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diazepam/infark

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Progressive encephalopathy with cerebral oedema and infarctions associated with valproate and diazepam overdose.

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Valproic Acid (VPA) in overdose is known to cause encephalopathy with or without cerebral odema, hyperammonaemia, hepatotoxicity, bone marrow suppression and non gap acidosis. Most of these conditions are reversible. We report a 45-year-old man who suffered permanent disability from the non

[Pharmacokinetics of antipyrine, nifedipine and diazepam in experimental myocardial infarct].

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It has been shown, that antipyrine, nifedipine, diazepam pharmacokinetics changes in different ways after myocardial infarction. On day 7, 14, and 21 after myocardial ischemia antipyrine T1/2 increased considerably, and antipyrine Cl and Kel decreased. Nifedipine T1/2 increased on day 7 only. There
Activation of the gamma-amino butyric acid (GABA)-ergic system might protect against the damage that occurs after cerebral ischaemia. We examined this hypothesis by administering diazepam to rats subjected to transient middle cerebral artery occlusion (MCAO) using the intraluminal thread method.

Diazepam in acute myocardial infarction. Clinical effects and effects on catecholamines, free fatty acids, and cortisol.

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Diazepam is a valuable drug in cases of acute myocardial infarction. The 10 mg intravenous loading dose and the subsequent 15 mg oral dose of diazepam administered three times daily produced safe, pleasant sedation, and reduced the need for analgesics. A much reduced excretion of catecholamines was

Diazepam in immediate post-myocardial infarct period. A double blind trial.

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One hundred and thirty-one male patients admitted to a coronary care unit with myocardial infarction, later confirmed, were randomly allocated to receive either 10 mg diazepam every six hours, or a matched placebo, for 48 hours. During this period, no differences were found between the treatment
Eighty-seven patients with an acute myocardial infarction and a pulse rate of greater than or equal to 80/min on admission were randomly allotted to one group given cardioselective beta-blockade, a second group given diazepam, and a third group given placebo. The three groups were comparable in age,

A double-blind evaluation of diazepam and amylobarbitone in acute myocardial infarction.

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Involuntary tonic spasms of a limb due to a brain stem lacunar infarction.

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OBJECTIVE Although repetitive involuntary movements are a well-recognized manifestation of carotid occlusive disease, similar movements have not been reported with a lacunar infarction outside of the basal ganglia or subthalamic nucleus. We describe a man with tonic spasms associated with a lacunar

Posttraumatic hemicerebral infarction in a four-year-old girl.

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BACKGROUND Brain infarction after trauma is uncommon. Injury of the carotid and vertebrobasilar arteries can cause brain infarction due to occlusion of brain blood flow. METHODS Emergency medical service (EMS) brought a 4-year-old girl involved in a car accident to the emergency room. She had had

Effects of ambient particles and carbon monoxide on supraventricular arrhythmias in a rat model of myocardial infarction.

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The association between short-term increases in particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Recent studies suggest an association between particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and supraventricular arrhythmias (SVA),
Epidemiological studies have reported a positive association of short-term increases in ambient particulate matter (PM) with daily mortality and hospital admissions for cardiovascular disease. Although patients with cardiopulmonary disease appear to be most at risk, particulate-related cardiac

Cardiac effects of carbon monoxide and ambient particles in a rat model of myocardial infarction.

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Ambient air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants such as carbon monoxide (CO). The effect of exposure to CO, alone or in combination with ambient PM, on arrhythmia incidence is unclear. To evaluate these effects, left-ventricular myocardial infarction was

[Central type of sleep apnea syndrome caused by unilateral lateral medullary infarction].

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We reported here a 64-year-old man with a central apnea resulted from unilateral medullary infarction. He was admitted because of cerebellar ataxia, dysarthria and dysphasia of abrupt onset. After the injection of diazepam for alcohol forbidden syndrome, he induced complete apnea and required the
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