The implication of nitric oxide in the process of bacterial translocation.
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.
Eleftheriadis
E
E
Department of Surgery, Faculty of Medicine, University of Thessaloniki, Greece. elemakis@med.auth.gr
Kotzampassi
K
K
Heliadis
N
N
Herodotou
A
A
Hatjopoulou
E
E
Petridou
E
E
Sarris
K
K
D000818:Animals; D018988:Bacterial Translocation / Q000502:physiology*; D007249:Inflammation / Q000139:chemically induced; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000382:microbiology*; D015054:Zymosan
D009599:Nitroprusside; D009569:Nitric Oxide; D015054:Zymosan; D019331:NG-Nitroarginine Methyl Ester