Mt. Littletonkearney et al., INCOMPLETE GLOBAL CEREBRAL-ISCHEMIA ALTERS PLATELET BIOLOGY IN NEONATAL AND ADULT SHEEP, American journal of physiology. Heart and circulatory physiology, 43(4), 1998, pp. 1293-1300
Platelets are implicated as etiologic agents in cerebral ischemia and
as modulators of neural injury following an ischemic insult. We examin
ed the effects of severe, transient global ischemia on platelet aggreg
ation during 45-min ischemia and 30-, 60-, and 120-min reperfusion in
adult and neonatal lambs. We also examined postischemic platelet depos
ition in brain and other tissues (120-min reperfusion) using indium-11
1-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 depr
essed platelet aggregation response (P < 0.01) to 4 mu g collagen in l
ambs and sheep (20.4 +/- 29.2 and 26 +/- 44.7% of control, respectivel
y). Marked platelet deposition occurred in brain and spleen in sheep,
whereas significant platelet entrapment occurred only in brain in lamb
s. Our findings suggest that ischemia causes platelet activation and d
eposition in brain and noncerebral tissues.