Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction

Sambol, Justin T.; Lee, Marlon A.; Caputo, Francis J.; Kawai, Kentaro; Badami, Chirag D.; Kawai, Tomoko; Deitch, Edwin A.; Yatani, Atsuko

doi:10.1152/japplphysiol.90937.2008

Cited by 39 publications

(25 citation statements)

References 41 publications

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“…Barlos et al [16] observed intestinal ischemia after trauma-hemorrhagic shock (T/HS) results in gut barrier dysfunction and the production/release of biologically active and tissue injurious factors in the mesenteric lymph, which in turn, causes acute lung injury and a systemic inflammatory state. Acute T/HS-induced myocardial dysfunction is likely because of gut-derived factors present in the mesenteric lymph [17]. Furthermore, in an animal model of T/HS, the TNF-a, IL-6, and MIP-2 levels were significantly elevated compared with sham-injured mice [18].…”

Section: Discussionmentioning

confidence: 95%

Omega-3 polyunsaturated fatty acids inhibit the increase in cytokines and chemotactic factors induced in vitro by lymph fluid from an intestinal ischemia-reperfusion injury model

Zhang¹,

He²,

Wang³

et al. 2015

Nutrition

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Section: Discussionmentioning

confidence: 95%

Omega-3 polyunsaturated fatty acids inhibit the increase in cytokines and chemotactic factors induced in vitro by lymph fluid from an intestinal ischemia-reperfusion injury model

Zhang¹,

He²,

Wang³

et al. 2015

Nutrition

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“…In 1998, Magnotti et al had confirmed that mesenteric lymph carried gut-derived mediators of endothelial permeability and lung injury following hemorrhagic shock (12). Post-shock mesenteric lymph (PSML) was subsequently shown to be a bioactive body fluid capable of inciting remote organ dysfunction in the lung (11), kidney (13), and heart (14, 15). Further, mesenteric lymph serves to prime quiescent neutrophils for enhanced respiratory burst (16) potentially via mechanisms related to the release of inflammatory lipid mediators such as phospholipase A2 and 5-lipoxygenase products (13, 17).…”

Section: Discussionmentioning

confidence: 99%

A “Clean Case” of Systemic Injury

Slaughter¹,

Kotter

Moore

et al. 2015

Shock

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Post-injury multiple organ failure results from an inappropriate, overwhelming immune response to injury. During trauma and hemorrhagic shock (T/HS), mesenteric ischemia causes gut mucosal breakdown with disruption of the intestinal barrier. It has been proposed that this releases the gut microbiota systemically via post-shock mesenteric lymph, engendering infectious complications. Despite extensive investigation, no clear evidence has been presented for gut bacterial translocation after resuscitation from T/HS. However, such previous studies were limited by available technologies. More sensitive methods, such as quantitative polymerase chain reaction (PCR), have since emerged for detection of bacterial presence and danger-associated molecular patterns (DAMPs). Quantitative PCR was applied to post-shock mesenteric lymph (PSML) derived from a rat model of T/HS. No bacterial presence was detected in a series of 12 samples, whereas multiple lymph samples showed presence of DAMPs after T/HS. Thus, we confirmed that bacterial translocation does not exist in PSML following resuscitation from T/HS-associated mesenteric ischemia. However, T/HS does increase the presence of mitochondrial DAMPs in PSML. These results support our current position that PSML elaborates remote organ injury by multiple inflammatory mechanisms, including lipid-mediated pro-inflammatory stimuli, and by contribution from gut-derived DAMPS.

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“…The report form Sambol et al 8 found that MLDL could prevent trauma/ hemorrhage shock-induced increases in LVDP and ±dP/dt max of isolated hearts form trauma/hemorrhage shocked rats. In the present study, we found that PSML drainage also could increase the LVSP and ±dP/dt max , which was consistent with the role of MLDL on cardiac function.…”

Section: Discussionmentioning

confidence: 96%

“…After a 15-min stabilization period, these indices of isolated heart function, including the left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), heart rate (HR), and the maximum rates of left ventricular developed pressure (LVDP) rise (+dP/dt max ) and fall (-dP/dt max ), were assessed by measuring the intraventricular pressure with a fluidfilled balloon (polyethylene film) that had been inserted into the left ventricle via the mitral valve from the left atrium as previously described 8,9,11 . This balloon was connected to a pressure transducer (ADInstruments), LVDP was calculated as the difference between the peak LVSP and LVEDP.…”

Section: Measurement Of Cardiac Function Of Isolated Heart From Hemormentioning

confidence: 99%

“…Our previous studies showed that blockage of PSML return by mesenteric lymph duct ligation (MLDL) could alleviate the myocardium injury in rats following hemorrhagic shock with fluid resuscitation, and its mechanism was related to decreasing free radical injury and inflammation 7 . Recently, Sambol et al 8 found that the MLDL could prevent hemorrhagic shock-induced cardiac contractile dysfunction, and PSML intravenous infusion into naïve rats induced myocardial contractile dysfunction 9 . Thus, the current study further tests the hypothesis that PSML is involved in cardiac dysfunction after hemorrhagic shock.…”

Section: Introductionmentioning

confidence: 99%

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Post-hemorrhagic shock mesenteric lymph is an important contributor to cardiac dysfunction following hemorrhagic shock

Si-hai

Zhao

et al. 2015

Acta Cir. Bras.

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PURPOSE:To evaluate whether post-hemorrhagic shock mesenteric lymph (PSML) is involved in cardiac dysfunction induced by hemorrhagic shock. METHODS:The hemorrhagic shock model (40±2 mmHg, 3h) was established in rats of the shock and shock+drainage groups; and PSML drainage was performed from hypotension 1-3h in the shock+drainage rats. Then, the isolated hearts were obtained from the rats for the examination of cardiac function with Langendorff system. Subsequently, the isolated hearts were obtained from normal rats and perfused with PSML or Krebs-Henseleit solution, and the changes of cardiac function were observed. RESULTS:The left ventricular systolic pressure (LVSP) and the maximal rates of LV developed pressure (LVDP) rise and fall (±dP/ dt max ) in the shock and shock+drainage groups were lower than that of the sham group; otherwise, these indices in the shock+drainage group were higher compared to the shock group. In addition, after isolated hearts obtained from normal rats perfusing with PSML, these cardiac function indices were gradual decline along with the extension of time, such as heart rate, LVSP, ±dP/dt max , etc. CONCLUSION:Post-hemorrhagic shock mesenteric lymph is an important contributor to cardiac dysfunction following hemorrhagic shock.

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Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction

Abstract: Deitch EA, Yatani A. Mesenteric lymph duct ligation prevents trauma/hemorrhage shock-induced cardiac contractile dysfunction.

Cited by 39 publications

References 41 publications

Omega-3 polyunsaturated fatty acids inhibit the increase in cytokines and chemotactic factors induced in vitro by lymph fluid from an intestinal ischemia-reperfusion injury model

Omega-3 polyunsaturated fatty acids inhibit the increase in cytokines and chemotactic factors induced in vitro by lymph fluid from an intestinal ischemia-reperfusion injury model

A “Clean Case” of Systemic Injury

Post-hemorrhagic shock mesenteric lymph is an important contributor to cardiac dysfunction following hemorrhagic shock

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