Prostaglandin E-major urinary metabolites as a new biomarker for acute mesenteric ischemia.

BACKGROUND: Acute mesenteric ischemia (AMI) is an emergent vascular disease caused by cessation of the blood supply to the small intestine. Despite advances in the diagnosis, intervention, and surgical procedures, AMI remains a life-threatening condition. Prostaglandin E2 major urinary metabolite (PGE-MUM), the urinary metabolite of prostaglandin E2, is known to be stable in urine and has been suggested to be a valuable biomarker for intestinal mucosal inflammation, such as ulcerative colitis. We therefore investigated whether or not PGE-MUM levels reflect the degree of ischemia in an intestinal ischemia-reperfusion model. METHODS: Male rats were used to establish a superior mesenteric artery occlusion (SMAO) group, in which the superior mesenteric artery was clamped, and a sham group. The clamping times in the SMAO group were either 30 minutes or 60 minutes, and reperfusion times were either 3 hours or 6 hours, after which PGE-MUM values were measured. RESULTS: The histological injury score of the SMAO (30-minute ischemia and 6-hour reperfusion group, 1.8 ± 0.4; 60-minute ischemia and 6-hour reperfusion group, 4.7 ± 0.5) and were significantly greater than that of the sham group (0.4 ± 0.7, p < 0.05). The PGE-MUM levels in the SMAO group (30-minutes ischemia and 6-hour reperfusion group, 483 ± 256; 60-minutes ischemia and 6-hour reperfusion group, 889 ± 402 ng/mL) were significantly higher than in the sham group (30-minute and 6-hour observation group, 51 ± 20; 60-minute and 6-hour observation group, 73 ± 32 ng/mL; p < 0.05). Furthermore, the PGE-MUM value was corrected by the concentration of urinary creatinine (Cr). The PGE-MUM/urinary Cr levels in the SMAO group were also significantly higher than in the sham group ( p < 0.05). CONCLUSION: We found that intestinal ischemia-reperfusion increased urinary PGE-MUM levels depending on the ischemic time. This suggests the potential utility of PGE-MUM as a noninvasive marker of intestinal ischemia.

Hormonas vasodilatadoras en la insuficiencia cardíaca crónica: efecto de la inhibición de la enzima convertidora de angiotensina / Vasodilator hormones in chronic heart failure: effect of the inhibition of angiotensine converting enzyme

To evaluate the chronic effect of enalapril, in addition to digitalis and diuretics, in patients with chronic heart failure, nine patients with an idopathic dilated cardiomyopathy (8 males, aged 48 to 76 years old) under treatment with digitalis and diuretics, received enalapril 20 mg bid during eigth weeks. Before and after this treatment period resting left ventricular ejection fraction, functional class, plasma levels of atrial natriuretic factor and bradykinins (BK) and urinary excretion of kalikreins (BK) and prostaglandins E2 (PGE2) were measured. After enalapril therapy, there was a significant increase in maximal O2 consumption (14.8ñ1.2 to 18.6ñ1.5 ml/kg/min, p<0.05) and radionuclide LV ejection fraction (27.4ñ1.1 to 31.4ñ0.9 percent p<0.05). This was associated with a significant decrease in plasma ANP levels (559ñ158 to 178ñ54.8 pg/ml) and UK (391ñ112 to 243ñ92 Cu/24 h). The decrease in ANP levels, which is a well known marker of prognosis in CHF, could contribute to explain the sustained clinical benefits observed with ACE inhibitors in patients with CHF

Renal function conscious one kidney-one clip hypertensive rats. Effect on indomethacin

Los presentes experimentos han analizado: a) la Presión Arterial (PA) y la función renal en ratas un riñón-un clip (IRIC) dos semanas después de la estenosis arterial; b) efecto de la inhibición de la ciclooxigenasa (CO) sobre la PA y la regluación de la función renal durante el período hipertensivo. Se estudiaron tres grupos de ratas utilizando animales sin anestesia, con libertad de movimiento y crónicamente instrumentados: grupo "Sham" (con operación simulada), Clip 0.31mm de luz, Clip 0.29mm de luz. Los animales fueron examinados antes (período Control) y durante la infusión de indometacina (IND, 5 mg/Kg por la cánula aórtica, n = 11 en cada grupo). La efectiva inhibición de la CO por IND fue confirmada por la determinación de prostaglandín E2 (PGE) en orina. La PA Control (mmH, media ñ ES) difirió significativamente entre los grupos (P < 0.001): Sham, 114 ñ 3; Clip 0.31, l35 ñ 2; Clip 0.29, 154 ñ 4 y los valores no variaron la infusión de IND, sugiriendo que la participación de los eicosanoides derivados de la CO, particularmente la PGE2, en la regulación de la hemodinamia renal de las ratas sham e hipertensas no es significativa. La excreción de sodio fue menor en el período Control de las ratas Clip 0.29 (P<0.01). El significativo efecto natriurético observado en este grupo Clip 0.29 por la infusión de IND sugiere la contribución de um metabolito del AA para el manejo renal del sodio en la hipertensión renovascular más severa