scholarly journals Local Cerebral Blood Flow in the Recovery Period following Complete Cerebral Ischemia in the Rat

1983 ◽  
Vol 3 (2) ◽  
pp. 170-182 ◽  
Author(s):  
Erik Kågström ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö

This study examines reflow patterns in the recirculation period following complete, global ischemia. Cerebrospinal fluid (CSF) compression ischemia was induced in ventilated rats for 5–30 min, and local cerebral blood flow (CBF) was measured autoradiographically after 5, 60, and 90 min of recirculation, Ischemia of 15 min duration was induced by four-vessel occlusion combined with arterial hypotension in two additional groups, with recovery periods of 5 or 60 min, In the immediate recirculation period (5 min), following 15 min of ischemia, local CBF was markedly heterogeneous, Thus, whereas most structures gave clear evidence of “reactive hyperemia,” others showed perfusion defects of the “no-reflow” type, Typically these defects affected the striatum, thalamus, and hippocampus, as well as the frontal, sensorimotor, and parietal cortices. Areas of no-reflow appeared after 10 min, were more extensive after 15 min, and occupied a major part of the brain after 30 min of ischemia. When recirculation was instituted for 60 or 90 min, following 15 min of ischemia, flow returned in previously unperfused areas. However, a delayed hypoperfusion developed, which differed widely between structures (range of CBF values, 20–80% of control). When the ischemic period was prolonged to 30 min, some perfusion defects remained, even after 90 min of recirculation.

1984 ◽  
Vol 4 (1) ◽  
pp. 82-87 ◽  
Author(s):  
Petter A. Steen ◽  
Leslie A. Newberg ◽  
James H. Milde ◽  
John D. Michenfelder

Ten minutes of complete cerebral ischemia was produced in 26 dogs by temporary ligation of the aorta and the venae cavae. Twenty dogs received nimodipine, a calcium entry blocker, 10 μg kg−1 i. v. 2 min after the ischemic period, followed by 1 μg kg−1 min−1 for 2–3 h. Six dogs received only the solvent used for nimodipine. Fourteen dogs received nimodipine for 3 h and were subsequently evaluated neurologically up to 48 h postischemia. In the 12 other dogs, CBF and metabolism were followed for 2 h postischemia while either nimodipine or the solvent only was infused. The results were compared to previously published results for untreated dogs and dogs given nimodipine before the ischemic event. Nimodipine had the same effect on postischemic CBF whether started before or after the ischemic event, nearly doubling the flow when compared with untreated controls, whereas the solvent alone caused only a slight increase in CBF over control. By contrast, nimodipine initiated in the preischemic period significantly improved the neurologic outcome, but when initiated in the post-ischemic period the results were equivocal, such that the outcome was not significantly different from either the untreated group or the group in which nimodipine was initiated preischemia. Metabolic measurements did not give any indication of a specific effect of nimodipine, nor could the metabolic results be used as an indicator of neurologic outcome. The results are consistent with a beneficial effect of nimodipine following complete cerebral ischemia; however, evaluation of neurologic functional effects will require a more sensitive model.


2018 ◽  
Vol 08 (03) ◽  
Author(s):  
Yasuyuki Matsuura ◽  
Toru Tanimura ◽  
Daisuke Iida ◽  
Hiroki Takada

1988 ◽  
Vol 10 (3) ◽  
pp. 151-155 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Cordell E. Gross ◽  
Geoff R. Adey ◽  
Ted S. Keller ◽  
Ken Nagata ◽  
...  

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