scholarly journals Effects of clentiazem on cerebral ischemia induced by carotid artery occlusion in stroke-prone spontaneously hypertensive rats.

Stroke ◽  
1994 ◽  
Vol 25 (2) ◽  
pp. 474-480 ◽  
Author(s):  
K Kikkawa ◽  
R Yamauchi ◽  
T Suzuki ◽  
K Banno ◽  
S Murata ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Spontaneously Hypertensive Rats ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Effects of Carotid Artery Occlusion and Reflow on Cerebral Circulation in Normotensive and Spontaneously Hypertensive Rats

1976 ◽  
Vol 17 (3) ◽  
pp. 384-386 ◽  
Author(s):  
TAKESHI SHIMA ◽  
Noboru YOKOYAMA ◽  
Hirofumi ISHIHARA ◽  
SATOSHI KUWABARA ◽  
Takahiko IGUCHI ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Cerebral Circulation ◽  
Spontaneously Hypertensive Rats ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals The CBF Threshold and Dynamics for Focal Cerebral Infarction in Spontaneously Hypertensive Rats

1992 ◽  
Vol 12 (3) ◽  
pp. 359-370 ◽  
Author(s):  
Michael Jacewicz ◽  
Jody Tanabe ◽  
William A. Pulsinelli
Keyword(s):  
Cerebral Infarction ◽  
Spontaneously Hypertensive Rats ◽  
Infarct Volume ◽  
Maximum Size ◽  
Threshold Value ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Flow Threshold

Two strategies were used to estimate the blood flow threshold for focal cerebral infarction in spontaneously hypertensive rats (SHRs) subjected to permanent middle cerebral artery and common carotid artery occlusion (MCA/CCAO). The first compared the volume of cortical infarction (24 h after ischemia onset) to the volumes of ischemic cortex (image analysis of [14C]iodoantipyrine CBF autoradiographs) perfused below CBF values <50 (VIC50) and <25 ml 100 g−1 min−1 (VIC25) at serial intervals during the first 3 h of ischemia. The infarct process becomes irreversible within 3 h in this model. In the second, measurements of CBF at the border separating normal from infarcted cortex at 24 h after ischemia onset were used as an index of the threshold. During the first 3 h of ischemia, VIC50 increased slightly to reach a maximum size at 3 h that closely matched the 24 h infarct volume. VIC25, in contrast, consistently underestimated the infarct volume by a factor of 2–3. CBF at the 24 h infarct border averaged 50 ml 100 g−1 min−1. Taken together, the results indicate that the CBF threshold for infarction in SHRs approaches 50 ml 100 g−1 min−1 when ischemia persists for ≥3 h. This threshold value is approximately three times higher than in primates. Since cortical neuronal density is also threefold greater in rats than in primates, the higher injury threshold in the rat may reflect a neuronal primacy in determining the brain's susceptibility to partial ischemia.

scholarly journals Glucosylceramide Synthase Activity and Ceramide Levels are Modulated during Cerebral Ischemia after Ischemic Preconditioning

2004 ◽  
Vol 24 (6) ◽  
pp. 623-627 ◽  
Author(s):  
Kenzo Takahashi ◽  
Irene Ginis ◽  
Ryoji Nishioka ◽  
Dace Klimanis ◽  
Frank C. Barone ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Spontaneously Hypertensive Rats ◽  
Artery Occlusion ◽  
Hypertensive Rats ◽  
Glucosylceramide Synthase ◽  
Ceramide Level ◽  
Spontaneously Hypertensive ◽  
Ischemic Core ◽  
Ceramide Accumulation ◽  
Cerebral Artery Occlusion

After 24-hour middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats, brain ceramide level increased from baseline reached 595% (ischemic core) and 460% (perifocal/penumbral areas); brain glucosylceramide synthase (GCS) activities in these areas simultaneously decreased by 70% and 50%, respectively. Ten-minute MCAO preconditioning significantly attenuated 24-hour MCAO-induced ceramide accumulation by 40% to 60% in ischemic core and perifocal areas, and GCS activities improved by 60% to 70% in both areas. Thus, potentially toxic levels of brain ceramide induced by MCAO were attenuated to intermediate levels in preconditioned animals; brain GCS activity was relatively preserved. In ischemic tolerance, GCS appears to modulate otherwise high levels of brain ceramide.

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