Acetylsalicylic acid reduces perfusion deficit in ischemic injured brain in rats

Acetylsalicylic acid (ASA) is an antiplatelet agent which has been used in treatment and prevention of stroke in humans. In the present study, the effects of ASA on perfusion deficits in the brain have been studied in an embolic model of stroke. Data showed that perfusion deficits were observed in all rats sacrificed immediately after middle cerebral artery (MCA) occlusion. Treatment with ASA significantly reduced perfusion deficits 1 h but not 3 h after the MCA occlusion. These findings thus support that ASA is useful agent in treatment and prevention of stroke, and show that its mechanism of action is likely through the reopening of cerebral microvessels.

[1]  K. Hossmann,et al.  The effect of intravascular saline perfusion on the sequelae of transient cerebral ischemia , 1971, Acta Neuropathologica.

[2]  Tao Yang,et al.  An improved version of embolic model of brain ischemic injury in the rat , 2001, Journal of Neuroscience Methods.

[3]  M. Tantucci,et al.  Nitro-aspirin (NCX4016) reduces brain damage induced by focal cerebral ischemia in the rat , 2001, Neuroscience Letters.

[4]  K. Todd,et al.  Patency of Cerebral Microvessels after Focal Embolic Stroke in the Rat , 2001, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[5]  J. Orozco,et al.  Leukocyte accumulation and hemodynamic changes in the cerebral microcirculation during early reperfusion after stroke. , 2000, Stroke.

[6]  B. Siesjö,et al.  Capillary patency after transient middle cerebral artery occlusion of 2 h duration , 1998, Neuroscience Letters.

[7]  K. Hossmann REPERFUSION OF THE BRAIN AFTER GLOBAL ISCHEMIA: HEMODYNAMIC DISTURBANCES , 1997, Shock.

[8]  M. Bednar,et al.  Intravenous aspirin causes a paradoxical attenuation of cerebrovascular thrombolysis. , 1995, Stroke.

[9]  W. Kuschinsky,et al.  Gross Persistence of Capillary Plasma Perfusion after Middle Cerebral Artery Occlusion in the Rat Brain , 1994, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[10]  G. D. del Zoppo,et al.  Inhibition of Polymorphonuclear Leukocyte Adherence Suppresses No‐Reflow After Focal Cerebral Ischemia in Baboons , 1992, Stroke.

[11]  G. FitzGerald Mechanisms of platelet activation: thromboxane A2 as an amplifying signal for other agonists. , 1991, The American journal of cardiology.

[12]  B. Siesjö,et al.  Recirculation in the Rat Brain following Incomplete Ischemia , 1983, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[13]  P. Coyle,et al.  Dorsal cerebral arterial collaterals of the rat , 1982, The Anatomical record.

[14]  K. Ohno,et al.  Transient Appearance of “No‐Reflow” Phenomenon in Mongolian Gerbils , 1980, Stroke.

[15]  A. Farah,et al.  Potential therapeutic applications of aspirin and other cyclo-oxygenase inhibitors. , 1980, British journal of clinical pharmacology.

[16]  A. Schafer,et al.  The role of platelets in thrombotic and vascular disease. , 1979, Progress in cardiovascular diseases.

[17]  R. Russell,et al.  No-reflow phenomenon in the cerebral circulation of the gerbil. , 1975, Journal of neurology, neurosurgery, and psychiatry.

[18]  M. Hamberg,et al.  Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides. , 1975, Proceedings of the National Academy of Sciences of the United States of America.

[19]  M. Kowada,et al.  Cerebral ischemia. II. The no-reflow phenomenon. , 1968, The American journal of pathology.

[20]  C. Fisher Observations of the fundus oculi in transient monocular blindness , 1959, Neurology.