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Lappuse 1 no 170 rezultātiem
Reduction of experimental myocardial infarct size by combined treatment with methylprednisolone sodium succinate and betahistine hydrochloride.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
This laboratory and others have shown that methylprednisolone sodium succinate and betahistine hydrochloride can each reduce the size of experimental myocardial infarct in dogs at six hours. In light of the fact that these two agents probably act via different mechanisms, a study was carried out to
Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left
Catecholamine-Induced Chest Pain Mimicking Infarction Due to an MIBG-Negative and DOPA-Positive Succinate Dehydrogenase Syndrome Subunit B-Related Pheochromocytoma.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
This 16-year-old boy presented with acute retrosternal pain possibly representing acute myocardial infarction. Cardiac enzymes were within reference ranges. There were marked increases in metanephrine to 3299 μg/24 h (reference, <400 μg/24 h), normetanephrine to 1309 μg/24 h (reference, 0-390 μg/24
Metabolomic Profiling in Acute ST-Segment-Elevation Myocardial Infarction Identifies Succinate as an Early Marker of Human Ischemia-Reperfusion Injury.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
BACKGROUND
Ischemia-reperfusion injury following ST-segment-elevation myocardial infarction (STEMI) is a leading determinant of clinical outcome. In experimental models of myocardial ischemia, succinate accumulation leading to mitochondrial dysfunction is a major cause of ischemia-reperfusion
Triphenylphosphonium and D-α-tocopheryl polyethylene glycol 1000 succinate-modified, tanshinone IIA-loaded lipid-polymeric nanocarriers for the targeted therapy of myocardial infarction.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
UNASSIGNED
Cardiovascular diseases (CVDs) are the leading causes of mortality worldwide. Currently, the best treatment options for myocardial infarction focus on the restoration of blood flow as soon as possible, which include reperfusion therapy, percutaneous coronary intervention, and therapeutic
Succinate dehydrogenase inhibition with malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
OBJECTIVE
Previous studies demonstrated that pre-treatment with malonate, a reversible inhibitor of succinate dehydrogenase, given before ischaemia, reduces infarct size. However, it is unknown whether administration of malonate may reduce reperfusion injury.
RESULTS
Isolated mice hearts were
Selective Inhibition of Succinate Dehydrogenase in Reperfused Myocardium with Intracoronary Malonate Reduces Infarct Size.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Inhibition of succinate dehydrogenase (SDH) with malonate during reperfusion reduces infarct size in isolated mice hearts submitted to global ischemia. However, malonate has toxic effects that preclude its systemic administration in animals. Here we investigated the effect of intracoronary malonate
[Effect of experimental myocardial infarct on the succinate oxidation rate and succinate dehydrogenase activity in the heart mitochondria].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
The rate of oxidation of NADH and 3-hydroxybutyrate was studied in heart mitochondria after short-term (60 min) occlusion of coronary artery and the subsequent reperfusion. Addition of NAD increased the rate of 3-hydroxybutyrate oxidation, lowered in mitochondria of impaired tissue, but no complete
The value of succinate dehydrogenase stain in the post-mortem diagnosis of early acute myocardial infarction. A forensic study.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
In consecutive medicolegal material comprising 79 persons, the formazan test revealed recent myocardial infarction in 16 cases (20%). Only 4 of these cases (25%) were demonstrated by macroscopic examination. By means of microscopic examination, the 4 infarctions recognized macroscopically and 5
[Methylprednisolone sodium succinate in acute myocardial infarct].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Author Correction: Selective Inhibition of Succinate Dehydrogenase in Reperfused Myocardium with Intracoronary Malonate Reduces Infarct Size.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
[Use of sodium succinate in patients with a history of myocardial infarction].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
[Evaluation of the effectiveness of methylprednisolone sodium succinate in reducing the infarct area].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
[WATER-SOLUBLE PREDNISOLONE SODIUM SUCCINATE IN THE TREATMENT OF COLLAPSE EPISODES DURING MYOCARDIAL INFARCT].
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Metoprolol CR/XL in postmyocardial infarction patients with chronic heart failure: experiences from MERIT-HF.
Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
BACKGROUND
The benefit of beta-blockers post-myocardial infarction (MI) was established in the late 1970s. Major advances in the treatment of MI have since occurred. However, patients with chronic heart failure (CHF) were excluded from those trials. The purpose of this study was to assess the effect
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