Peripheral vasculature, effect

Amiodarone dilates arteriolar vascular smooth muscle, especiady coronary arteries, and thus exhibits antianginal effects. Its effects on the peripheral vasculature to decrease resistance leads to a decrease in left ventricular stroke work and a decrease in myocardial oxygen consumption. The dmg rarely produces hypotension that requires discontinuation of the dmg (1,2). 

Mechanism of Action An alpha-adrenergic agonist that stimulates alphaj-adrenergic receptors. Inhibits sympatheticcardioaccelerat or and vasoconstrictor center to heart, kidneys, peripheral vasculature. Therapeutic Effect Decreases systolic, diastolic blood pressure (BP). Chronic use decreases peripheral vascular resistance. Pharmacohinetics Well absorbed from gastrointestinal (GI) tract. Widely distributed. Protein binding 90%. Metabolized in liver. Excreted in urine and feces. Not removed by hemodialysis. Half-life 6 hr. 

Combining agonists with some local anesthetics greatly prolongs the duration of infiltration nerve block the total dose of local anesthetic (and the probability of toxicity) can therefore be reduced. Epinephrine, 1 200,000, is the favored agent for this application, but norepinephrine, phenylephrine, and other agonists have also been used. Systemic effects on the heart and peripheral vasculature may occur even with local drug administration but are usually minimal. 

Diltiazem (Cardizem, Dilacor). Like the other calcium channel blockers, diltiazem is able to vasodilate the coronary arteries and the peripheral vasculature. Diltiazem also produces some depression of electrical conduction in the sinoatrial and atrioventricular nodes, an effect that may cause slight bradycardia. This bradycardia can be worsened by beta blockers or in patients with myocardial conduction problems, and diltiazem should probably be avoided in these individuals.32,45... 

The calcium channel blockers inhibit the entrance of calcium into cardiac and smooth muscle cells of the coronary and systemic arterial beds. All calcium channel blockers are therefore vasodilators that cause a decrease in smooth muscle tone and vascular resistance. (See p. 187 for a description of the mechanism of action of this group of drugs.) At clinical doses, these agents affect primarily the resistance of vascular smooth muscle and the myocardium. [Note Verapamil mainly affects the myocardium, whereas nifedipine exerts a greater effect on smooth muscle in the peripheral vasculature. Diitiazem is intermediate in its actions.]... 

Halothane can be used as an anesthetic by maternal inhalation for fetal surgery and improves surgical exposure by relaxing the uterus. However, the effects of halothane on fetal cardiovascular homeostasis have been evaluated, and the authors concluded that halothane had a significant negative effect on the fetal heart and peripheral vasculature it was therefore considered a poor anesthetic for this purpose (57). 

In addition to their prominent function in heart, P-ARs are located on vascular smooth muscle cells, where they mediate vasodilating effects of catecholamines. The P2-AR has been proposed to play a dominant role in catecholamine-induced vasodilation in both pulmonary and peripheral vasculature. Surprisingly, isomet-... 

Direct effect on peripheral vasculature, responds poorly to vasopressors... 

The occurrence of "Ca -selective", voltage activated "channels" is not limited to the myocardium. They occur in most smooth muscle cells - including those in the coronary, cerebral and peripheral vasculature (30). The normal activity of pacemaker, nodal and conducting tissues (31) is also largely dependent upon them. Because of their widespread distribution it follows that substances which affect the functioning of these channels will have a profound effect on the circulation. By contrast, skeletal muscle is relatively unaffected (32). 

Class II drugs can be further subdivided into at least three subgroups (Figure 3). For example the effect of diltiazem on the slow channels is more marked in the smooth muscle cells of the coronary (51) than the peripheral vasculature. Nimodipine (52) acts preferentially on slow channel transport in the cerebral vessels, where it blocks thromboxane-induced contractions (53) ... 

Apart from catecholamine secretion, it is not obvious what role increased endocrine activity would have in homeostasis after injury. In adrenalectomized dogs subjected to hemorrhagic injury, cortisol and aldosterone will each cause an expansion of extracellular fluid volume by mobilization of cell water within 6 hours of administration. Cortisol, but not aldosterone, also will cause an expansion of plasma volume which can be attributed to its effects on the peripheral vasculature. Spironolactone will prevent the shift of water from the body cell mass to the interstitial fluid (M3). The above experimental evidence clearly im-... 

These drugs decrease the activation of a, receptors in the peripheral vasculature, resulting in net vasodilatation and decreased TPR. In addition, venous capacitance is increased, effectively... 

If the combination of a beta-blocker and a diuretic does not produce sufficient lowering of pressure, a calcium channel blocker (e.g., verapamil, nifedipine) may be used. This class of drugs blocks type L calcium channels in the myocardium and peripheral vasculature in a dose-depen-dent manner, resulting in decreased cardiac output and peripheral resistance (see chapter 12 for a full discussion of calcium channel blockers). The individual drugs within the class vary as to effect on cardiac muscle and/or vasculature. Therefore, the drug used dictates the relative decrease in cardiac output and/or TPR. 

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