Clinical

Nitrate donors in frequent clinical use are displayed in figure 3 . From a clinical perspective, the circulatory effects of NTG can be viewed in two ways - venous and arterial. As a venodilator, NTG induces venous pooling and reduces venous return. The resulting reduction in ventricular preload has found an important place in the treatment of heart failure [18] - in acute heart failure with intravenous NTG and in chronic heart failure with oral preparations. The venodilatory effect of NTG also plays a role in the relief of angina pectoris by reducing left ventricular end-diastolic pressure, ventricular wall tension and improving subendocardial blood flow. Long-term use of organic nitrates for heart failure has been limited because of nitrate tolerance.

The use of NTG for more than a century in the treatment of angina pectoris has long been attributed to its effects on the arterial side of the circulation. NTG has a powerful dilating effect on muscular arteries. Coronary arterio-graphic studies have shown increased diameter of normal coronary segments and reduction in the narrowing of coronary stenoses, with a resultant decrease in the resistance to blood flow across these stenoses (fig. 4) [19, 20]. NTG also improves the function of collateral vessels distal to proximal stenoses (fig. 5) [21]. In contrast to inorganic nitrates, as described earlier, NTG must undergo biotransformation before it becomes active. Resistance vessels <100 ^m in diameter in the coronary circulation lack the biochemical machinery to activate NTG and are therefore not dilated by the drug. Larger microvessels (>200 ^m) are able to biotransform NTG and these vessels are therefore responsive to the

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