Vol. 274, Issue 4, H1293-H1300, April 1998
Incomplete global cerebral ischemia alters platelet
biology in neonatal and adult sheep
Marguerite T.
Littleton-Kearney,
Patricia D.
Hurn,
Thomas S.
Kickler, and
Richard J.
Traystman
Department of Anesthesiology/Critical Care Medicine, The Johns
Hopkins Hospital, Baltimore, Maryland 21287-2725
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 g1 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.
platelet aggregation; platelet entrapment; chronological age
