adenosine/infarction

Lyen an sove nan clipboard la

Chwazi kalite sòt

Paj 1 soti nan 2466 rezilta yo

Infarct size-limiting effect of ischemic preconditioning is blunted by inhibition of 5'-nucleotidase activity and attenuation of adenosine release.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND We have previously reported that ischemic preconditioning increases 5'-nucleotidase activity and adenosine release during ischemia and reperfusion. However, its direct cause-and-effect relation has not been proven. To test the idea that the infarct size-limiting effect of ischemic

Extracellular Hydrolysis of Adenine Nucleotides and Nucleoside Adenosine is Higher in Patients with ST Elevation than Non-ST Elevation in Acute Myocardial Infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND The hydrolysis of adenine nucleotide linked to the membrane of the platelets is changed in acute myocardial infarction (AMI) probably due to a greater arterial blockage and cell damage in patients with ST elevation (STEMI) than in those without ST segment elevation (NSTEM). METHODS This

Reactive oxygen species and mitochondrial adenosine triphosphate-regulated potassium channels mediate helium-induced preconditioning against myocardial infarction in vivo.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE Helium produces preconditioning by activating prosurvival kinases, but the roles of reactive oxygen species (ROS) or mitochondrial adenosine triphosphate-regulated potassium (K(ATP)) channels in this process are unknown. The authors tested the hypothesis that ROS and mitochondrial K(ATP)

Antimuscarinics suppress adenosine triphosphate and prostaglandin E2 release from urothelium with potential improvement in detrusor overactivity in rats with cerebral infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE Antimuscarinics improve detrusor overactivity. We evaluated the effects and action mechanisms of imidafenacin (Kyorin Pharmaceutical, Tokyo, Japan), a novel therapeutic agent for overactive bladder with antimuscarinic activity, on mediator release from urothelium and detrusor overactivity

Association of recurrent cerebral infarction with adenosine diphosphate- and collagen-induced platelet aggregation in patients treated with ticlopidine and/or aspirin.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Although the platelet aggregation test is the most common method for evaluating response to antiplatelet therapy, little is known about the association of recurrent cerebral infarction with platelet aggregation in the presence of various different antiplatelet drugs. We prospectively evaluated

Roles of mitochondrial ATP-sensitive K channels and PKC in anti-infarct tolerance afforded by adenosine A1 receptor activation.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE This study intended to assess the role of mitochondrial ATP-sensitive potassium (mitoK ATP) channels and the sequence of signal transduction with protein kinase C (PKC) and adenosine A1 receptors in rabbits. BACKGROUND To our knowledge, the link between trigger receptors of

Bimakalim, an ATP-sensitive potassium channel opener, mimics the effects of ischemic preconditioning to reduce infarct size, adenosine release, and neutrophil function in dogs.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND The primary goal of the present study was to determine whether the infarct size-reducing effect of preconditioning is associated with an increase in adenosine release from the ischemic myocardium during a prolonged occlusion period or the subsequent reperfusion period and by a decrease in

Pretreatment with morin, a flavonoid, ameliorates adenosine triphosphatases and glycoproteins in isoproterenol-induced myocardial infarction in rats.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

The aim of this investigation was to evaluate the preventive role of morin, a flavonoid, on cardiac marker enzymes such as aspartate transaminase, lactate dehydrogenase, creatine kinase and creatine kinase-MB, membrane-bound enzymes such as sodium potassium-dependent adenosine triphosphatase,

Pravastatin reduces myocardial infarct size via increasing protein kinase C-dependent nitric oxide, decreasing oxyradicals and opening the mitochondrial adenosine triphosphate-sensitive potassium channels in rabbits.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND Statins reportedly protect against myocardial infarction, but the precise mechanism is unclear. RESULTS Rabbits underwent 30 min of coronary occlusion followed by 48 h of reperfusion. Pravastatin (1 or 5 mg/kg) or saline was intravenously administered 10 min before ischemia. Pravastatin

Adenosine-enhanced ischemic preconditioning provides enhanced postischemic recovery and limitation of infarct size in the rabbit heart.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE The purpose of this study was to determine the effect of an intracoronary bolus injection of adenosine used in concert with ischemic preconditioning on postischemic functional recovery and infarct size reduction in the rabbit heart and to compare adenosine-enhanced ischemic preconditioning

Effects of adenosine triphosphate dependent potassium channel opener on bladder overactivity in rats with cerebral infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

OBJECTIVE We evaluated the effect of the adenosine triphosphate dependent K channel opener KRN2391 (N-cyano-N' -(2-nitroxyethyl)-3-pyridinecarboximidamide methanesulfonate) (Kirin Brewery Co., Gunma, Japan) on bladder overactivity induced by middle cerebral artery occlusion. METHODS At 7 days after

Beneficial effects of intracoronary adenosine as an adjunct to primary angioplasty in acute myocardial infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND The benefits of vessel recanalization in acute myocardial infarction (AMI) are limited by reperfusion damage. In animal models, adenosine limits reperfusion injury, reducing infarct size and improving ventricular function. The aim of this study was to evaluate the safety and feasibility

Intracoronary adenosine administered during percutaneous intervention in acute myocardial infarction and reduction in the incidence of "no reflow" phenomenon.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

Percutaneous intervention in acute myocardial infarction has been associated with a high incidence of "no reflow," ranging from 11% to 30%, with an increased risk of complications. The role of intracoronary adenosine for the prevention of this phenomenon has not been evaluated fully. We studied the

Adenosine sestamibi SPECT post-infarction evaluation (INSPIRE) trial: A randomized, prospective multicenter trial evaluating the role of adenosine Tc-99m sestamibi SPECT for assessing risk and therapeutic outcomes in survivors of acute myocardial infarction.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

BACKGROUND Preliminary studies indicate that adenosine myocardial perfusion single photon tomography (SPECT) can safely and accurately stratify patients into low and high risk groups early after acute myocardial infarction (AMI). RESULTS INSPIRE is a prospective, randomized multicenter trial which

The hemodynamic effects of adenosine infusion after experimental right heart infarct in young swine.

Se sèlman itilizatè ki anrejistre yo ki ka tradwi atik yo

The use of a vasodilator selective to the pulmonary circulation may be beneficial in cases with right-ventricle failure, as it will decrease right-heart afterload without concurrent systemic hypotension. Adenosine has recently been advocated as such a drug, although its clinical efficacy in this

Antre nan paj
facebook nou an

Herbal & Natural Medicine

Baz done ki pi konplè remèd fèy medsin te apiye nan syans

Travay nan 55 lang
Geri èrbal te apiye nan syans
Remèd fèy rekonesans pa imaj
Kat entèaktif GPS - tag zèb sou kote (vini byento)
Li piblikasyon syantifik ki gen rapò ak rechèch ou an
Search remèd fèy medsin pa efè yo
Izeganize enterè ou yo ak rete kanpe fè dat ak rechèch la nouvèl, esè klinik ak rive

Tape yon sentòm oswa yon maladi epi li sou remèd fèy ki ta ka ede, tape yon zèb ak wè maladi ak sentòm li itilize kont.
* Tout enfòmasyon baze sou rechèch syantifik pibliye