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Vasodilators venous

Milrinone is a bipyridine derivative that inhibits phosphodiesterase 111 and produces positive inotropic and arterial and venous vasodilating effects hence, milrinone has been referred to as an inodilator. It has supplanted use of amrinone, which has a higher rate of thrombocytopenia. [Pg.106]

Sodium nitroprusside is a mixed arterial-venous vasodilator that acts directly on vascular smooth muscle to increase cardiac index and decrease venous pressure. Despite its lack of direct inotropic activity, nitroprusside exerts hemodynamic effects that are qualitatively similar to those of dobutamine and milrinone. However, nitroprusside generally decreases PAOP, SVR, and blood pressure more than those agents do. [Pg.107]

Possible uses. Arteriolar vasodilators are given to lower blood pressure in hypertension (p. 312), to reduce cardiac work in angina pectoris (p. 308), and to reduce ventricular afterload (pressure load) in cardiac failure (p. 132). Venous vasodilators are used to reduce venous filling pressure (preload) in angina pectoris (p. 308) or cardiac failure (p. 132). [Pg.118]

Hydralazine and dihydralazine are predominantly arterial vasodilators which cause a reduction in peripheral vascular resistance but also reflex tachycardia and fluid retention. They were used in the treatment of hypertension, in combination with a -blocker and a diuretic. Long-term use of these compounds may cause a condition resembling lupus erythematodes with arthrosis, dermatitis and LE-cells in the blood. This risk is enhanced in women and in patients with a slow acetylator pattern. When combined with the venous vasodilator isosorbide (an organic nitrate) hydralazine was shown to be mildly beneficial in patients with congestive heart failure (V-HEFT I Study). Hydralazine and dihydralazine have been replaced by other therapeutics, both in hypertension treatment and in the management of heart failure. [Pg.329]

Nifedipine (Table 3) is a potent vasodilator that selectively dilates resistance vessels and has fewer effects on venous vessels. It does not cause reflex tachycardia during chronic therapy. Nifedipine is one of the first-line choices for black or elderly patients and patients having concomitant angina pectoris, diabetes, or peripheral vascular diseases. Nifedipine, sublingually, is also suitable for the treatment of hypertensive emergencies. Nifedipine does not impair sexual function or worsen blood Hpid profile. The side effects are flushing, headache, and dizziness. [Pg.142]

Nitroprusside. Nitropmsside is a poteat, fast-actiag vasodilator that has to be administered iatravenously by iafusion. It relaxes arterial and venous vascular smooth muscle. Its use is mainly ia hyperteasive crises. Its effects terminate as sooa as iafusioa of the dmg is stopped. [Pg.143]

Nicorandil. Nicorandil is a potassium channel opener that can lower blood pressure 21, 20, and 29 mm Hg after single oral doses of 10, 20, and 30 mg, respectively (250). There are no significant changes ia heart rate. Headache is the primary side effect. Nicorandil has potent coronary vasodilator effects. It causes sustained vasodilation of arteriolar resistance and venous capacitance blood vessels, thus reduciag cardiac preload and aftedoad. [Pg.143]

Vasodilators are a group of dtugs, which relax the smooth muscle cells of the blood vessels and lead to an increased local tissue blood flow, a reduced arterial pressure and a reduced central venous pressure. Vasodilators reduce the cardiac pre-load as well as after-load and thereby reduce cardiac work. They are used in a variety of conditions including hypertension, cardiac failure and treatment/prevention of angina pectoris. Major groups are Ca2+-channel blockers (e.g. dihydropyridines), NO-donators (e.g. organic nitrates), K+-channel openers (minoxidil), phosphodiesterase inhibitors (e.g. sildenafil), Rho-kinase inhibitors (e.g. Y27632) or substances with unknown mechanism of action (e.g. hydralazine). Inhibitors of the... [Pg.1272]

