Myocardial damage during

Ferrari, R., Ceconi, C., Curello, S., Guamieri, C., Caldarera, C., Albertini, A. and Visioli, O. (1985). Oxygen-mediated myocardial damage during ischaemia and reperfusion role of the cellular defences against oxygen toxicity. J. Mol. Cell. Cardiol. 17, 937-945. 

Magnesium sulfate Heart block or myocardial damage IV magnesium to patients with preeclampsia during the 2 hours preceding delivery. 

As with other antiarrhythmics, in the elderly or patients with marked previous myocardial damage, increase dose more gradually during initial treatment phase. 

Angiogenesis driven by myocardial hypoxia may permit collateral formation, relief of angina, and minimize tissue damage during myocardial infarction. On the other hand, hypoxic drive to retinal neovascularization can contribute to retinal hemorrhage and blindness. 

Although the major thrust of this chapter is centered on the free radical hypothesis of myocardial injury, it is essential to realize that calcium overload in myocardial cells during ischemia and reperfusion could be the primary cause of myocardial injury [40,41]. It is also likely that mechanisms of free radical production and calcium overload are related and not mutually exclusive [40]. Alterations in intracellular calcium homeostasis are often accompanied by depletion of cellular antioxidants [42]. The mitochondrial Ca2+ homeostasis has been shown to affect oxy radicals produced through the electron-transport chain [43], Reperfusion and reoxygenation of hearts are characterized by marked increase in cytosolic and mitochondrial levels of Ca2+ [44]. Ruthenium red, which inhibits mitochondrial Ca2+ uptake, also protects the heart against reperfusion-induced damage [45,46],... 

Q4 Cardiac enzymes are released into the blood following heart muscle damage during a heart attack. Creatine kinase, particularly its MB isoenzyme, is one of the most specific of these enzymes, which reaches a peak 24 hours after infarction. It rises and then falls within the first 72 hours of the heart attack. Aspartate transaminase is also released, but levels of this enzyme can be raised in several other conditions, so it is less specific than creatine kinase MB. Troponin T is also specific for myocardial damage and is raised for approximately two weeks following infarction. Finding a high concentration of these enzymes in a patient s blood therefore supports the evidence obtained from the ECG and confirms that the patient has suffered a myocardial infarction. 

Beckmann S, Bocksch W, Muller C, Schartl M. Does dobutamine stress echocardiography induce damage during via-bihty diagnosis of patients with chronic regional dysfunction after myocardial infarction J Am Soc Echocardiogr 1998 ll(2) 181-7. 

In preliminary studies, GP-BB was significantly more sensitive than CK and CK-MB for AMI diagnosis during the first 3 to 4 hours after the onset of chest pain. Therefore GP-BB may be an important marker for the early diagnosis of AMI. Similar to other cytoplasmic proteins, such as myoglobin and CK-MB, the time course of GP-BB can be notably influenced by early reperfusion of the infarct-related coronary artery, with a more rapid increase and earlier peak. GP-BB is, however, not a heart-specific protein and its specificity as a marker for myocardial damage is limited. 

Mel B is less toxic than tryparsamide. However, its use may be associated with renal and myocardial damage, albuminuria, hypertension and colic. Other side effects of the drug are jaundice, diarrhea and conjunctival infections [9,12]. About 1% of the treated patients may develop encephalopathy [37]. The drug is also known to cause headache, tremor, fever, convulsion, coma and death. It is contraindicated during epidemics of influenza and G-6-PD deficiency [36,38]. 

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