Ischaemia myocardial

PI (adenosine) receptors were explored as therapeutic targets before P2 receptors. Adenosine was identified early and is in current use to treat supraventricular tachycardia. A2a receptor antagonists are being investigated for the treatment of Parkinson s disease and patents have been lodged for the application of PI receptor subtype agonists and antagonists for myocardial ischaemia and reperfusion injury, cerebral ischaemia, stroke, intermittent claudication and renal insufficiency. 

These detailed cell models can be used to study the development in time of processes like myocardial ischaemia (a reduction in coronary blood flow that causes under-supply of oxygen to the cardiac muscle), or effects of genetic mutations on cellular electrophysiology. They allow to predict the outcome of changes in the cell s environment, and may even be used to assess drug actions. 

Ferrari, R., Curello, S., Ceconi, C., Cargoni, A., Condorelli, E. and Albertini, A. (1986). Intracellular effects of myocardial ischaemia and reperfusion role of calcium and oxygen. Eur. Heart J. 7 (Suppl. A), 3-12. 

MI Myocardial ischaemia MIF Migration inhibition factor mIL Mouse interleukin MI/R Myocardial ischaemia/ reperfiision MIRL Membrane inhibitor of reactive lysis... 

Neri Semeri G. G., Gensini G. F., Poggessi L. Effect of heparin, aspirin oralteplase in reduction of myocardial ischaemia in refractory unstable angina. Lancet 1990 335,615-8. 

Q77 When starting levothyroxine, a baseline ECG is recommended. The baseline ECG is used to distinguish underlying myocardial ischaemia from changes induced by hypothyroidism. 

Adenosine 3 receptor ADORA3 Agonism Immunosuppression, hypotension, anti-ischaemic (cardioprotective), pro-ischaemic (cerebral), cell necrosis, cell proliferation and angiogenesis. Antagonism might cause myocardial ischaemia, proinflammatory effects, hypertension and interfere with the regulation of cell growth. 

Blockers are used as therapeutics in the treatment of hypertension, myocardial ischaemia (angina pectoris), tachyarrhythmias, and in the secondary prevention following myocardial infarction. More recently the cautious use of /3-blockers has been found to be of potential benefit in the treatment of congestive heart failure (NYHA stages II and III). 

All of the aforementioned beneficial effects of the /3-blockers are caused by the blockade of /3i-adrenoceptors. The beneficial effect of /3-blockers in the treatment of angina is largely caused by the reduction of heart rate and the concomitant decrease in myocardial oxygen consumption, thus improving the imbalance between oxygen supply and consumption which underlies myocardial ischaemia. 

Sodium nitroprusside (SNP) is both a venous and an arterial vasodilator. An important part of its vasodilator action is caused by the release of nitric oxide (NO), similarly as for the organic nitrates. SNP can only be administered via the intravenous route. It is a rapidly and short acting vasodilator. It has been used in the treatment of hypertensive emergencies and in the management of myocardial ischaemia. In spite of its vasodilator action it hardly influences heart rate, in contrast to hydralazine and minoxidil. The dosage of SNP should not be higher than 3 pg/kg/min within 48 h, in order to avoid the rise of cyanide ions and thiocyanate in the blood. 

Adverse effects are generally mild some nausea may occur. Its posihve inotropic action can result in myocardial ischaemia in patients with coronary artery disease. 

The most prominent effect of halothane on the circulation is a dose-related decrease in arterial blood pressure. This is due mainly to reduced myocardial contractility and ventricular slowing. Cardiac output falls due to a decrease in stroke volume and bradycardia. Systemic vascular resistance also falls but this is less pronounced than with some other agents. Although halothane reduces myocardial oxygen consumption it also reduces oxygen demand and it is suitable for patients with myocardial ischaemia. 

Unlike tubocurarine, pancuronium does not produce ganglionic block or histamine release. For this reason it became popular soon after its introduction and became the drug of choice for use in sick patients. However, it increases the heart rate, arterial pressure, and cardiac output in clinical doses. While this may be advantageous when using high-dose opiate anaesthesia in cardiac surgery, it can be associated with arrhythmias and myocardial ischaemia. The... 

