No abstract

Changes in transmembrane sodium fluxes have been reported in normotensive and in hypertensive subjects after ketanserin administration. In this study, the effects of the serotonergic system on transmembrane sodium transport mechanisms have been investigated in vitro. In erythrocytes drawn from ten healthy subjects, we studied the effects of serotonin (5HT) on the Na/K pump, Na/K cotransport, Na/Li countertransport, and passive permeability of Na. No significant changes were found. A direct, non-receptor-mediated action of ketanserin was then suspected, and the effects of two concentrations of ketanserin (5 x 10(-8) and 5 x 10(-7) M) were evaluated in erythrocytes from 12 normal volunteers. Both concentrations of ketanserin significantly decreased the activity of the Na/K pump and increased the activity of Na/Li countertransport. Na/K cotransport and passive permeability were not affected. Indirect evidence of the action of ketanserin on sodium transmembrane fluxes came from other experiments. In the red blood cells taken from five normal subjects and incubated for 2 hours in a plasma pool, we evaluated the changes in intracellular sodium concentration induced by the presence of 5HT or ketanserin. A significant decrease in intracellular sodium concentration occurred only with ketanserin. This study indicates that ketanserin has a direct influence on transmembrane sodium fluxes. If this action were also present in other cells, it might contribute to the actions of the drug at vascular, nervous, and renal tubular levels.

Atrial natriuretic factor (ANF) exerts a vasodilatory effect on the coronary bed in myocardial ischemia. Besides wall stretch, ANF release can also be triggered by endothelin in experimental models. We studied the time course of ANF release and its relationship with endothelin during transient myocardial ischemia in man. Twelve patients subjected to the dipyridamole echocardiography test (DET) in a single-blind, randomly balanced, placebo-controlled setting were studied. Circulating ANF and endothelin were monitored during both dipyridamole and placebo. Dipyridamole caused left ventricular (LV) dyssynergy in 6 patients (group 1: multiple or isolated coronary artery stenosis) and acute left atrial dilation in 5 out of 6. In these 5 patients, a progressive rise of circulating ANF was found soon after LY dyssynergy, starting from time +8 min (55 ± 12 vs. 40 ± 7 at time 0 and 42 ± 8 pmol/1 time-matched placebo, p < 0.05 for both), becoming highly significantly different from + 10 min (72 ± 13 vs. 40 ± 7 at time 0 and vs. 47 ± 5 pmol/1 time-matched placebo, p < 0.01 for both) up to the end of the study (+40 min). Circulating ANF and echocardiographie parameters did not vary in the other 6 patients undergoing the DET (group 2) as well as during placebo in both groups. The DET caused heart rate and the rate-pressure products to increase to the same extent in both groups (+12 and +13%; +13 and +15%, respectively). Circulating endothelin did not vary. The consistent and long-lasting rise of circulating ANF in patients with coronary artery disease during transient myocardial ischemia indicate that ANF measurements during chest pain may be an important marker of the reduction in myocardial perfusion and LV dysfunction. Further studies will indicate if ANF may play a physiological role to attenuate anginal attacks.

The influence of exercise training on left ventricular (LV) geometry and function was studied by 2Dguided M-mode computerized echocardiography in 14 athletes who underwent a predominantly endurance training program. Twenty age-matched untrained subjects served as controls. After a rigorous 28-week training, LV mass was increased (159 ± 27 g/m^2, p < 0.001 vs. 95 ± 20 of controls), with normal values of relative wall thickness (Th/R) and end-systolic meridional wall stress (ESS), suggesting an adequate LV eccentric hypertrophy. Fractional shortening values and the relation between LV ESS and fractional shortening excluded alterations in systolic pump performance. Also, no impairment in LV relaxation and filling indices was observed. When restudied 8 weeks after interruption of exercise, when the reconditioning had just begun, LV mass was still increased, though to a smaller degree (117 ±21 g/m^2, p < 0.001 vs. control values). Eccentric LV hypertrophy was adequate in 9 athletes, whereas 5 athletes showed low Th/R and high LV ESS values. This inadequate LV eccentric hypertrophy was probably due to an abrupt increase in workload. However, systolic and diastolic LV function analysis showed no abnormalities in any subject. We conclude that LV myocardial properties are not affected in exercise-induced LV eccentric hypertrophy. Our results provide new information on the regression of LV hypertrophy after cessation of training.

The case of a child with beta-thalassaemia major who developed a massive haemorrhagic pericardial effusion is reported and in whom the clinical picture completely resolved after pericardiocentesis. Possible causes are discussed and the role of echocardiography in the follow-up of thalassaemic patients is emphasized.