Brain ischemia alters platelet ATP diphosphohydrolase and 5'-nucleotidase activities in naive and preconditioned rats

Abstract

The effects of transient forebrain ischemia, reperfusion and ischemic preconditioning on rat blood platelet ATP diphosphohydrolase and 5'-nucleotidase activities were evaluated. Adult Wistar rats were submitted to 2 or 10 min of single ischemic episodes, or to 10 min of ischemia 1 day after a 2-min ischemic episode (ischemic preconditioning) by the four-vessel occlusion method. Rats submitted to single ischemic insults were reperfused for 60 min and for 1, 2, 5, 10 and 30 days after ischemia; preconditioned rats were reperfused for 60 min 1 and 2 days after the long ischemic episode. Brain ischemia (2 or 10 min) inhibited ATP and ADP hydrolysis by platelet ATP diphosphohydrolase. On the other hand, AMP hydrolysis by 5'-nucleotidase was increased after 2, but not 10, min of ischemia. Ischemic preconditioning followed by 10 min of ischemia caused activation of both enzymes. Variable periods of reperfusion distinctly affected each experimental group. Enzyme activities returned to control levels in the 2-min group. However, the decrease in ATP diphosphohydrolase activity was maintained up to 30 days of reperfusion after 10-min ischemia. 5'-Nucleotidase activity was decreased 60 min and 1 day following 10-min ischemia; interestingly, enzymatic activity was increased after 2 and 5 days of reperfusion, and returned to control levels after 10 days. Ischemic preconditioning cancelled the effects of 10-min ischemia on the enzymatic activities. These results indicate that brain ischemia and ischemic preconditioning induce peripheral effects on ecto-enzymes from rat platelets involved in nucleotide metabolism. Thus, ATP, ADP and AMP degradation and probably the generation of adenosine in the circulation may be altered, leading to regulation of microthrombus formation since ADP aggregates platelets and adenosine is an inhibitor of platelet aggregation. Correspondence

<i>Syzygium cumini</i> Extract Decrease Adenosine Deaminase, 5′Nucleotidase Activities and Oxidative Damage in Platelets of Diabetic Patients

“…3.1.3.5, CD73, 5'NT) is located in the platelet membrane and promotes the hydrolysis of AMP to its nucleoside, adenosine, in the extracellular medium [33,34]. Recent studies report that 5'NT is altered in type 2 DM and hypertensive patients probably related with the thromboregulation process [35,36].…”

An ultrastructural study of cell death in the CA1 pyramidal field of the hippocapmus in rats submitted to transient global ischemia followed by reperfusion

“…The 4-vessel occlusion (4VO) method of inducing ischemia involves cauterization of both vertebral arteries plus transient occlusion of the carotids and results in significant reduction of the cerebral blood flow (90% or more), producing approximately 90% of neuronal death 24 or 48 h after the ischemic insult (Pulsinelli & Brierley, 1979;Nunn et al 1994;Frassetto et al 2000). The hippocampus has been extensively utilized to evaluate neuronal death after cerebral ischemia due to its simple arrangement and homogeneous pattern of damage within each region.…”

Toxic effects of mercury, lead and gadolinium on vascular reactivity

“…NTPDase2 is another ectonucleotidase associated with the vasculature that preferentially converts ATP to ADP (50). Following the action of E-NTPDases, ecto-5'-nucleotidase is responsible for the end of nucleotide signaling by converting AMP to adenosine (51).…”