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Myocardial damage

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. [Pg.70]

To avoid myocardial damage, the interval between shocks should be >1 min... [Pg.11]

Cytotoxicity of methylamine [45], kidney liver and myocardial damage due to ethylamine [46], hepatosplenomegaly and eosinophilia due to aniline [47], euphoria, dyspnea, teratogenicity, renal failure, hematuria, proteinurea, anorexia and methanoglobinemia due to a-naphthylamine and diphenylamine have been reported in the literature [48-54]. Therefore the remediation and mineralization of amines is... [Pg.316]

The enzyme responsible for this topping-up ATP in active muscle is CK. CK is found in high concentration in muscle cells, both free within the sarcoplasm and also associated with membranes of mitochondria and the sarcoplasmic reticulum. Structurally, creatine kinase is a dimeric enzyme of B and/or M subunits, each of about 40 kDa. Three quaternary structure isoenzyme forms arise CK-MM, CK-BB and CK-MB. The predominant form in all muscles is CK-MM, but cardiac muscle also contains a significant amount of CK-MB and this isoenzyme can be used as a specific marker of myocardial damage (see Case Notes at the end of this chapter). [Pg.247]

Over a 9-year period (1967-76), 11 cases of jaundice were reported from a company that mixed preground MDA with silicon dioxide. In one instance, transient signs of myocardial damage in addition to transient signs of hepatic damage were observed after MDA exposure from a defective filter system. ... [Pg.474]

Magnesium sulfate Heart block or myocardial damage IV magnesium to patients with preeclampsia during the 2 hours preceding delivery. [Pg.25]

Parenteral therapy The dangers of parenteral use of quinidine are increased in the presence of AV block or absence of atrial activity. Administration is more hazardous in patients with extensive myocardial damage. Use of quinidine in digitalis-induced cardiac arrhythmia is extremely dangerous because the cardiac glycoside may already have caused serious impairment of intracardiac conduction system. Too rapid IV administration of as little as 200 mg may precipitate a fall of 40 to 50 mm Hg in arterial pressure. [Pg.425]

As with other antiarrhythmics, in the elderly or patients with marked previous myocardial damage, increase dose more gradually during initial treatment phase. [Pg.447]

Hypotension If hypotension (systolic blood pressure up to 90 mm Hg) occurs, discontinue drug and carefully assess patient s hemodynamic status and extent of myocardial damage. [Pg.525]

The antiarrhythmic drugs in class I suppress both normal Purkinje fiber and His bundle automaticity in addition to abnormal automaticity resulting from myocardial damage. Suppression of abnormal automaticity permits the sinoatrial node again to assume the role of the dominant pacemaker. [Pg.169]

This effect of tolbutamide, if it occurs, has been attributed to prevention of ischemic preconditioning, a protective manoeuvre that reduces myocardial damage after temporary stoppage of coronary blood flow (25). [Pg.443]

L-Ascorbic acid serves as a reductant for several important enzymatic biotransformations. These characteristic biological activities result from its enediol structure, which confers a strong electron-donating ability. In addition, there is considerable evidence that biological antioxidants, including ascorbic acid, play an important role in the prevention of a large number of chronic diseases such as cancer, cerebral apoplexy, diabetes, myocardial damage, and AIDS.367,368... [Pg.254]

In rabbits burned by an unknown amount of white phosphorus, electrocardiogram alterations (prolongation of QT interval, ST segment depression, T-wave changes, bradycardia, and low voltage QRS complex) indicative of myocardial damage were observed however, no histological alterations were observed in the heart (Bowen et al. 1971). [Pg.91]

Qualitative biomarkers of acute oral exposure that are shared with other toxic compounds include a variety of electrocardiogram alterations. Postmortem biomarkers include fatty hepatic degeneration, pulmonary edema and/or congestion, widespread internal hemorrhaging, widespread intracellular fatty deposits, various myocardial damage, hepatic necrosis, hepatic fibrosis, and increased liver weight (see Section 2.2 for more detail). [Pg.146]

Ibraev SA, Kulkybaev GA, Rys-Uly M. 1992. Morphological mechanisms of myocardial damage with chronic phosphorus intoxication. Zdravookhr Kaz 12 13-15. [Pg.223]

A large number of studies have shown that mild-to-moderate elevations of biochemical markers of myocardial damage... [Pg.48]

Abbreviations. DVT, deep venous thrombosis ESTEEM, Efficacy and Safety of the oral Thrombin inhibitor ximelagatran in combination with aspirin, in patiEnts with rEcent Myocardial damage ... [Pg.113]


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