Brain death causes structural and inflammatory changes in donor intestine

Koudstaal, Lyan G.; Hart, Tony; Berg, van den Anke; Olinga, Peter; Goor, van Harry; Ploeg, Rutger J.; Leuvenink, Henri G. D.

doi:10.1016/j.transproceed.2004.12.258

Cited by 27 publications

(12 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The morphologic integrity of the small bowel graft is paramount to preventing bacterial translocation and subsequent infectious complications of the recipients. Koudstaal et al 14,15 found that intestinal mucosal injury was clearly present 1-hour after brain death in rats compared to controls. Nevertheless, we found no significant change in small bowel tissue pathology observed 4 hours after hypotensive brain death, and that the reversible damage increased gradually 4 to 12 hours after hypotensive brain death.…”

Section: ■ Discussionmentioning

confidence: 99%

Characterization of the intestinal graft in a swine hypotensive after brain death model

Li¹,

Gao

Chen

et al. 2019

Acta Cir. Bras.

View full text Add to dashboard Cite

To establish a hypotensive brain death pig model and observe the effects of hypotension on small bowel donors. Methods: The hypotensive brain death model was produced using the modified intracranial water sac inflation method in ten domestic crossbred pigs. Effects of hypotensive brain death on small bowel tissue morphology were evaluated through changes in intestinal tissue pathology, tight junction protein of the intestinal mucosa and plasma intestinal fatty acid-binding protein (i-FABP) levels. The pathophysiological mechanism was examined based on changes in superior mesenteric artery (SMA) blood flow and systemic hemodynamics. Results: After model establishment, SMA blood flow, and the mean arterial pressure (MAP) significantly decreased, while heart rate increased rapidly and fluctuated significantly. Small bowel tissue morphology and levels of tight junction protein of the intestinal mucosa showed that after model establishment, small bowel tissue injury was gradually aggravated over time (P<0.05). Plasma i-FABP levels significantly increased after brain death (P<0.05). Conclusions: A hypotensive brain death pig model was successfully established using an improved intracranial water sac inflation method. This method offers a possibility of describing the injury mechanisms more clearly during and after brain death.

show abstract

Section: ■ Discussionmentioning

confidence: 99%

Characterization of the intestinal graft in a swine hypotensive after brain death model

Li¹,

Gao

Chen

et al. 2019

Acta Cir. Bras.

View full text Add to dashboard Cite

show abstract

“…El corazón y los demás órganos de los fallecidos en ME frecuentemente tienen cambios inflamatorios secundarios a una combinación de los fenómenos de isquemia-reperfusión y del medio inflamatorio que se produce en el seno de la muerte encefálica. La activación del sistema inmunitario aumenta la inmunogenicidad de los órganos, y puede causar un aumento en la incidencia de rechazo precoz, así como afectar negativamente a la supervivencia a medio y largo plazo del órgano trasplantado [32][33][34][35][36][37] .…”

Section: Discussionunclassified

Modulación hormonal del donante de órganos. Utilidad de los esteroides

Michelena¹,

Chamorro

Falcón

et al. 2009

Medicina Intensiva

View full text Add to dashboard Cite

Recently, the work group made up of the National Transplant Organization (Organización Nacional de Trasplantes, ONT), Spanish Society of Intensive, Critical Medicine and Coronary Units (Sociedad Española de Medicina Intensiva, Crítica y de Unidades Coronarias, SEMICYUC) and other Scientific Societies have recommended using 15 mg/kg of methyl prednisolone during the management of lung donors after brain death. This recommendation is based on descriptive and retrospective studies. However, the review of different experimental and clinical studies also suggests a potential benefit of using steroids in either thoracic or abdominal organ donors during management strategies. In brain death management, early steroid administration may decrease cytokine production and also may prevent alterations induced by proinflammatoy mediators, stabilize cell membranes, reduce expression of cell surface adhesion molecules and avoid lipid peroxidation after the ischemic period. This could be beneficial in increasing number and quality of organs harvested and in decreasing rejection episodes after transplant. It would be very recommendable to carry out prospective and comparative studies to demonstrate these potential utilities. Meanwhile and knowing the deleterious effects of inflammatory activity arising during and after brain death, we recommend using 15 mg/kg of methyl prednisolone in the organ donor management, as soon as possible. The potential benefit of its immunomodulation effects, its low cost and the absence of major side effects can justify this recommendation.

show abstract

“…Additionally, the existence of a loop of CCL2 secretion, involving the IL‐6/IL‐6Ralpha/gp130 complex (52), suggests that ischemia may be a major trigger of CCL2 secretion (53). However, since brain death also promotes the release of hormones and other inflammatory mediators, what triggers increased CCL2 production is still unknown (19,54–59).…”

Section: Discussionmentioning

confidence: 99%

High Levels of Donor CCL2/MCP-1 Predict Graft-Related Complications and Poor Graft Survival After Kidney-Pancreas Transplantation

Ogliari

Caldara

Socci

et al. 2008

American Journal of Transplantation

View full text Add to dashboard Cite

In this study we analyzed the role of CCL2, a member of the chemokine family, in early graft damage. Using simultaneous kidney-pancreas transplantation (SPK) as a model, we showed that brain death significantly increases circulating CCL2 levels in humans. We found that in such situations, high donor CCL2 levels (measured before organ recovery and at the onset of cold preservation) correlate with increased postreperfusion release of CCL2 by both the graft and recipient throughout the week following transplantation (n = 28). In a retrospective study of 77 SPK recipients, we found a significant negative association between high donor levels of CCL2 and graft survival. Decreased survival in these patients is related to early posttransplant complications, including a higher incidence of pancreas thrombosis and delayed kidney function. Taken together our data indicate that high CCL2 levels in the donor serum predict both an increase in graft/recipient CCL2 production and poor graft survival. This suggests that the severity of the inflammatory response induced by brain death influences the posttransplant inflammatory response, independent of subsequent ischemia and reperfusion.

show abstract

Brain death causes structural and inflammatory changes in donor intestine

Cited by 27 publications

References 4 publications

Characterization of the intestinal graft in a swine hypotensive after brain death model

Characterization of the intestinal graft in a swine hypotensive after brain death model

Modulación hormonal del donante de órganos. Utilidad de los esteroides

High Levels of Donor CCL2/MCP-1 Predict Graft-Related Complications and Poor Graft Survival After Kidney-Pancreas Transplantation

Contact Info

Product

Resources

About