Mesenteric lymph duct ligation prevents shock-induced RBC deformability and shape changes

Zaets, Sergey B.; Berezina, Tamara L.; Caruso, Joseph M.; Xu, Dakang; Deitch, Edwin A.; Machiedo, George W.

doi:10.1016/s0022-4804(02)00024-0

Cited by 35 publications

(26 citation statements)

References 21 publications

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“…In published and unpublished rodent studies, similar relationships were found between T/HS lymph and bone marrow failure (31) as well as RBC dysfunction (32). However, because of the potential limitations of extrapolating rodent studies to the clinical arena, the gut lymph hypothesis of lung injury was tested in a non-human primate baboon model (33).…”

Section: The Gut Lymph Hypothesis Of Acute T/hsinduced Lung Injury Fumentioning

confidence: 77%

Gut lymph hypothesis of early shock and trauma-induced multiple organ dysfunction syndrome: A new look at gut origin sepsis

Deitch

2006

Journal of Organ Dysfunction

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Trauma is the leading cause of death in people agedB/40 years and multiple organ dysfunction syndrome (MODS) is the leading cause of death in intensive care units. Consequently, understanding the mechanisms by which trauma/hemorrhagic shock (T/HS) leads to acute (non-infectious) MODS is of major health importance in the USA. One of the major hypotheses being studied to explain the development of sepsis and MODS after trauma is the gut hypothesis of MODS. Additionally, there is recent experimental and clinical information that the response to injury and sepsis may differ between males and females. Thus, the overall global hypothesis of this review is that T/HS-induced early distant organ injury and cellular dysfunction is secondary to gut injury and is primarily mediated by factors exiting the gut via the mesenteric lymphatics. A secondary major hypothesis which will be presented is that gender and sex hormones modulate gut and hence distant organ and cellular dysfunction after T/HS. These hypotheses are supported by our studies indicating that T/HSinduced lung injury and endothelial cell activation/dysfunction, neutrophil activation, red blood cell dysfunction and bone marrow failure in male rats are mediated primarily by factors exiting the gut in the mesenteric lymph. Additionally, our studies show that proestrus female rats are resistant to these T/HS-induced injuries. Based on these results supporting the gut lymph hypothesis of systemic inflammatory response syndrome and MODS, and studies showing that female rats are more resistant to T/HS than male rats, the effects of gut-derived factors in lymph, as well as the effects of gender and sex hormones on cellular and organ dysfunction after T/HS, appear to be fruitful areas for further investigation.

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Section: The Gut Lymph Hypothesis Of Acute T/hsinduced Lung Injury Fumentioning

confidence: 77%

Gut lymph hypothesis of early shock and trauma-induced multiple organ dysfunction syndrome: A new look at gut origin sepsis

Deitch

2006

Journal of Organ Dysfunction

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“…Based on our recent work in male rats, it appears that, after an episode of splanchnic ischemia, gut-derived factors are critical for the development of shock-induced distant organ and cellular dysfunction (2,6,16,27,41,43). However, some human (8,23,32,37) and animal (4, 5) studies suggest that females may tolerate sepsis and shock better than males, and recent animal work suggests that the reduction in shockinduced acute lung injury is the result of the relative resistance of the female rat to T/HS-induced gut injury (1,9).…”

Section: Discussionmentioning

confidence: 99%

The female intestine is more resistant than the male intestine to gut injury and inflammation when subjected to conditions associated with shock states

Homma¹,

Hoy²,

Xu³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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108

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. The female intestine is more resistant than the male intestine to gut injury and inflammation when subjected to conditions associated with shock states. Am J Physiol Gastrointest Liver Physiol 288: G466 -G472, 2005. First published October 21, 2004; doi:10.1152/ajpgi.00036.2004.-Having documented that proestrus female rats are more resistant to shock-induced acute gut and hence lung injury than male rats, we tested the hypothesis that the female gut is more resistant to injury and produces less of an inflammatory response than the male gut when exposed to conditions associated with shock states (hypoxia and acidosis) utilizing the ex vivo Ussing chamber system. Ileal mucosal membranes harvested from normal male and female rats mounted in Ussing chamber systems were exposed to normoxia or 40 min of hypoxia at a normal pH (pH 7.3) or acidosis (pH 6.8). Cytokine and nitric oxide levels in the serosal compartment of the Ussing chamber were measured at the end of the 3-h experimental period to assess the immunoinflammatory response, whereas FITC-dextran (mol wt 4,300) was employed to assess barrier function. Histomorphological changes were used to quantitate gut mucosal injury. Hypoxia, acidosis, or hypoxia plus acidosis was associated with a significant increase in proinflammatory cytokine production [interleukin (IL)-6, tumor necrosis factor, and macrophage inflammatory protein (MIP)-2] by the male compared with the female intestinal segments. In contrast, the female gut manifested a higher anti-inflammatory response (nitric oxide and IL-10) and improved intestinal barrier function as well as less evidence of mucosal injury than the male intestinal segments. Administration of estradiol or the testosterone receptor antagonist, flutamide, to male rats abrogated the increase in gut injury and the increased IL-6 and MIP-2 response observed after hypoxia plus acidosis. These results suggest that gender differences in the ex vivo intestinal response to stresses, such as hypoxia and acidosis, exist and that the administration of estradiol or blockade of the testosterone receptor to male rats mitigates these gender differences.Ussing chamber; gender; ileal membrane; hypoxia/low pH; nitric oxide ALTHOUGH MULTIPLE ORGAN DYSFUNCTION syndrome (MODS) is the leading cause of death in intensive care units today (14), effective therapies have been slow to be developed, at least in part, because of an incomplete understanding of its basic biology (14). Consequently, studies directed at elucidating the pathophysiology of MODS have assumed major clinical importance. Over the years, we and others have focused on the role of gut ischemia/injury as a factor in the subsequent development of MODS (7, 13). Most recently, these studies have documented that, after trauma-hemorrhagic shock (T/ HS), the gut becomes a cytokine-generating organ (17) and that factors exiting the gut via the mesenteric lymphatics contribute to lung injury, endothelial cell dysfunction, and neutrophil activation (2, 14 -16, 19, 41). Although these studies illust...

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“…However, rats in Group 4 acquired endotoxin tolerance despite the apparent absence of portal endotoxins due to luminal sterilization by antibiotics. The route of bacterial and/or microbial translocation is considered to derive not only from portal venous circulation but also from intestinal lymphatic systems [17,18]. Because we did not evaluate the level of endotoxin in mesenteric lymph node or fluid, we cannot exclude the role of luminal endotoxin in the acquisition of LPS-tolerance via the lymphatic systems.…”

Section: Discussionmentioning

confidence: 99%

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

Unno

Uchiyama

Yamamoto

et al. 2006

Journal of Surgical Research

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Mesenteric lymph duct ligation prevents shock-induced RBC deformability and shape changes

Cited by 35 publications

References 21 publications

Gut lymph hypothesis of early shock and trauma-induced multiple organ dysfunction syndrome: A new look at gut origin sepsis

Gut lymph hypothesis of early shock and trauma-induced multiple organ dysfunction syndrome: A new look at gut origin sepsis

The female intestine is more resistant than the male intestine to gut injury and inflammation when subjected to conditions associated with shock states

Portal Triad Occlusion Induces Endotoxin Tolerance: Role of Portal Congestion

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