As a result, the inhibitory effect of this complex interaction of actin and myosin. Enhancing myocardial contractions (positive inotropic effect) due to the fact that cardiac glycosides inhibit Na +, K + ATOa3y (competing with K + ions breathing binding sites of Na +, K + ATFazy) - Mg2 +-dependent thiol breathing (containing SHgruppy) Lipoprotein the cell membrane of cardiomyocytes. Impact and minute breathing of the heart becomes larger, better blood supply to organs and tissues removed edema. Solutions of potassium chloride intravenously breathing . Apparently this is due to a decrease in excessive sympathetic nervous system influences on the heart, as well as antianginal and antiarrhythmic action. All this increases the burden on under- the heart and causes functional and structural changes of the myocardium, termed «remodeling». Cardiotonic strengthen contractions of the heart. Sodium nitroprusside breathing expands the arteries and veins, lowers arterial and venous pressure (reduces Posti preload on the heart). Slowing breathing heart rate (negative chronotropic effect) due to the fact that under the action of cardiac glycosides increased vagal tone, which has a braking effect on the automatism of the sinoatrial breathing Under the action cardiac glycosides breathing kardiokardialny reflex: stimulation of afferent fibers entered the centers of the vagus breathing and vagal efferent fibers back to the heart. Sometimes used in acute heart failure; slowly injected glucose solution. To eliminate the toxic effects of cardiac glycosides used in the preparation of potassium (K + ions prevent breathing binding of glycosides with Na +, K + ATPase) and magnesium (Na +, K + ATPase - Mg2 +-dependent enzyme). The yield of Ca2 + from sarcoplasmic reticulum, breathing breathing Ca2 + in the cytoplasm increases. Blockers are traditionally regarded means contraindicated in heart failure, as these substances weaken the contraction of the heart. Lanatozid C (Celanidum) - glycoside digitalis woolly, from which it is formed digoxin. For a systematic treatment of chronic heart failure, ACE inhibitors are used - captopril, enalapril, lisinopril, and others. Cardiotonic properties are cardiac glycosides and 1adrenomimetiki. Diuretics used in heart failure - hydrochlorothiazide furosemide, and others to increase excretion of Na + and water, resulting in: decreases the volume of extracellular fluid (Reduces swelling), decreases the volume of blood plasma (reduces the load breathing the heart). In acute heart failure intravenously administered high-vasodilator Tools - sodium nitroprusside, nitroglycerin. Application drugs that reduce the workload on the heart - ACE inhibitors, vasodilators, diuretics urelichivaet cardiac output, improves the condition of patients, slows the progression of cardiac remodeling and failure. When you receive systematic digitoksina it possible material accumulation. Nitroglycerin increasingly expanding venous and to a lesser degree of arterial vessels. The most frequently from use of cardiac glycosides digoxin, extracted from the woolly foxglove (Digitalis lanata). In this case, myocardial contractility increases, breathing cardiac output. Currently, the most upotrebitelen drug glycoside woolly foxglove - digoxin. In chronic heart failure used isosorbide dinitrate, isosorbide mononitrate, similar to the action of nitroglycerin. Digitoxin - glycoside digitalis purple. For Coronary Heart Disease treatment of chronic heart failure is especially suitable carvedilol (dilatrend), who adrenoblokiruyuschee properties combined with a vasodilator (the blockade aadrenoretseptor) and antioxidant action. Spironolactone - a weak diuretic, but the mechanism of action is an antagonist of aldosterone and therefore is effective in chronic heart failure. Na +, K + transport contributes ATFaza Na + ions from breathing cell and K + ions into the cell. Blocking the formation of angiotensin II, these drugs enhance arterial and venous vessels, reduce the arterial and venous pressure (reduce fasting and preload on the heart).
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