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Halaman 1 dari 16 hasil
Effects of SUN-1165, N-(2,6-dimethylphenyl)-8-pyrrolizidine acetamide hydrochloride hemihydrate, a new class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the refractory period in canine myocardial infarction.
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Effects of SUN-1165, a class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the effective refractory period (ERP) were examined in a canine model of myocardial infarction and compared with those of lidocaine. The antiarrhythmic effects were examined on the
PET molecular imaging of angiogenesis with a multiple tyrosine kinase receptor-targeted agent in a rat model of myocardial infarction.
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OBJECTIVE
Angiogenesis plays a major role in tissue remodeling and repair after myocardial infarction (MI), and imaging it could provide information on the healing process. During angiogenesis, vascular endothelial growth factor receptors (VEGFRs), platelet-derived growth factor receptors (PDGFRs),
Development of the chymase inhibitor as an anti-tissue-remodeling drug: myocardial infarction and some other possibilities.
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Chymase leading to tissue remodeling is expected to be a potent pharmaceutical target. Its functions in vivo are still unclear, because of lack of orally available inhibitors. Recently, however, the chymase inhibitor NK3201
Combined therapy with PJ34, a poly(ADP-ribose)polymerase inhibitor, reduces tissue plasminogen activator-induced hemorrhagic transformations in cerebral ischemia in mice.
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Recombinant tissue-type plasminogen activator (rt-PA) is presently the only pharmacological treatment approved for thrombolysis in patients suffering from ischemic stroke. Although reperfusion of ischemic tissue is essential, the use of rt-PA is limited due to its narrow therapeutic window and risk
The orally active urotensin receptor antagonist, KR36676, attenuates cellular and cardiac hypertrophy.
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OBJECTIVE
Blockade of the actions of urotensin-II (U-II) mediated by the urotensin (UT) receptor should improve cardiac function and prevent cardiac remodelling in cardiovascular disease. Here, we have evaluated the pharmacological properties of the recently identified UT receptor antagonist,
Antiarrhythmic efficacy of combined I(Ks) and beta-adrenergic receptor blockade.
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Suppression of malignant ventricular arrhythmias by selective blockade of the cardiac slowly activating delayed rectifier current (I(Ks)) has been demonstrated with the benzodiazepine L-768673
PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke.
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Neuroinflammation is central to the pathological cascade following ischemic stroke. Non-invasive molecular imaging methods have the potential to provide critical insights into the temporal dynamics and role of certain neuroimmune interactions in stroke. Specifically, Positron Emission Tomography
Neuroprotective effects of a novel broad-spectrum cation channel blocker, LOE 908 MS, on experimental focal ischemia: a multispectral study.
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Thirty-four rats undergoing 90 minutes of temporary middle cerebral artery occlusion were randomly and blindly assigned to vehicle or (RS)-(3,4-dihydro-6, 7-dimethoxyisoquinoline-1-gamma1)-2-phenyl-N,N-di-2-(2, 3, 4-trimethoxyphenyl)ethyl acetamide (LOE 908 MS; 0.5 mg/kg) i.v. bolus at 30 minutes
Inhibition of nonselective cation channels reduces focal ischemic injury of rat brain.
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The effect of the novel inhibitor of receptor-activated and calcium store-operated nonselective cation channels, (RS)-(3,4-dihydro-6,7-dimethoxyisoquinoline-1-gamma 1)-2-phenyl-N, N-di-[2(2,3,4-trimethoxyphenyl) ethyl]acetamide (LOE 908 MS), on focal cerebral ischemia was studied in
Role of peripheral benzodiazepine receptors in mitochondrial, cellular, and cardiac damage induced by oxidative stress and ischemia-reperfusion.
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Mitochondrial dysfunction has been identified as a possible early event in ischemia-reperfusion damage. The peripheral benzodiazepine receptor, a mitochondrial inner membrane protein, has already been proposed to play a role in mitochondrial regulation, although its exact function remains unclear.
Reduction of hemorrhagic transformation by PJ34, a poly(ADP-ribose)polymerase inhibitor, after permanent focal cerebral ischemia in mice.
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Hemorrhagic transformation is an aggravating event that occurs in 15 to 43% of patients suffering from ischemic stroke. This phenomenon due to blood-brain barrier breakdown appears to be mediated in part by matrix metalloproteinases (MMPs) among which MMP-2 and MMP-9 could be particularly involved.
Randomized placebo-controlled double-blind cross-over study on antihypoxidotic effects of piracetam using psychophysiological measures in healthy volunteers.
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The effects of two acute doses (1600 mg, 2400 mg) of 2-oxo-pyrrolidine-1-acetamide (piracetam, Normabraïn) on hypoxia resistance were screened vs placebo in a randomized, double-blind 3-way change-over design in 9 healthy male volunteers (mean age: 26.4 +/- 3.5 years; mean body weight: 74.9 +/- 8.4
[The effect of atenolol on contractility and hemodynamics of the infarcted heart in comparison to propranolol and practolol (author's transl)].
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In animals without myocardial infarction the new beta-sympathicolytic agent atenolol (4-[2'-hydroxy-3'-iso-propylaminopropoxy]-phenyl acetamide, ICI 66 082) dose-dependently decreased heart rate, systolic aortic pressure and cardiac output. Coronary mean flow, coronary resistance, stroke volume,
Myeloperoxidase inhibition in mice alters atherosclerotic lesion composition.
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Myeloperoxidase (MPO) is a highly abundant protein within the neutrophil that is associated with lipoprotein oxidation, and increased plasma MPO levels are correlated with poor prognosis after myocardial infarct. Thus, MPO inhibitors have been developed for the treatment of heart failure and acute
The positron emission tomography ligand DAA1106 binds with high affinity to activated microglia in human neurological disorders.
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Chronic microglial activation is an important component of many neurological disorders, and imaging activated microglia in vivo will enable the detection and improved treatment of neuroinflammation. 1-(2-chlorphenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinoline-carbox-amide (PK11195), a peripheral
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