Both vasoconstrictors and vasodilators have been used in the treatment of priapism. Vasoconstrictors are thought to work by forcing blood out of the cavernosum and into the venous return. Aspiration of the penile blood followed by intracavenous irrigation with epinephrine (1 1,000,000 solution) has been effective with minimal complications.37 In severe cases, surgical intervention to place penile shunts has been used, but there is a high failure rate, and the risk of complications, from skin sloughing to fistulas, limits its use. [Pg.1015]

The sympathetic system also innervates vascular smooth muscle and regulates the radius of the blood vessels. All types of blood vessels except capillaries are innervated however, the most densely innervated vessels include arterioles and veins. An increase in sympathetic stimulation of vascular smooth muscle causes vasoconstriction and a decrease in stimulation causes vasodilation. Constriction of arterioles causes an increase in TPR and therefore MAP. Constriction of veins causes an increase in venous return (VR) which increases end-diastolic volume (EDV), SV (Frank-Starling law of the heart), CO, and MAP. [Pg.203]

Vasodilators Arterial Arterial and venous Hydralazine Nitroprusside t 4 T... [Pg.212]

The answer is d. (Hardman, pp 794-795.) Hydralazine, minoxidil, diazoxide, and sodium nitroprusside are all directly acting vasodilators used to treat hypertension. Because hydralazine, minoxidil, nifedipine, and diazoxide relax arteriolar smooth muscle more than smooth muscle in venules, the effect on venous capacitance is negligible. Sodium nitroprusside, which affects both arterioles and venules, does not increase cardiac output, a feature that enhances the utility of sodium nitroprusside in the management of hypertensive crisis associated with MI. [Pg.126]

Nesiritide is manufactured using recombinant techniques and is identical to the endogenous B-type natriuretic peptide secreted by the ventricular myocardium in response to volume overload. Consequently, nesiritide mimics the vasodilatory and natriuretic actions of the endogenous peptide, resulting in venous and arterial vasodilation increases in cardiac output natriuresis and diuresis and decreased cardiac filling pressures, sympathetic nervous system activity, and renin-angiotensin-aldosterone system activity. [Pg.108]

Isolated tissues Vasoconstrictor/vasodilator assessment Isolated tissues (e.g., arterial/ venous rings) Krasner et al.,-84 Lefer et al85... [Pg.257]

In A, the clinically most important vasodilators are presented in the order of approximate frequency of therapeutic use. Some of these agents possess different efficacy in affecting the venous and arterial limbs of the circulation (width of beam). [Pg.118]

These vasodilator effects produce hemodynamic consequences that can be put to therapeutic use. Due to a decrease in both venous return (preload) and arterial afterload, cardiac work is decreased (p. 308). As a result, the cardiac oxygen balance improves. Spasmodic constriction of larger coronary vessels (coronary spasm) is prevented. [Pg.120]

Mention should also be made of the possibility of affecting cardiac function in angina pectoris (p. 306) or congestive heart failure (p. 132) by reducing venous return, peripheral resistance, or both, with the aid of vasodilators and by reducing sympathetic drive applying 3-blockers. [Pg.128]

Vasodilatation by venous occlusion plethysmography, laser doppler Vasodilators... [Pg.163]


See other pages where Vasodilators venous is mentioned: [Pg.47]    [Pg.56]    [Pg.197]    [Pg.210]    [Pg.249]    [Pg.251]    [Pg.253]    [Pg.334]    [Pg.334]    [Pg.723]    [Pg.723]    [Pg.643]    [Pg.47]    [Pg.56]    [Pg.197]    [Pg.210]    [Pg.249]    [Pg.251]    [Pg.253]    [Pg.334]    [Pg.334]    [Pg.723]    [Pg.723]    [Pg.643]    [Pg.123]    [Pg.574]    [Pg.1002]    [Pg.246]    [Pg.56]    [Pg.56]    [Pg.56]    [Pg.58]    [Pg.98]    [Pg.234]    [Pg.107]    [Pg.289]    [Pg.308]    [Pg.81]    [Pg.220]    [Pg.237]   
See also in sourсe #XX -- [ Pg.122 ]




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