Mesenteric Lymphatic Ducts Ligation Decreases the Degree of Gut-Induced Lung Injury in a Portal Vein Occlusion and Reperfusion Canine Model

Intra-Abdominal Hypertension Causes Bacterial Growth in Lungs: An Animal Study

“…This was reported with the presence of an IAP of 10 mmHg [11]. In our study the mean IAP at rats was 13.8 mmHg and bacterial translocation may be suggested by the detection of several bacteria (i.e., E. coli , Enterococcus faecalis , Pseudomonas aeruginosa , and Peptostreptococcus ) in regional mesenteric lymph nodes but also in regional and distal organs such as the lungs of the animals.…”

“…However, it is clear that bacterial translocation may occur after a period of splanchnic ischemia in the setting of IAH. Liu et al [11] used a rodent model to examine the effect of raised IAP on ileal mucosal blood flow and on bacterial translocation. An increased IAP of 25 mmHg for 60 minutes resulted in significantly decreased mucosal blood flow (−63% from baseline) in rodents despite the maintenance of normal mean arterial blood pressure.…”

“…Moreover, in order to classify histologic results of animals' lungs we used a classification of severity of lung infection based on the classical description of pneumonia stages [11] where + means normal, ++ means congestion, +++ means consolidation, ++++ means grey hepatization, and +++++ means resolution.…”

Beta-1 blocker improves survival of septic rats through preservation of gut barrier function

“…Other investigators have shown that stimulation of gut motor function by administration of b-adrenergic blocker prevented overgrowth of intestinal bacteria and subsequent bacterial translocation [12]. It remains unclear, however, if either stimulation or inhibition of b-adrenergic activity may modulate gut barrier function and subsequent bacterial translocation [13,14]. Therefore, in the present study, we examined the effects of selective b1-blocker on survival of septic hosts, and simultaneously assessed the local (intraperitoneal) and systemic (into the bloodstream) release of inflammatory cytokines such as tumor necrosis factor-a (TNF-a), interleukin-1b (IL-1b), and high-mobility group box-1 (HMGB-1), with a focus on gut mucosal integrity and bacterial translocation into the mesenteric lymph nodes (MLNs).…”

Severe Acute Pancreatitis: Gut Barrier Failure, Systemic Inflammatory Response, Acute Lung Injury, and the Role of the Mesenteric Lymph

“…It thus was hypothesized that MODS in critical illness was not attributable primarily to the translocation of bacteria/endotoxins but rather to endogenous toxic factors produced by GALT in response to intestinal ischemia and disseminated into the mesenteric lymph. The beneficial effects of interruption of mesenteric lymph flow on the development of lung injury in critical illness of different etiologies have now been demonstrated in several animal models [45][46][47][48][49][50].…”