Incomplete global cerebral ischemia alters platelet biology in neonatal and adult sheep

1998 ◽  
Vol 274 (4) ◽  
pp. H1293-H1300 ◽  
Author(s):  
Marguerite T. Littleton-Kearney ◽  
Patricia D. Hurn ◽  
Thomas S. Kickler ◽  
Richard J. Traystman
Keyword(s):  
Platelet Aggregation ◽  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Ischemic Insult ◽  
Aggregation Response ◽  
Etiologic Agents ◽  
Platelet Deposition ◽  
Incomplete Global Cerebral Ischemia ◽  
Indium 111 ◽  
Neonatal Lambs

Platelets are implicated as etiologic agents in cerebral ischemia and as modulators of neural injury following an ischemic insult. We examined the effects of severe, transient global ischemia on platelet aggregation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in adult and neonatal lambs. We also examined postischemic platelet deposition in brain and other tissues (120-min reperfusion) using indium-111-labeled platelets. Ischemic cerebral blood flow fell to 5 ± 1 and 5 ± 2 ml ⋅ min−1⋅ 100 g−1in lambs and sheep, respectively. During ischemia, platelet counts fell to 47.5 ± 5.1% of control ( P < 0.05) in lambs and 59 ± 4.9% of control in sheep ( P < 0.05). Ischemia depressed platelet aggregation response ( P < 0.01) to 4 μg collagen in lambs and sheep (20.4 ± 29.2 and 26 ± 44.7% of control, respectively). Marked platelet deposition occurred in brain and spleen in sheep, whereas significant platelet entrapment occurred only in brain in lambs. Our findings suggest that ischemia causes platelet activation and deposition in brain and noncerebral tissues.

Parallel Antioxidant and Antiexcitotoxic Therapy Improves Outcome After Incomplete Global Cerebral Ischemia in Dogs

Stroke ◽  
1997 ◽  
Vol 28 (1) ◽  
pp. 198-205 ◽  
Author(s):  
Steve Davis ◽  
Mark A. Helfaer ◽  
Richard J. Traystman ◽  
Patricia D. Hurn
Keyword(s):  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Incomplete Global Cerebral Ischemia

scholarly journals MK-801 (Dizocilpine) Protects the Brain from Repeated Normothermic Global Ischemic Insults in the Rat

1993 ◽  
Vol 13 (6) ◽  
pp. 925-932 ◽  
Author(s):  
Baowan Lin ◽  
W. Dalton Dietrich ◽  
Myron D. Ginsberg ◽  
Mordecai Y.-T. Globus ◽  
Raul Busto
Keyword(s):  
Cerebral Ischemia ◽  
Repeated Measures ◽  
Neuronal Damage ◽  
Brain Temperature ◽  
Global Cerebral Ischemia ◽  
Striatal Neurons ◽  
Ischemic Insult ◽  
Mk 801 ◽  
Bilateral Carotid ◽  
Ventrolateral Thalamus

We investigated the neuroprotective potential of MK-801 (dizocilpine), a noncompetitive N-methyl-d-aspartate (NMDA) antagonist, in the setting of three 5-min periods of global cerebral ischemia separated by 1-h intervals in halothane-anesthetized rats. Each ischemic insult was produced by bilateral carotid artery occlusions plus hypotension (50 mm Hg). Brain temperature was maintained at normothermic levels (36.5–37.0°C) throughout the experiment. MK-801 (3 mg/kg) (n = 6) or saline (n = 6) was injected intraperitoneally 45 min following the end of the first ischemic insult. Following 7-day survival, quantitative neuronal counts of perfusion-fixed brains revealed severe ischemic damage in hippocampal CA1 area, neocortex, ventrolateral thalamus, and striatum of untreated rats. By contrast, significant protection was observed in MK-801-treated rats. In area CA1 of the hippocampus, numbers of normal neurons were increased 11- to 14-fold by MK-801 treatment (p < 0.01). The ventrolateral thalamus of MK-801-treated rats showed almost complete histologic protection, and neocortical damage was reduced by 71% (p < 0.01). The degree of MK-801 protection of striatal neurons was less complete than that seen in other vulnerable structures, amounting to 63% for central striatum (p = 0.02, Mann–Whitney U test) and 48% in the dorsolateral striatum (NS). A repeated-measures analysis of variance demonstrated a highly significant overall protective effect of MK-801 treatment ( F1,10 = 37.2, p = 0.0001). These findings indicate that excitotoxic mechanisms play a major role in neuronal damage produced by repeated ischemic insults and that striking cerebroprotection is conferred by MK-801 administered following the first insult in animals with cerebral normothermia. NMDA antagonists may prove useful in patients at risk of repeated episodes of cerebral ischemia.

