Serum adenosine deaminase levels in reactional and non-reactional leprosy.

BACKGROUND AND AIMS: Altered serum adenosine deaminase (ADA) levels have been recorded in various diseases involving lymphocytes and/or lymphoreticular system including leprosy. The study was planned to evaluate alterations in serum ADA levels, if any, in reactional and non-reactional leprosy. METHODS: Eighty patients of leprosy, comprising 60 patients of non-reactional leprosy and 20 patients of reactional leprosy were studied along with 20 normal healthy controls. Five milliliters of venous blood was collected and ADA levels were estimated by the method of Giusti (1974). RESULTS: There were 54 males and 26 females. The age of the patients ranged from 5 years to 62 years. The duration of leprosy ranged from 15 days to 3 years. The mean serum ADA level in normal controls was 10.31 +/- 0.58 u/L. The serum ADA levels were raised in leprosy patients, significantly so in multibacillary patients. The serum ADA levels were higher in patients of leprosy with reaction. CONCLUSIONS: The study showed significantly high serum ADA levels in multibacillary leprosy and this was further increased in patients of leprosy with reaction. This may be because of increased lymphoreticular activity during the reactional phases.

Papel de la adenosina sobre la acción antiarrítmica de los digitálicos / Role of adenosine on the antiarrhythmic action of digitalis

La acción de la adenosina sobre el periodo refractario funcional de los tejidos auriculares y en la cancelación del flutter auricular, es semejante a la de los digitálicos. Tal hecho sugiere la posible existencia de una participación adenílica en la acción digitálica. Por ello medimos las concentraciones plasmáticas de adenosina al infundir ouabaína, e investigamos el efecto del digitálico sobre el periodo refractario de tejidos auriculares y sobre el flutter en condiciones de inhibición colinérgico y bloqueo purinérgico. En perros, se administró ouabaína hasta inducir fibrilación ventricular. Se obtuvo sangre del seno coronario y de la vena femoral, midiendo la adenosina por cromatagrafía de líquidos. El periodo refractario se midió con la ténica del estímulo extra acoplado. El flutter se indujo al estimular el haz internodal posterior. Los resultados muestran que la concentración de adenosina se elevó más de 100 por ciento en plama de seno coronario; el efecto de la ouabaína sobre el periodo refractario no se modificó con la inhibición colinérgica, pero sí fue inhibido por aminofilina; el digitálico modificó su acción en la cancelación del flutter en presencia de aminofilina. Conclusión: en la acción antiarrítmica de los digitálicos parece participar un componente adenílico que resulta de la liberación de adenosina del corazón

Laboratory and field comparisons of adenosine influx in Plasmodium falciparum and Plasmodium vivax infected erythrocytes with genetic abnormalities from patients in Myanmar.

Influx of the purine nucleoside, adenosine, was assessed in erythrocytes from both normal subjects and from subjects with a range of genetically determined erythrocyte disorders from Myanmar. The latter included alpha-thalassemia major (Myanmar variant), beta-thalassemia major (Myanmar variant), beta-thalassemia trait, HbEE and HbAE erythrocytes and two variants of glucose-6-phosphate dehydrogenase (G6PDH) deficiency. Significant reductions (p < 0.01) of adenosine influx were observed in erythrocytes from individuals with alpha- and beta-thalassemia major and severe G6PDH deficiency. Abnormal erythrocytes infected with the malarial parasites, Plasmodium falciparum or Plasmodium vivax, demonstrated a reduction in adenosine transport which correlated with the proportion of abnormal erythrocytes present in the samples obtained. The effect of nitrobenzylthioinosine (NBMPR) on adenosine influx was explored in normal and abnormal erythrocytes. In all these cases, NBMPR completely inhibited the transport of adenosine. However, transport of adenosine into P. falciparum and P. vivax-infected normal erythrocytes and abnormal cells was only inhibited 50-60% by NBMPR. The combination of tubercidin and NBMPR completely blocked adenosine transport into both normal and abnormal erythrocytes infected with either P. falciparum or P. vivax.

Relative participation of adenosine and endothelium derived mediators in coronary reactive hyperemia in the dog

The metabolites that mediate coronary reactive hyperemia have not been definitely identified. Although adenosine and endothelium derived substances seem to be involved, their relative contributions have not been defined yet. In the canine coronary circulation, we studied the relative participation of adenosine, nitric oxide and prostacyclin in reactive hyperemia, by measuring the changes produced by interfering with the synthesis or action of these metabolites. The dose-response curve for flow changes vs intracoronary administration of adenosine was displaced to the right after the inhibition of nitric oxide synthesis with N-omega-nitro-L-arginine, revealing that nitric oxide release partly mediates the vasodilator action of adenosine. The inhibition of PGI-2 synthesis with indomethacin did not modify reactive hyperemia. Interference with adenosine action, by administration of adenosine deaminase plus theophylline, decreased reactive hyperemia by 31.0 +/- 4.0 percent (p < 0.001). Inhibition of nitric oxide synthesis decreased reactive hyperemia by a larger (p < 0.005) magnitude, 41.0 +/- 3.9 percent (p < 0.001), revealing the existence of other stimuli for nitric oxide release in reactive hyperemia besides adenosine. Simultaneous inhibition of nitric oxide and PGI-2 syntheses and of adenosine action reduced reactive hyperemia, but the effect was not additive, reaching 49.5 +/- 4.5 percent of control. Since nitric oxide and adenosine are the most important mediators in reactive hyperemia so far described, our results suggest that other metabolites, acting directly or through mediators other than adenosine or nitric oxide, are responsible for about 50 percent of coronary reactive hyperemia