scholarly journals Failure of flunarizine to improve cerebral blood flow or neurologic recovery in a canine model of complete cerebral ischemia.

Stroke ◽  
1984 ◽  
Vol 15 (4) ◽  
pp. 666-671 ◽  
Author(s):  
L A Newberg ◽  
P A Steen ◽  
J H Milde ◽  
J D Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Canine Model ◽  
Neurologic Recovery ◽  
Complete Cerebral Ischemia

scholarly journals Nicardipine Increases Cerebral Blood Flow but Does Not Improve Neurologic Recovery in a Canine Model of Complete Cerebral Ischemia

1986 ◽  
Vol 6 (6) ◽  
pp. 684-690 ◽  
Author(s):  
Takefumi Sakabe ◽  
Ikuo Nagai ◽  
Toshizoh Ishikawa ◽  
Hiroshi Takeshita ◽  
Tsutomu Masuda ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Canine Model ◽  
Untreated Group ◽  
Outcome Studies ◽  
Neurologic Outcome ◽  
Calcium Entry Blocker ◽  
Neurologic Recovery ◽  
Complete Cerebral Ischemia

The effects of the calcium entry blocker nicardipine on CBF, CMRO2, and neurologic outcome following 10 min of complete cerebral ischemia were examined in dogs. In CBF and CMRO2 studies, the CBF in the untreated group (seven dogs) and the nicardipine group (seven dogs; 20 μg kg−1 at 30 min postischemia and a subsequent infusion of 2 μg kg−1 min−1 for 90 min) initially increased to 300–400% and then returned to preischemic values at 30 min postischemia. Thereafter the CBF in the untreated group significantly decreased to 50% of preischemic values for the following 90-min period (hypoperfusion), while the CBF in the nicardipine group did not differ from preischemic values. The CMRO2 in both groups decreased to ∼50–80% of preischemic values after 15 min postischemia and did not differ between the groups throughout the study. In neurologic outcome studies, 18 dogs were divided into three groups (of six dogs each): untreated; saline infusion only, posttreated; nicardipine as in CBF and CMRO2 studies, pretreated; nicardipine 20 μg kg−1 at 2 min preischemia and a subsequent infusion of 2 μg kg−1 min−1 from immediately postischemia to 120 min postischemia. Nicardipine treatment initiated either before or after ischemia failed to improve neurologic outcome at 48 h postischemia. Thus, the increase of postischemic global CBF by nicardipine is not accompanied by neurologic recovery in a canine model of complete cerebral ischemia.

scholarly journals Nimodipine Improves Cerebral Blood Flow and Neurologic Recovery after Complete Cerebral Ischemia in the Dog

1983 ◽  
Vol 3 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Petter A. Steen ◽  
Leslie A. Newberg ◽  
James H. Milde ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Protective Effect ◽  
Calcium Entry ◽  
Calcium Entry Blocker ◽  
Neurologic Recovery ◽  
Entry Blocker ◽  
Ischemic Episode ◽  
Complete Cerebral Ischemia

Ten minutes of complete ischemia was produced in 11 dogs by temporary ligation of the aorta. Immediately before the ischemic episode, the dogs received nimodipine, a new calcium entry blocker, 10 μg kg−1, i.v., followed by an infusion of 1 μg kg−1 min−1 for 2 h. Post-ischemic cerebral blood flow and metabolism were measured for 120 min in six dogs. Neurologic recovery was evaluated 48 h post-ischemia in five dogs. The results were compared to previously determined controls. Nimodipine nearly doubled cerebral blood flow in the delayed post-ischemic hypoperfusion period, compared to untreated dogs (approximately 45% versus 25% of pre-ischemic control values), but had no significant effect on metabolism. Nimodipine also improved neurologic recovery. Four of five treated dogs were normal and one was moderately damaged, whereas six of seven controls were either severely damaged or dead. This suggests that the delayed hypoperfusion state occurring after complete cerebral ischemia probably does contribute to the ultimate neurologic damage, and that nimodipine offers a potential protective effect.

scholarly journals Delayed Treatment with Nimodipine Improves Cerebral Blood Flow after Complete Cerebral Ischemia in the Dog

1986 ◽  
Vol 6 (3) ◽  
pp. 332-337 ◽  
Author(s):  
Leslie Newberg Milde ◽  
James H. Milde ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Cerebral Metabolism ◽  
Cerebral Hypoperfusion ◽  
Constant Infusion ◽  
Calcium Entry Blocker ◽  
Delayed Treatment ◽  
Venae Cavae ◽  
Complete Cerebral Ischemia

Ten minutes of complete cerebral ischemia was produced in 18 dogs by temporary ligation of the aorta and venae cavae. Dogs were randomly assigned to one of three groups. A bolus dose of 10 μg kg−1 nimodipine, a dihydropyridine calcium entry blocker, followed by a constant infusion of 1 μg kg−1 min−1 was given at 15, 30, or 60 min post ischemia. Cerebral blood flow and metabolism were measured for 2 h postischemia. Delayed treatment with nimodipine ameliorated or reversed the cerebral hypoperfusion that routinely occurs after complete ischemia. In the groups treated at 15 and 30 min, CBF remained above 60 ml min−1 100 g−1. In the group treated at 60 min, there was a progressive decline in CBF to 37 ml min−1 100 g−1. Following treatment with nimodipine, CBF immediately increased and was maintained above 50 ml min−1 100 g−1 for the remainder of the study. Once treatment with nimodipine was begun, CBF was approximately double that of an untreated group. Changes in CBF reflected changes in cerebrovascular resistance. Nimodipine had no effect on cerebral metabolism. Since the postischemic hypoperfusion state is believed to contribute to the ultimate neurologic damage following complete ischemia, treatment with nimodipine, even if delayed up to 60 min, may improve the outcome.

Effect of Lidoflazine on Cerebral Blood Flow and Neurologic Outcome When Administered After Complete Cerebral Ischemia in Dogs

1987 ◽  
Vol 66 (3) ◽  
pp. 304-311 ◽  
Author(s):  
Jerry E. Fleischer ◽  
William L. Lanier ◽  
James H. Milde ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Neurologic Outcome ◽  
Complete Cerebral Ischemia

scholarly journals Cerebral Blood Flow and Neurologic Outcome When Nimodipine is Given after Complete Cerebral Ischemia in the Dog

1984 ◽  
Vol 4 (1) ◽  
pp. 82-87 ◽  
Author(s):  
Petter A. Steen ◽  
Leslie A. Newberg ◽  
James H. Milde ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Specific Effect ◽  
Neurologic Outcome ◽  
Calcium Entry Blocker ◽  
Ischemic Event ◽  
Venae Cavae ◽  
Ischemic Period ◽  
Complete Cerebral Ischemia

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.

Post-ischemic neurologic recovery and cerebral blood flow using a compression model of complete “bloodless” cerebral ischemia in dogs

Resuscitation ◽  
1988 ◽  
Vol 16 (4) ◽  
pp. 271-286 ◽  
Author(s):  
William L. Lanier ◽  
Jerry E. Fleischer ◽  
James H. Milde ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Neurologic Recovery ◽  
Compression Model
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