Cyanide toxicity, overshoot hypotension, and myocardial ischaemia. Hypoxia caused by increased ventilation-perfusion mismatch due to pulmonary vasodilatation and inhibition of hypoxic pulmonary vasoconstriction. Rebound hypertension after discontinuation of SNP infusion. 

Angina pectoris, hypertension, congestive heart failure, acute myocardial ischaemia, acute pulmonary oedema, unstable coronary syndromes especially when associated with elevated filling pressures. Nitrate therapy may exaggerate outflow obstruction in hypertrophic obstructive cardiomyopathy. 

These result from over-stimulation of the sympathetic nervous system anxiety, sweating, tachycardia, arrhythmia, hypertension, myocardial ischaemia, headache, cerebral haemorrhage, pulmonary oedema. Adrenaline may cause pupillary dilatation which must be distinguished from pupillary dilatation due to other causes, e.g. severe brain injury. 

Isoprenaline stimulates pi and 32 adrenoceptors (pi>32) resulting in increased myocardial contractility and reduced peripheral vascular resistance. It does not act on a adrenoceptors. Cardiac output increases partly due to reduced afterload and an increase in heart rate. There is a diversion of blood to non-essential tissues, e.g. skeletal muscle and skin. Because of the decrease in peripheral vascular resistance arterial blood pressure and coronary perfusion pressure may decrease, which may predispose to myocardial ischaemia. 

Dopamine does not cross the blood-brain barrier and so there are no CNS side effects when given intravenously. Tachyarrhythmias, myocardial ischaemia, headache, nausea and vomiting may occur. Interactions... 

Hiraishi S, Iwanami N, Ogawa N. Images in cardiology. Enlargement of cardiac rhabdomyoma and myocardial ischaemia during corticotropin treatment for infantile spasm. Heart 2000 84(2) 170. 

Schulte-Sasse U. Life threatening myocardial ischaemia associated with the use of prostaglandin El to induce abortion. BJOG 2000 107(5) 700-2. 

Moran C, Ni Bhuinneain M, Geary M, Cunningham S, McKenna P, Gardiner J. Myocardial ischaemia in normal patients undergoing elective Caesarean section a peripar-tum assessment. Anaesthesia 2001 56(11) 1051—8. 

Myocardial ischaemia (Severe) Intramyocardial injection VEGF-C Naked DNA Isner, J.M. et al./ Vascular Genetics Inc St. Elizabeth s Medical Center, Boston, MA, USA... 

The most serious toxic effects of cocaine involve changes in the cardiovascular system. These include cardiac arrhythmias, myocardial ischaemia and infarction, and cerebrovascular spasm, all of which can be largely explained by the facilitation of the action of catecholamines on the cardiovascular system. Another explanation of the cardiotoxicity of cocaine lies in the direct vasoconstrictive properties of its major metabolite, norcocaine. It seems likely... 

Drory X Shapira I, Fisman EZ, et al. Myocardial ischaemia during sexual activity in patients with coronary artery disease. Am J Cardiol 1995 75 835-837. 

Halcox JPJ, Nour KRA, Zalos G, et al. The effect of sildenafil on human vascular function, platelet activation and myocardial ischaemia. J Am Coll Cardiol 2002 40 1232-1240. 

Chi, N.C., and Karliner, J.S. 2004. Molecular determinants of responses to myocardial ischaemia-reperfusion injury focus on hypoxia-inducible and heat shock factors. Cardiovasc. Res. 61 437-447. 

Banai, S., Shweiki, D., Pinson, A., Chandra, M., Lazarovici, G., and Keshet, E. 1994a. Upregula-tion of vascular endothelial growth factor expression induced by myocardial ischaemia implications for coronary angiogenesis. Cardiovasc. Res. 28 1176-1179. 

Squadrito F, Altavilla D, Squadrito G, Saitta A, Deodato B, Arlotta M, et al. Tacrolimus limits polymorphonuclear leucocyte accumulation and protects against myocardial ischaemia-reperfusion injury. J Mol Cell Cardiol 2000 32 429 140. 

Angina pectoris describes the classic symptoms of chest pain, and is caused by transient myocardial ischaemia. In stable angina, the blood flow through the coronary arteries may be limited due to the development of atherosclerotic plaques that restrict blood and therefore oxygen to the cardiac muscle myocardium. Episodes of angina are typically caused by exertion or emotion and are relieved by rest. 

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