ObjectiveTransfusion-Related Acute Lung Injury （TRALI） is a common fatal transfusion adverse reaction. Major Histocompatibility Complex （MHC） class I is an important factor involved in the pathogenesis of TRALI； however， the role of complement in itspathogenesis has not been fully elucidated. This study aims to explore the role of complement in MHC class I antibody-mediated TRALI， so as to provide a theoretical basis for clinical prevention and treatment. MethodsThis study established a murine model of transfusion-related acute lung injury （TRALI） based on the "two-hit" theory， with lipopolysaccharide （LPS） as the first hit and MHC class I antibody as the second hit. Male Balb/c mice were randomly divided into seven groups （n=5 per group per experiment）： Naive （blank control）， LPS （first hit only）， Isotype （isotype antibody control）， TRALI （model group）， C5aR1 inhi （C5aR1 antagonist intervention）， C5aR2 inhi （C5aR2 antagonist intervention）， and Anti-C5 （anti-complement C5 antibody intervention）. Rectal temperature was monitored after MHC class I antibody injection. After sample collection， the severity of pulmonary edema was assessed by measuring the lung wet-to-dry weight ratio， histological analysis， and immunohistochemistry. Serum and bronchoalveolar lavage fluid were collected to measure cytokine and complement levels. ResultsMice in the TRALI group exhibited a significant decrease in rectal temperature， an increased lung wet-to-dry weight ratio， elevated serum cytokine levels， and markedly heightened complement C5a levels in bronchoalveolar lavage fluid （P＜0.000 1）. Histopathological examination revealed substantial infiltration of inflammatory cells， predominantly neutrophils accompanied by fewer lymphocytes， plasma cells， and monocytes， along with increased deposition of the membrane attack complex C5b-9 in lung tissues. In contrast， mice treated with anti-C5 antibody demonstrated no significant decrease in rectal temperature. The lung wet-to-dry weight ratio in this group showed no statistical difference compared to either the Naive or Isotype control groups （P＞0.05）. Furthermore， these mice displayed reduced serum cytokine levels， a significant attenuation of inflammatory cell infiltration in the lungs， and a 100% survival rate at the 2-hour time point. However， mice administered either the C5aR1 antagonist or the C5aR2 antagonist failed to be protected and subsequently developed TRALI. ConclusionComplement activation， which forms the membrane attack complex C5b-9， plays a critical role in MHC class I antibody-mediated TRALI. Blocking complement C5 activation can effectively prevent the occurrence of TRALI.

OBJECTIVETo explore the diagnostic value of MRI and SPECT in early postburn brain edema in severely burned dogs.

METHODSTwenty-six mongrel dogs were randomized into control (n = 6) and burned groups in which every 5 dogs were allotted to each of following time points: 6, 12, 18 and 24 postburn hours (PBHs). The dogs in burn groups were inflicted with 50% TBSA of III degree skin burn and were infused with 5% glucose solution after 6 PBHs, so that severe early postburn brain edema was produced. MRI and SPECT were employed to observe dynamically the brain of dogs in all groups. The results were collected and compared with one another.

RESULTSThe results indicated that with MRI brain morphological change of early brain edema could be shown as early as within 12 PBH and diffuse brain edema became more obvious with elapse of time. The changes might be difficult to be found by MRI when T(1)WISIR decreased below 10%. T(2)WI SIR increased by 8.29% at 24 PBH with blurred demarcation between the brain gray and white matters. There was diffused and progressive nuclide ((99)TCm-ECD) concentration in the brain tissue as shown by SPECT at 6 PBH. The radio-nuclide taking ratio increased significantly after 12 PBH, especially at 24 PBH (P < 0.01) when compared with that before burn.

CONCLUSIONCombined application of MRI and SPECT could evidently increase sensitivity and specificity in the diagnosis of early postburn brain edema.

Animals ; Brain Edema ; diagnosis ; diagnostic imaging ; Burns ; complications ; Dogs ; Magnetic Resonance Imaging ; Male ; Tomography, Emission-Computed, Single-Photon

Objective: To investigate the correlation between MRI features and pathology in brain edema at the early stage of severe burn (50％ TBSA Ⅲ degree) in dogs.Methods: Fifty-two dogs were randomized into control, simple burn (SB), burn plus sodium lactate (BSL), and burn plus glucose solution groups (BGS). The manifestation of the brain of control group was compared with that of burn groups at 6, 12, 18 and 24 hours postburn with MRI and pathological examination (gross appearance, electron microscopy and light microscopy).Results: The earliest findings of brain edema were seen at 12 hours after burn in BGS group, in which brain swelling was the main feature of MRI. The decrease of SIR on T1WI was not observed until it was exceeded 10％.Signal of T2WI increased by 8.29％ at 24 hours after burn.It was difficult to distinguish the gray matter from the white matter at the boundary line, which became blurred later. Histological changes of brain edema were observed as early as 6 hours after burn, being accompanied by swelling of endothelial cells and peri-vescular astrocytes, and vacuolation took place in neurons at 12 hours after burn, with different degrees of necrosis of capillary endothelimn,neurons, and axons. These changes became more marked with elapse of time. The BGS group showed the most obvious changes mentioned above at 24 hours after burn.Conclusions: The model of the brain edema after severe burn has the feature of both vasogenic edema and cytotoxic edema on the MRI and pathology. Positive MRI findings lagged behind that of the pathomorphological changes.