OBJECT: The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH. METHODS: Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls. The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH. CONCLUSIONS: The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.
OBJECT: The mechanisms underlying acute cerebral ischemia after subarachnoid hemorrhage (SAH) are not well established. Platelets aggregate within major cerebral vessels hours after SAH, but this has not been studied in the microvasculature. Platelet aggregates within the microvasculature could mechanically obstruct the lumen and initiate events that injure vessel structure. In the present study the authors examined the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH. METHODS:Subarachnoid hemorrhage was induced in the rat by using the endovascular perforation model. The animals were killed between 10 minutes and 48 hours after SAH. Immunostaining for the platelet surface receptor glycoprotein (GP)IIb/IIIa, which mediates platelet aggregation, was used to detect platelet aggregation. Sham-operated animals were used as controls. The GPIIb/IIIa immunoreactive platelet aggregates were abundant in the microvasculature of the basal and frontal cortex, striatum, and hippocampus 10 minutes after SAH. These aggregates decreased in number from 1 to 6 hours post-SAH and then increased to a peak at 24 hours. No immunoreactive aggregates were observed 48 hours after SAH. CONCLUSIONS: The data indicate that widespread platelet aggregation occurs very rapidly in response to SAH followed by a decrease within 6 hours and a subsequent increase 24 hours after SAH. Microvascular platelet aggregates may contribute to decreased cerebral blood flow and ischemic injury after SAH via a number of mechanisms.
Authors: Jared M Pisapia; Xiangsheng Xu; Jane Kelly; Jamie Yeung; Geneive Carrion; Huaiyu Tong; Sudha Meghan; Omar M El-Falaky; M Sean Grady; Douglas H Smith; Sergei Zaitsev; Vladimir R Muzykantov; Michael F Stiefel; Sherman C Stein Journal: Exp Neurol Date: 2011-11-04 Impact factor: 5.330
Authors: Jennifer A Frontera; J Javier Provencio; Fatima A Sehba; Thomas M McIntyre; Amy S Nowacki; Errol Gordon; Jonathan M Weimer; Louis Aledort Journal: Neurocrit Care Date: 2017-02 Impact factor: 3.210
Authors: Simone C Oudshoorn; Gabriel J E Rinkel; Andrew J Molyneux; Richard S Kerr; Sanne M Dorhout Mees; Daan Backes; Ale Algra; Mervyn D I Vergouwen Journal: Neurocrit Care Date: 2014-08 Impact factor: 3.210