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Pulse--synchronous sympathetic burst power as a new index of sympatho-excitation in patients with heart failure. Am J Physiol Heart Circ Physiol 287: H1821-H1827, 2004. First published June 3, 2004; 10.1152/ajpheart.00252.2003.--The upper limit of incidence of muscle sympathetic neural bursts can lead to underestimation of sympathetic activity in patients with severe heart failure. This study aimed to evaluate the pulse-synchronous burst power of muscle sympathetic nerve activity (MSNA) as a more specific indicator that could discriminate sympathetic activity in patients with heart failure. In 54 patients with heart failure, the pulse-synchronous burst power at the mean heart rate was quantified by spectral analysis of MSNA. Thirteen patients received a central sympatholytic agent (guanfacine) for 5 days to validate the feasibility of this new index. Both burst incidence and plasma norepinephrine level showed no significant difference between patients in New York Heart Association functional class III (94 [+ or -] 6 per 100 heartbeats and 477 [+ or -] 219 pg/ml, respectively) and class II (79 [+ or -] 14 per 100 heartbeats and 424 [+ or -] 268 pg/ml, respectively). In contrast, the burst power was useful for discriminating patients in class III from those in class II (61 [+ or -] 8% vs. 39 [+ or -] 10%; p < 0.05). Inhibition of sympathetic nerve activity by guanfacine was more sensitively reflected by the change of burst power (-36 [+ or -] 25%) than by that of burst incidence (-12 [+ or -] 14%; P < 0.001). The sympathetic burst power reflects both burst frequency and amplitude independently of the absolute values and provides a sensitive new index for interindividual comparisons of sympathetic activity in patients with heart failure. muscle sympathetic nerve activity; [alpha][sub.2]-adrenoceptor agonist; spectral analysis

The aortic depressor nerve (ADN) activity and sympathetic nerve discharge (SND) in rat arteries were measured after electrical stimulation and phenylephrine infusion to determine whether sustained elevation in arterial pressure elicits nonuniform sympathetic nerve responses. Using rats as experimental animals, it was shown that prolonged electrical stimulation which causes activation of arterial baroreceptors results in nonuniform responses of efferent SND.

Inhibition of nitric oxide synthase (NOS) generates nonuniform alterations in sympathetic nerve discharge (SND) independent of arterial pressure in baroreceptor-denervated rats. Mean arterial pressure (MAP), renal SND, and lumbar SND are measured before and after the injection of N(super G)-nitro-L-arginine methyl ester (L-NAME) in baroreceptor innervated rats. MAP increases, whereas renal and lumbar SND decreases by injecting L-NAME. The experimental procedure for the inhibition of NOS is discussed.

A recent study has reported that angina patients who have had 20 treatments with heparin (a clot-dissolving drug) prior to exercise periods improved their capacity to exercise by developing collateral circulation. When a patient has a blocked coronary artery, a collateral vessel may develop, providing an alternate route to maintain blood flow. Heparin has been associated with the growth of new blood vessels, but whether it initiates this new growth is not clear. Fourteen patients with chronic stable effort angina (chest pain caused by insufficient blood flow to the heart during exercise) were included in a study to determine the role of heparin in the development of collateral circulation. Seven patients were assigned to strenuous exercise periods twice a day, preceded by heparin treatment; seven others were given daily injections of heparin only. Each treatment regimen lasted for 10 days, and the total dose of heparin was the same for both groups. Patients who received heparin, but did not exercise, did not improve significantly, while patients who received heparin before exercising increased the amount of time they were able to exercise by 43 percent. In an earlier study, 20 periods of strenuous exercise without heparin pretreatment similarly did not result in improved exercise capacity. The results of this study indicate that the development of collateral circulation is related to heparin treatment combined with exercise, but not to heparin treatment alone. (Consumer Summary produced by Reliance Medical Information, Inc.)

The coronary collateral circulation refers to the circulation of blood in small blood vessels branching from the coronary arteries, the major blood vessels supplying the heart. Collateral circulation is important in improving blood flow when the main artery is obstructed. The function of the coronary collateral circulation in the reversible asynergy or impaired coordination of the function of the left ventricle was assessed. Nitroglycerin, a drug that dilates blood vessels and is used to treat angina pectoris (chest pain due to inadequate coronary blood flow), was given to 19 patients with a recent heart attack and complete occlusion or blockage in a portion of their left anterior descending coronary artery. Nine patients with significant collateral circulation to the blocked artery showed improved function and coordination of the left ventricle with the administration of nitroglycerin. However, the remaining 10 patients, who did not have adequate collateral circulation, showed no changes in ventricular function when nitroglycerin was administered. Heart rates and pressures within the ventricles were not altered by nitroglycerin and were similar in patients with and without collateral circulation. These findings show that, in the presence of intact coronary collateral circulation, nitroglycerin can improve the function of the left ventricle when blood flow in the main coronary arteries is blocked and heart tissue has been damaged by a heart attack. (Consumer Summary produced by Reliance Medical Information, Inc.)

Myocardial infarction (MI, heart attack) is the deterioration of heart tissue due to cessation of the heart's blood supply, which may result from a blood clot obstructing the coronary arteries, the major blood vessels supplying the heart. Heparin is a polysaccharide, or glucose compound, that prevents the coagulation of blood and the formation of blood clots. The effects of heparin on the development of coronary collaterals (small blood vessels that supplement circulation to the heart when a coronary artery is blocked) and on the function of the heart were examined in 18 patients recovering from an MI. Collateral development was greater in patients receiving heparin than in patients without this treatment. Heart function was indicated by measurements of left ventricular ejection fraction, or the amount of blood emptied from the left ventricle during contraction, and muscle shortening of the infarcted heart tissue. These characteristics improved to a greater extent in patients receiving heparin treatment, compared with patients receiving no treatment. The results demonstrate that heparin preserves left ventricular function as a result of collateral development in patients who have sustained an MI. (Consumer Summary produced by Reliance Medical Information, Inc.)