Coronary vessels

Bakhai A, Booth J, Delahunty N et al (2005) The SV stent study a prospective, multicentre, angiographic evaluation of the BiodivYasio phosphorylcholine coated small vessel stent in small coronary vessels. Int J Cardiol 102 95-102... 

The answer is a. (Hardman, pp 762-764.) Experimentally, nitrates dilate coronary vessels. This occurs in normal subjects, resulting in an overall increase in coronary blood flow. In arteriosclerotic coronaries, the ability to dilate is lost, and the ischemic area may actually have less blood flow under the influence of nitrates. Improvement in the ischemic conditions is the result of decreased myocardial oxygen demand because of a reduction of preload and afterload. Nitrates dilate both arteries and veins and thereby reduce the work of the heart. Should systemic blood pressure fall, a reflex tachycardia will occur. In pure coronary spasm, such as Prinzmetal s angina, the effect of increased coronary blood flow is relevant, while in severe left ventricular hypertrophy with minimal obstruction, the effect on preload and afterload becomes important. 

Currently, more than 400 human somatic cell gene therapy protocols are being tested. Most of these involve the use of genetically modified cells to treat noninherited diseases. For example, normal copies of the p53 tumor suppressor gene are inserted into lung tumors to halt tumor progression, and genetically modified cells have been used to create new coronary vessels in patients with coronary heart disease. Success has also been achieved in the treatment of hereditary disease (most notably, the recent successful treatment of X-linked severe combined immune deficiency see Clinical Correlate). 

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. 

More than 100 years ago, it was observed that amylnitrate and nitroglycerine relieve pain in angina pectoris, and since nitrites and nitrates have the ability to dilate vessels, thus moderately increasing blood flow to the myocardium, it became customary to think that dilation of coronary vessels alleviates the condition of angina pectoris. 

Although several factors can influence the flow of blood through the coronary vessels, the most important of these is the local production of vasodilator metabolites that results from stimulation-induced increased work by the heart. a-Adrenoreceptors and -adrenoceptors in the coronary vascular beds do not play a major role in determining the vasodilator effects of the administration of epinephrine or norepinephrine. 

Sevoflurane, in common with all volatile agents, reduces cardiac output and systemic blood pressure. It does so mainly through a reduction in peripheral vascular resistance. Although it is a systemic vasodilator it does not appear to produce significant dilatation of small coronary vessels and there is no possibility of coronary steal as hypothesised for isoflurane. A small increase in heart rate may be observed. This is less pronounced than with isoflurane and desflurane and is almost certainly the result of reflex activity secondary to the reduction in peripheral vascular resistance. Sevoflurane is associated with a stable heart rhythm and does not predispose the heart to sensitisation by catecholamines. In children, halothane causes a greater decrease in heart rate, myocardial contractility and cardiac output than sevoflurane at all concentrations. For these reasons sevoflurane is advocated for use in outpatient dental anaesthesia, especially in children. 

Dopamine is an endogenous catecholamine and an immediate precursor of adrenaline and noradrenaline. At low doses it stimulates vascular DAI dopaminergic receptors, especially those in renal, mesenteric and coronary vessels. As the dose increases it progressively stimulates 31 and al adrenoceptors. Thus, depending on the dose it may act as a renal vasodilator, a myocardial inotrope, or a peripheral vasoconstrictor. Dopamine also causes release of noradrenaline from autonomic nerve endings (DA2 receptors). 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

Epimedium brevicorum Maxim. E. koreanum Nakai E. macranthum Moore et Decne. Jin Yang Huo (aerial part) Icarlin, noricariin, korepimedoside A, korepimedoside B, icariine, des-O-methyl-licariine, magnoflorine, epimedoside A, polysaccharides, 33 48 Dilate the coronary vessels and increase the coronary flow by reducing vascular resistance. 

Verapamil (CalanIsoptin). Verapamil has been used to treat angina because of its ability to vasodilate the coronary vessels. Verapamil, however, seems to be moderately effective compared to the other antiangi-nal drugs, and verapamil also depresses myocardial excitability and decreases heart rate.9,32 Because of its negative effects on cardiac excitation, verapamil is probably more useful in controlling certain cardiac arrhythmias (see Chapter 23). 

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