Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats

Simas, Rafael; Ferreira, Sueli Gomes; Menegat, Laura; Zanoni, Fernando Luiz; Correia, Cristiano de Jesus; Silva, Isaac A.; Sannomiya, Paulina; Moreira, Luíz Felipe Pinho

doi:10.6061/clinics/2015(06)11

Cited by 10 publications

(4 citation statements)

References 36 publications

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“…Regarding lung intravital microscopic data, Ivanov and co-workers describe that the alveolus is a spherical body surrounded by a microvascular network. (7) On the other hand, Sack et al (2) showed that pulmonary microcirculation exhibits a significant number of no-reflow areas with extremely reduced red blood cell velocities after lung transplantation in pigs, situation that was probably triggered by the ischemia-reperfusion injury. The analogous observation regarding the lung microcirculation documented in the current study after BD induction indicates another cause to this phenomenon and reinforces the relevance of microvascular injury since the donor management.…”

Section: Discussionmentioning

confidence: 99%

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Brain death effects on lung microvasculature in an experimental model of lung donor

Simas¹,

Zanoni²,

Silva³

et al. 2020

J Bras Pneumol.

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Objective: Brain death (BD) triggers important hemodynamic and inflammatory alterations, compromising the viability of organs suitable for transplantation. To better understand the microcirculatory alterations in donor lungs caused by BD. The present study investigated the pulmonary microcirculation in a rodent model of BD via intravital microscopy. Methods: Male Wistar rats were anaesthetized and mechanically ventilated. They were trepanned and BD was induced through the increase in intracranial pressure. As control group, sham-operated (SH) rats were trepanned only. In both groups, expiratory O 2 and CO 2 were monitored and after three hours, a thoracotomy was performed, and a window was created to observe the lung surface using an epi-fluorescence intravital microscopy. Lung expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) was evaluated by immunohistochemistry, and cytokines were measured in lung samples. Results: Three hours after the surgical procedures, pulmonary perfusion was 73% in the SH group. On the other hand, BD animals showed an important decrease in organ perfusion to 28% (p = 0.036). Lung microcirculatory compromise after BD induction was associated with an augmentation of the number of leukocytes recruited to lung tissue, and with a reduction in eNOS expression and an increase in ICAM-1 expression on lung endothelial cells. BD rats showed higher values of expiratory O 2 and lower values of CO 2 in comparison with SH animals after three hours of monitoring. Conclusion: Data presented showed that BD triggers an important hypoperfusion and inflammation in the lungs, compromising the donor pulmonary microcirculation.

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Section: Discussionmentioning

confidence: 99%

“…The sample size was based on similar studies previously performed by our group. (5,7) All data are presented as mean±SEM (standard error of the mean). The results between groups were compared by a non-parametric Mann-Whitney test using Graph Pad Prism software version 6.1.…”

Section: Statistical Analysesmentioning

confidence: 99%

Brain death effects on lung microvasculature in an experimental model of lung donor

Simas¹,

Zanoni²,

Silva³

et al. 2020

J Bras Pneumol.

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“…Nevertheless, sublingual microvascular blood flow is equally altered in brain dead patients, suggesting additional factors. Brain death is typically followed by hemodynamic instability and endothelial dysfunction, with or without a prior autonomic storm [ 26 , 27 ].…”

Section: Discussionmentioning

confidence: 99%

Conjunctival microcirculatory blood flow is altered but not abolished in brain dead patients: a prospective observational study

et al. 2016

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BackgroundThe conjunctival microcirculation has potential as a window to cerebral perfusion due to related blood supply, close anatomical proximity and easy accessibility for microcirculatory imaging technique, such as sidestream dark field (SDF) imaging. Our study aims to evaluate conjunctival and sublingual microcirculation in brain dead patients and to compare it with healthy volunteers in two diametrically opposed conditions: full stop versus normal arterial blood supply to the brain.MethodsIn a prospective observational study we analyzed conjunctival and sublingual microcirculation using SDF imaging in brain dead patients after reaching systemic hemodynamic targets to optimize perfusion of donor organs, and in healthy volunteers. All brain death diagnoses were confirmed by cerebral angiography. Microcirculatory images were obtained and analyzed using standardized published recommendations. Study registered at ClinicalTrials.gov, number NCT02483273.ResultsEleven brain dead patients and eleven apparently healthy controls were enrolled in the study. Microvascular flow index (MFI) of small vessels was significantly lower in brain dead patients in comparison to healthy controls in ocular conjunctiva (2.7 [2.4–2.9] vs. 3.0 [2.9–3.0], p = 0.01) and in sublingual mucosa (2.8 [2.6–2.9] vs. 3.0 [2.9–3.0], p = 0.02). Total vessel density (TVD) and perfused vessel density (PVD) of small vessels were significantly lower in brain dead patients in comparison to healthy controls in ocular conjunctiva (10.2 [6.6–14.8] vs. 18.0 [18.0–25.4] mm/mm2, p = 0.001 and 5.0 [3.5–7.3] vs. 10.9 [10.9–13.5] 1/mm, p = 0.001), but not in sublingual mucosa.ConclusionIn comparison to healthy controls brain dead patients had a significant reduction in conjunctival microvascular blood flow and density. However, the presence of conjunctival flow in case general cerebral flow is completely absent makes it impossible to use the conjunctival microcirculation as a substitute for brain flow, and further research should focus on the link between the ocular microcirculation, intracranial pressure and alternative ocular circulation.

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“…Furthermore, it remains challenging to discern whether damages to the graft are caused by brain death per se or by supportive clinical treatment of the patient. Most studies have focused on the inflammatory changes in liver grafts that are evoked by brain death, revealing that these inflammatory events are independent of the autonomic storm (4). Alternatively, the liver can be viewed as the largest "chemical works" of the body, with metabolic activity and involvement in the synthesis, decomposition and detoxification of most substances.…”

Section: Introductionmentioning

confidence: 99%

Intestinal microbiota dysbiosis and liver metabolomic changes during brain death

Wang

Tao

Guo

et al. 2022

Preprint

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Background The causative link between brain death and intestinal microbiota dysbiosis is unclear, and the distortion in liver metabolism caused by brain death requires further exploration. Material and Methods A rat model of brain death was constructed and sustained for 9 hours. Intestinal contents and portal vein plasma were collected for microbiota sequencing and microbial metabolite detection. Liver tissue was resected to investigate metabolic alterations, and the results were compared with those of a sham group. Results Microbiota dysbiosis occurred at the family and genus levels after 9 hours of brain death. Microbial metabolites remained unchanged in both the intestinal contents and portal vein plasma. Liver metabolic function deteriorated, and the levels of 80% of the differential metabolites decreased in the brain-dead rats. Most of the differential metabolites were related to energy metabolism. Conclusions Brain death resulted in microbiota dysbiosis in rats; however, this dysbiosis did not alter microbial metabolites. Deterioration in liver metabolic function during extended periods of brain death may reflect a continuous worsening in energy deficiency.

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Mesenteric hypoperfusion and inflammation induced by brain death are not affected by inhibition of the autonomic storm in rats

Cited by 10 publications

References 36 publications

Brain death effects on lung microvasculature in an experimental model of lung donor

Brain death effects on lung microvasculature in an experimental model of lung donor

Conjunctival microcirculatory blood flow is altered but not abolished in brain dead patients: a prospective observational study

Intestinal microbiota dysbiosis and liver metabolomic changes during brain death

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