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

Marguerite T. Littleton-Kearney, Patricia D. Hurn, Thomas S. Kickler, Richard J. Traystman

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


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-1 in 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.

Original languageEnglish (US)
Pages (from-to)H1293-H1300
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4 43-4
StatePublished - Apr 1998


  • Chronological age
  • Platelet aggregation
  • Platelet entrapment

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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