Myocardial oxidation

Curello, S., Ceconi, C.. Cargnoni, A., Connacchian, A., Ferrari, R. and Albertini, A. (1987). Improved procedure for determining glutathione in plasma as an index of myocardial oxidative stress. Clin. Chem. 33, 1448-1449. 

A recent study aiming at validating the fatty acid analog FTP in the isolated perfused rat heart showed that FTP as a metabolically trapped FAO probe is capable of indicating rates of myocardial oxidation of exogenous long-chain fatty acids [187]. 

I I I Clermont G, Vergely C, Jazayeri S, et al. Systemic free radical activation is a major event involved in myocardial oxidative stress related to cardiopulmonary bypass. Anesthesiology 2002 96 80-87. 

Nishizawa, T., Iwase, M., Kanazawa, H., Ichihara, S., Ichihara, G., Nagata, K., Obata, K., Kitaichi, K., Yokoi, T., Watanabe, M., Tsunematsu, T., Ishikawa, Y., Murohara, T., and Yokota, M. 2004. Serial alterations of beta-adrenergic signaling in dilated cardiomyopathic hamsters possible role of myocardial oxidative stress. Circ. J. 68 1051-1060. 

Nony P, GuastaUa JP, Rebattu P, Landais P, Lievre M, Bontemps L, Itti R, Beaune J, Andre-Fouet X, Janier M. In vivo measurement of myocardial oxidative metabolism and blood flow does not show changes in cancer patients undergoing doxorubicin therapy. Cancer Chemother Pharmacol 2000 45(5) 375-80. 

Qin, R, Simeone, M., and Patel, R. 2007. Inhibition of NADPH oxidase rednces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction. 43, 271-81. 

Akhlaghi, M. and Bandy, B. 2010. Dietary broeeoli sprouts protect against myocardial oxidative damage and eell death during isehemia-reperfusion. Plant Foods for Human Nutrition, 65(3), 193-9. doi 10.1007/slll30-010-0182-4... 

The results show that the consequences of the vessel occlusion are not limited to the damaged tissue, but will also affect the metabolism of myocardial cells in other parts of the left ventricle. It seems that the myocardial cells have lost the ability to increase their metabolic activity, as a necessary compensatory mechanism, in CHF due to the myocardial infarction. The results are unexpected, in fact previous studies have shown increased activity of myocardial oxidative enzymes, stimulated by enhanced sympathetic nervous system activity in CHF. Heat production rale in the ischemic myocardium indicated a persistent metabolic activity with continuous demand of oxygen and fuel supply. This finding is of interest with regard to the possibility to use drugs that may improve the metabolic condition and survival of the damaged myocardium. 

Nitrous oxide produces respiratory depression (38,39). It has been shown to produce a direct myocardial depressant effect in dogs (40) and in humans breathing a 40% N2O/60% oxygen mixture (41) however, this may be offset by the activation of the sympathetic nervous system (42). The combination of nitrous oxide and opioids can produce decreases in myocardial contractiHty, heart rate, and blood pressure (43). 

Oxidant Stress-induced Alterations in Myocardial Glutathione Status... 

Ferrari, R., Ceconi, C., Curello, S., Caignoni, A., De Giuli, F. and Visioli, O. (1992). Occurrence of oxidative stress during myocardial reperfusion. Mol. Cell. Biochem. Ill, 61-69. 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

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