thrombolysis in Rabbits Is Dependent on the Rate and Route of Administration , 1992, Stroke.

[7]  H. Fukasawa,et al.  Attenuated neuropathology by nilvadipine after middle cerebral artery occlusion in rats. , 1991, Stroke.

[8]  G. Schmid-Schönbein,et al.  Polymorphonuclear Leukocytes Occlude Capillaries Following Middle Cerebral Artery Occlusion and Reperfusion in Baboons , 1991, Stroke.

[9]  J. Cervós-Navarro,et al.  The Cerebral Vessel Wall , 1977 .

[10]  P. Weinstein,et al.  Reversible middle cerebral artery occlusion without craniectomy in rats. , 1989, Stroke.

[11]  W D Heiss,et al.  Flow thresholds of functional and morphological damage of brain tissue. , 1983, Stroke.

[12]  P. Lyden,et al.  Incidence of cerebral hemorrhage after treatment with tissue plasminogen activator or streptokinase following embolic stroke in rabbits [corrected]. , 1990, Stroke.

[13]  M. Chopp,et al.  Duration dependent post-ischemic hypothermia alleviates cortical damage after transient middle cerebral artery occlusion in the rat , 1993, Journal of the Neurological Sciences.

[14]  M Chopp,et al.  Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. , 1993, The American journal of pathology.

[15]  R. Rosenwasser,et al.  Leukocyte involvement in cerebral ischemia and reperfusion injury. , 1990, Surgical neurology.

[16]  J. Garcìa,et al.  CEREBRAL INFARCTION: EVOLUTION OF HISTOPATHOLOGICAL CHANGES AFTER OCCLUSION OF A MIDDLE CEREBRAL ARTERY IN PRIMATES , 1974 .

[17]  M D Ginsberg,et al.  The Significance of Brain Temperature in Focal Cerebral Ischemia: Histopathological Consequences of Middle Cerebral Artery Occlusion in the Rat , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[18]  P. Kochanek,et al.  Indomethacin, prostacyclin, and heparin improve postischemic cerebral blood flow without affecting early postischemic granulocyte accumulation. , 1987, Stroke.

[19]  G. Schmid-Schönbein Capillary plugging by granulocytes and the no-reflow phenomenon in the microcirculation. , 1987, Federation proceedings.

[20]  H. Pasantes‐Morales,et al.  Effect of guanidinoethane sulfonate on taurine uptake by rat retina , 1984, Journal of neuroscience research.

[21]  J. Toole,et al.  Blood cell rheology in acute cerebral infarction. , 1989, Stroke.

[22]  K. Kogure,et al.  Correlation between cerebral blood flow and histologic changes in a new rat model of middle cerebral artery occlusion. , 1989, Stroke.

[23]  R. Busto,et al.  Histopathological and Hemodynamic Consequences of Complete versus Incomplete Ischemia in the Rat , 1987, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[24]  A. Leaf Cell Swelling: A Factor in Ischemic Tissue Injury , 1973, Circulation.

[25]  B. Siesjö,et al.  Penumbral Tissues Salvaged by Reperfusion Following Middle Cerebral Artery Occlusion in Rats , 1992, Stroke.

[26]  S. O’Gorman,et al.  Reassessment of Cerebral Capillary Changes in Acute Global Ischemia and Their Relationship to the "No-Reflow Phenomenon" , 1977, Stroke.

[27]  W. Pulsinelli,et al.  Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia. , 1991, Stroke.

[28]  Michael M. Todd,et al.  Mild Hypothermia Reduces Infarct Size Resulting From Temporary but Not Permanent Focal Ischemia In Rats , 1992, Stroke.

[29]  M. Chopp,et al.  Sequential neuronal and astrocytic changes after transient middle cerebral artery occlusion in the rat , 1993, Journal of the Neurological Sciences.

[30]  Y. Olsson,et al.  Regional cerebral blood flow and histopathologic changes after middle cerebral artery occlusion in rats. , 1989, Stroke.

[31]  M Chopp,et al.  The Effect of Hypothermia on Transient Middle Cerebral Artery Occlusion in the Rat , 1992, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[32]  R. Busto,et al.  The dissociation of cerebral blood flow, metabolism, and function in the early stages of developing cerebral infarction , 1980, Annals of neurology.