scholarly journals Ischemic Preconditioning Preserves Mitochondrial Function after Global Cerebral Ischemia in Rat Hippocampus

2001 ◽  
Vol 21 (12) ◽  
pp. 1401-1410 ◽  
Author(s):  
Kunjan R. Dave ◽  
Isabel Saul ◽  
Raul Busto ◽  
Myron D. Ginsberg ◽  
Thomas J. Sick ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Cerebral Ischemia ◽  
Oxidative Phosphorylation ◽  
Ischemic Preconditioning ◽  
Global Cerebral Ischemia ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Ischemic Insult ◽  
Bilateral Carotid ◽  
Consumption Rates ◽  
Induction Of Tolerance

Ischemic tolerance in brain develops when sublethal ischemic insults occur before “lethal” cerebral ischemia. Two windows for the induction of tolerance by ischemic preconditioning (IPC) have been proposed: one that occurs within 1 hour after IPC, and another that occurs 1 or 2 days after IPC. The authors tested the hypotheses that IPC would reduce or prevent ischemia-induced mitochondrial dysfunction. IPC and ischemia were produced by bilateral carotid occlusions and systemic hypotension (50 mm Hg) for 2 and 10 minutes, respectively. Nonsynaptosomal mitochondria were harvested 24 hours after the 10-minute “test” ischemic insult. No significant changes were observed in the oxygen consumption rates and activities for hippocampal mitochondrial complexes I to IV between the IPC and sham groups. Twenty-four hours of reperfusion after 10 minutes of global ischemia (without IPC) promoted significant decreases in the oxygen consumption rates in presence of substrates for complexes I and II compared with the IPC and sham groups. These data suggest that IPC protects the integrity of mitochondrial oxidative phosphorylation after cerebral ischemia.

Effect of peptide Semax and its C-terminal fragment PGP on Vegfa gene expression during incomplete global cerebral ischemia in rats

2013 ◽  
Vol 47 (3) ◽  
pp. 406-410 ◽  
Author(s):  
V. V. Stavchanskii ◽  
T. V. Tvorogova ◽  
A. Yu. Botsina ◽  
S. A. Limborska ◽  
V. I. Skvortsova ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Terminal Fragment ◽  
Incomplete Global Cerebral Ischemia ◽  
Vegfa Gene

Effect of fentanyl on the electrophysiological recovery following incomplete global cerebral ischemia

1991 ◽  
Vol 23 (3) ◽  
pp. 227-232 ◽  
Author(s):  
Usha S. Vasthare ◽  
Sharon Rubin ◽  
Howard A. Riina ◽  
Robert H. Rosenwasser ◽  
Christer Carlsson ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Incomplete Global Cerebral Ischemia

Ultrastorcture of Cerebellar Purkinje Cells in Rats Subjected To Partial Global Cerebral Ischemia

1985 ◽  
Vol 43 ◽  
pp. 674-675
Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros
Keyword(s):  
Cerebral Ischemia ◽  
Purkinje Cells ◽  
Cell Types ◽  
Microscopic Level ◽  
Global Cerebral Ischemia ◽  
Light Microscopic Level ◽  
Cerebellar Damage ◽  
Cerebellar Injury ◽  
Cerebellar Purkinje Cells ◽  
Cell Changes

In severe cerebral ischemia, Purkinje cells of the cerebellum are one of the cell types most vulnerable to anoxic damage. In the partial (forebrain) global ischemic (PGI) model of the rat, Paljärvi noted at the light microscopic level that cerebellar damage is inconsistant and when present, milder than in the telencephalon, diencephalon and rostral brain stem. Cerebellar injury was observed in 3 of 4 PGI rats following 5 minutes of reperfusion but in none of the rats after 90 min of reperfusion. To evaluate a time between these two extremes (5 and 90 min), the present investigation used the PGI model to study the effects of ischemia on the ultrastructure of cerebellar Purkinje cells in rats that were sacrificed after 30 min of reperfusion. This time also was chosen because lactic acid that is thought to contribute to ischemic cell changes in PGI is at a maximum after 30 min of reperfusion.

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