ABSTRACT
In order to investigate the correlation between traumatic servity and blood cAMP and cGMP levels in the patients with acute trauma and its clinical significance, 120 cases of trauma were randomly selected and divided into 4 groups (n = 30 in each group): mildly traumatic group (ISS 25). The cAMP and cGMP levels were assayed in sera, leucocytes and platelets respectively in 6 h and 24 h after trauma. The results showed that cAMP and cGMP levels were elevated significantly in sera and platelets (P < 0.05 or P < 0.01), meanwhile cGMP levels in leucocytes (P < 0.05). It was concluded that cAMP and cGMP might play an important role in traumatic stress, participate in the cellular signal transducation and promote the immune function of leucocytes and the coagulation founction of platelets. Serum cAMP and cGMP levels were upregulated correspondingly as ISS increased, and positively correlated to the traumatic severity.
Subject(s)
Blood Platelets/metabolism , Cyclic AMP/blood , Cyclic GMP/blood , Injury Severity Score , Leukocytes/metabolism , Wounds and Injuries/bloodABSTRACT
The purpose of this study was to analyze the effect of fluoxetine upon human T lymphocyte proliferation, and to assess the early signals elicited after T cell triggering and cAMP formation. Blood samples from normal human volunteers were drawn from venipuncture and T cells were cultured in the presence or absence of Concanavalin A (Con A) and fluoxetine. Protein Kinase C (PKC) levels and cyclic adenosine monophosphate (cAMP) formation were also measured. Fluoxetine exerted dual effect, depending on the degree of lymphocyte activation: at mitogenic concentrations of Con A (2 mug/ml), we observed na inhibitory effect on cellular proliferation. This inhibitory effect involves PKC degradation and cAMP formation. On the other hand, when submitogenic Con A concentrations (1mug/ml) were used, fluoxetine stimulated the cellular response and increased PKC traslocation. The participation of extracellular calcium mobilization could be involved in these mechanisms. According to our results, fluoxetine seems to modulate calcium influx which, in turn, would influence PKC traslocation, thus modulating the immune response through a mechanism that could be involving cAMP participation.
Subject(s)
Adult , Female , Humans , Concanavalin A/pharmacology , Cyclic AMP/metabolism , Fluoxetine/pharmacology , Protein Kinase C/metabolism , Selective Serotonin Reuptake Inhibitors/pharmacology , T-Lymphocytes/cytology , T-Lymphocytes/drug effects , Cell Division/drug effects , Cyclic AMP/blood , Protein Kinase C/bloodABSTRACT
Chronic renal failure (CRF) is accompanied by adaptive changes in renal and extrarrenal epithelial ionic transport. Fluid reabsorption in the thick ascending limb of Henle is increased and the capacity to lower the urine osmolality in water diuresis is preserved. To study the cellular mechanism of this adaptation, we measured intracellular cAMP in microdissected medullary thick ascending limb (mTAL) segments in rats with CRF. mTAL exhibited in CRF nephrons an increase of basal cAMP from 6.0 +/- 1.5 in controls to 47.0 + 10.3 fmol. mm-1 tubule in CRF (P < 0.05). Maximally stimulated cAMP levels (10(-3) M IBMX plus 10(-5) M Forskolin) were different from basal levels in controls (6.0 + 1.5 vs 63.1 +/- 18.8, P < 0.05) but not from basal levels in CRF (47.0 +/- 10.3 vs 63.0 +/- 16.0, P = N.S.). Preincubation with the adenylate cyclase inhibitor 2'5' -dideoxyadenosine (DDA) 10(-4) M produced no changes in cAMP in controls (93.7 +/- 10.3 percent of DDA untreated samples) whereas it decreased to 76.2 +/- 8.8 percent (24 percent inhibition) in CRF (P < 0.05). No differences between controls and CRF groups were found in basal and stimulated cAMP in red blood cells and distal colon. The data would suggest that the cAMP pathway is an intracellular signal for mTAL adaptation in epithelial transport and that the adenylate-cyclase system is specifically activated in CRF.
Subject(s)
Animals , Male , Rats , Loop of Henle/cytology , Cyclic AMP/physiology , Renal Insufficiency, Chronic/physiopathology , Cyclic AMP/blood , Enzyme Activation , Ion Transport , Radioimmunoassay , Rats, WistarABSTRACT
Se realizó la determinación de los valores de AMP-cíclico plasmático en 19 pacientes con el diagnóstico confirmado de infarto cardíaca agudo, en los cuales no existían antecedentes conocidos de trastornos endocrinos; el rango de edad fue de 36 a 80 años y ambos sexos, donde predomina el masculino. El estudio se realizó en el período de 21 días posteriores a la fecha de ingreso. El AMP-cíclico fue valorado en plasma por el método radionuclídico con reactivos de la firma Amersham y como marcador del nucleótido, el tritio (8 - H3 adenosin 3,5; fosfato cíclico). Los niveles de AMP-cíclico se encuentran aumentados durante los 21 días posteriores al infarto en el grupo estudiado. En la primera semana en siete casos el promedio fue de X + 29,40 + ou - 1,4 mol/I, lo que difiere significativamente con el control (P <0.005). En la segunda semana X + 37,7 + ou - 2,35 n mol/I (P <0.005) y en la tercera semana el promedio fue X + 27,50 + ou - 4,09 n mol/I, sin encontrarse diferencia (P > 0.05). Grupo control X + 22,50 + ou - 1,00 n mol/I. Se discuten estos resultados y los datos obtenidos fueron estadísticamente precesados