RESUMEN
Since there is increasing evidence indicating nitric oxide [NO] would play a role in sepsis, we decided to investigate whether this multifaceted mediator is directly implicated in the process of bacterial translocation. A total of 48 rats received intraperitoneal either Zymosan A (group Z) for systemic inflammation production or sodium chloride solution (controls); they were then further subdivided into three groups of eight animals each, being given, through the tail vein: L-NAME (N-nitro-L-arginine] for inhibition of NO production; SNP (sodium nitroprusside) as NO donor; or sodium chloride as control. After 2 h, the mesenteric lymph node complex was excised, under sterile conditions, and, using standard bacteriological techniques, bacterial translocation was assessed as colony forming units per gram of tissue (CFU/g). Statistical evaluation of the bacteriological data revealed a significant increase of bacterial translocation in all rats subjected to systemic inflammation (group Z) versus controls (P = 0.01) Control rats that were subjected to L-NAME treatment exhibited a statistically significant increase (P = 0.001) in CFU/g compared to sodium chloride treated rats, while SNP treatment revealed no difference in relation to sodium chloride treated rats. Group Z rats, subjected to L-NAME treatment, similarly exhibited a statistically significant increase (P = 0.01) in CFU/g compared to sodium chloride treated rats, while SNP treatment led to a statistical increase of bacterial translocation in relation to sodium chloride treated rats (P = 0.05). The results of this study lead us to suggest that NO appears to participate in the process of bacterial translocation.
Asunto(s)
Traslocación Bacteriana/fisiología , Óxido Nítrico/fisiología , Sepsis/microbiología , Animales , Inflamación/inducido químicamente , Ganglios Linfáticos/microbiología , Masculino , NG-Nitroarginina Metil Éster/farmacología , Óxido Nítrico/antagonistas & inhibidores , Nitroprusiato/farmacología , Ratas , Ratas Wistar , ZimosanRESUMEN
BACKGROUND: We verified the possibility of using laser Doppler fluxmetry for prolonged monitoring of hepatic perfusion; we confirm the ability of an implantable laser Doppler microprobe to be in constant 'optical contact' with the liver and thus to transmit a stable microcirculatory signal for a prolonged period of time, and we correlate the response of liver microcirculation to the hepatic artery blood flow reduction in order to estimate this flow by continuous monitoring of microcirculation. METHOD: Hepatic microcirculation was recorded by a single-fiber microprobe implanted in the livers of 8 dogs and of 5 surgical ICU patients. In another 7 dogs, liver microcirculation as well as hepatic artery blood flow were recorded digitally, while an occluder was used to decrease hepatic artery flow. RESULTS: Analysis of the initial data of microcirculation revealed a nonsignificant variation between consecutive time segments, a finding confirming the hypothesis that laser Doppler gives a very stable signal over a long period of time. Polynomial regression analysis, performed on data pairs obtained from microcirculation and hepatic artery blood flow revealed a regression coefficient y = -54.22 + 1.07x + 0.0046x2 (y = hepatic artery blood flow, x = liver microcirculation). CONCLUSION: This finding means that it is possible to watch the hepatic artery flow values continuously by the use of this equation and simple monitoring of liver microcirculation. Thus, the use of laser Doppler fluxmetry with implantable microprobes seems promising as a novel method for continuous assessment of hepatic artery blood flow.
Asunto(s)
Arteria Hepática/fisiología , Flujometría por Láser-Doppler , Hígado/irrigación sanguínea , Animales , Perros , Femenino , Arteria Hepática/diagnóstico por imagen , Humanos , Hígado/fisiología , Modelos Logísticos , Masculino , Microcirculación/fisiología , Persona de Mediana Edad , Valores de Referencia , Flujo Sanguíneo Regional , Sensibilidad y Especificidad , UltrasonografíaRESUMEN
Bleeding from esophageal varices is highly lethal in cirrhotics, the main cause of death being liver failure. Because adequate hepatic perfusion is a prerequest for the maintenance of liver function, the present study was designed to evaluate the influence of hemorrhagic shock on liver microcirculation in rats with portal hypertension due to cirrhosis of the liver induced by CCl4. In 16 cirrhotic rats and an equal number of controls, hepatic microcirculation was continuously assessed--by means of laser-Doppler flowmetry, through a self-adhesive probe attached to the liver surface, before and during a 15 min period of arterial hypotension (40 mmHg) induced by blood withdrawal. Our findings revealed that immediately following hemorrhage there is a statistically significant reduction of microcirculation in cirrhotics versus controls. The results of this study assist in the better understanding of the hemodynamic conditions which prevail in the cirrhotic liver during the first minutes of hemorrhage.