nucleotidase/accident vascular cerebral

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Histochemical study on 5'-nucleotidase in the cerebrovascular system in stroke-prone spontaneously hypertensive rats.

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5'-Nucleotidase activity in the cerebrovascular system in stroke-prone spontaneously hypertensive rats was histochemically investigated. In the hypertensive rats, an enhancement of 5'-nucleotidase activity was observed already in the early stage of hypertension and the enzyme activity increased with

A comparative study on lipid peroxidation in cerebral cortex of stroke-prone spontaneously hypertensive and normotensive rats.

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1. Lipid peroxidation and membrane-related enzyme changes in the cerebral cortex of stroke-prone rats (SHRSP) and normotensive rats were examined at 5 and 20 weeks of age. 2. In vivo formation of thiobarbituric acid-reactant substances was higher in SHRSP at 20 weeks of age and in vitro generation

Successful use of clopidogrel for cerebrovascular accident in a patient with suspected ticlopidine-induced hepatotoxicity.

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OBJECTIVE To report a case of successful clopidogrel use in a patient who developed suspected ticlopidine-induced hepatotoxicity during therapy for a cerebrovascular accident. METHODS A 79-year-old white woman with a history of hypertension, type 2 diabetes, Alzheimer disease, and coronary artery

Engineered human soluble calcium-activated nucleotidase inhibits coagulation in vitro and thrombosis in vivo.

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Human soluble calcium-activated nucleotidase (human SCAN) is a homologue of the salivary anti-coagulant apyrases injected by insects into their hosts to allow blood feeding. However, the human enzyme, unlike its insect counterparts, does not efficiently hydrolyze the platelet agonist, ADP. By

Adenosinergic System Involvement in Ischemic Stroke Patients' Lymphocytes.

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Adenosine modulates many physiological processes through the interaction with adenosine receptors (ARs) named as A₁, A_2A, A_2B, and A₃ARs. During ischemic stroke, adenosine mediates neuroprotective and anti-inflammatory effects through ARs activation. One

Tissue-resident ecto-5' nucleotidase (CD73) regulates leukocyte trafficking in the ischemic brain.

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Ectoenzymes expressed on the surface of vascular cells and leukocytes modulate the ambient nucleotide milieu. CD73 is an ecto-5' nucleotidase that catalyzes the terminal phosphohydrolysis of AMP and resides in the brain on glial cells, cells of the choroid plexus, and leukocytes. Though CD73

Metabolic control of excessive extracellular nucleotide accumulation by CD39/ecto-nucleotidase-1: implications for ischemic vascular diseases.

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Platelets are responsible for maintaining vascular integrity. In thrombocytopenic states, vascular permeability and fragility increase, presumably due to the absence of this platelet function. Chemical or physical injury to a blood vessel induces platelet activation and platelet recruitment. This is

Elastin and elastase-like enzyme change in aorta of rat with malignant hypertension.

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In order to study the role of elastin in arteries with respect to hypertension and hypertensive arterial disease, aortic elastin content and elastase-like enzyme activity were examined and compared in stroke-prone spontaneously hypertensive rats (SHRSP), which show malignant hypertension, and

Impact of cardiac-specific expression of CD39 on myocardial infarct size in mice.

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OBJECTIVE Prior work suggests that ischemic preconditioning increases the level of CD39 in the heart and contributes to cardiac protection. Therefore, we examined if targeted cardiac expression of CD39 protects against myocardial injury. METHODS Mice with cardiac-specific expression of human CD39

In vitro effect of homocysteine on nucleotide hydrolysis by blood serum from adult rats.

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During the past few years, elevated blood levels of homocysteine (Hcy) have been linked to increased risk of premature coronary artery disease, stroke and thromboembolism. These processes can be also related to the ratio adenine nucleotide/adenosine, since extracellularly these nucleotides are

Astrocytes affect the profile of purines released from cultured cortical neurons.

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Adenosine (ADO) is produced by cultured neurons and astrocytes, albeit by different pathways, during in vitro stroke models (Parkinson and Xiong [2004] J. Neurochem. 88:1305-1312). Expression of ecto-5' nucleotidase (e-N), the enzyme responsible for extracellular dephosphorylation of AMP to ADO, is

AMP-dependent hypothermia affords protection from ischemic brain injury.

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In light of the relevance of therapeutic hypothermia to stroke treatment, we investigated whether 5'-adenosine monophosphate (AMP)-dependent cooling affords protection from ischemic brain injury. We show that hypothermia by AMP is because of adenosine A1 receptor (A1R) activation and is not

Effects of pressure overload, left ventricular hypertrophy on beta-adrenergic receptors, and responsiveness to catecholamines.

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Pressure overload left ventricular (LV) hypertrophy was produced by banding the ascending aorta of puppies and allowing them to grow to adulthood. LV free wall weight per body weight increased by 87% from a normal value of 3.23 +/- 0.19 g/kg. Hemodynamic studies of conscious dogs with LV hypertrophy

CD39: Interface between vascular thrombosis and inflammation.

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Extracellular nucleotides play a critical role in vascular thrombosis and inflammation. Alterations in purinergic extracellular nucleotide concentrations activate pathways that result in platelet degranulation and aggregation, and endothelial and leukocyte activation and recruitment. CD39, the

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