Demonstrates transient focal neurological deficits caused by endogenous platelet microemboli in baboons, highlighting a clinically relevant model for evaluating acute stroke therapies.
To investigate the pathophysiological process of transient ischaemic events in a clinically relevant model, we produced transient focal cerebral ischaemia in five baboons using endogenously generated platelet microemboli. Thrombogenic segments of Dacron vascular graft were incorporated as unilateral carotid arterio-arterial shunts to produce endogenous platelet microemboli. The embolized microparticles were quantified by isotopic imaging using 111In-platelets and by transcranial Doppler ultrasonography. Platelet microemboli accumulated rapidly in the shunted carotid territory and reached a maximum value of 3.2 +/- 0.8 x 10(9) in the embolized hemisphere 20 min after initiating blood flow through the graft segment. Sixty min after removing the grafts 111In-platelets were largely cleared from hemispheric vasculature. Recovered animals exhibited mild contralateral hemiparesis which disappeared completely within 24 h. We conclude that endogenously generated platelet microemboli accumulate transiently in the dependent cerebral circulation and produce corresponding transient focal neurological dysfunction. This model may be useful in the evaluation of new therapeutic strategies in acute stroke.
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Kessler et al. (1992) studied this question.
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