Traumatic stressor could lead to a series of neuroendocrine responses, such as increased sympathetic activity and secretion of stress hormones, because of the local-pathological-changed tissues and stress response. These changes will have a huge impact on nutrient metabolism. In this article, we reviewed the researches on the change in lipid metabolism after trauma, associated factors, possible mechanisms and possible interventions.
Lipid Metabolism ; Risk Factors ; Wounds and Injuries ; metabolism

ObjectiveMechanical ventilation (MV) has long been used as a life-sustaining approach for several decades. However, researchers realized that MV not only brings benefits to patients but also cause lung injury if used improperly, which is termed as ventilator-induced lung injury (VILI). This review aimed to discuss the pathogenesis of VILI and the underlying molecular mechanisms.

Data SourcesThis review was based on articles in the PubMed database up to December 2017 using the following keywords: "ventilator-induced lung injury", "pathogenesis", "mechanism", and "biotrauma".

Study SelectionOriginal articles and reviews pertaining to mechanisms of VILI were included and reviewed.

ResultsThe pathogenesis of VILI was defined gradually, from traditional pathological mechanisms (barotrauma, volutrauma, and atelectrauma) to biotrauma. High airway pressure and transpulmonary pressure or cyclic opening and collapse of alveoli were thought to be the mechanisms of barotraumas, volutrauma, and atelectrauma. In the past two decades, accumulating evidence have addressed the importance of biotrauma during VILI, the molecular mechanism underlying biotrauma included but not limited to proinflammatory cytokines release, reactive oxygen species production, complement activation as well as mechanotransduction.

ConclusionsBarotrauma, volutrauma, atelectrauma, and biotrauma contribute to VILI, and the molecular mechanisms are being clarified gradually. More studies are warranted to figure out how to minimize lung injury induced by MV.

Animals ; Barotrauma ; metabolism ; Humans ; Reactive Oxygen Species ; metabolism ; Ventilator-Induced Lung Injury ; metabolism ; Wounds and Injuries ; metabolism

Trauma can induce a series of dynamic metabolic responses with different characteristics in three stages, including ebb phase, flow phase, and recovery phase. Nutrition support after trauma should be dynamically adjusted according to metabolic response and its individual phase, focusing on energy balance as well as metabolic modulation, adjusting immunological response to trauma by reduction of the exaggerated cytokines production, maintaining body protein balance, and enhancing wound healing.
Energy Metabolism ; Humans ; Nutritional Support ; Wound Healing ; Wounds and Injuries ; metabolism ; therapy

Animals ; Apoptosis ; Caspase 3 ; metabolism ; Male ; Myocardium ; pathology ; Rats ; Rats, Wistar ; Time Factors ; Wounds and Injuries ; physiopathology

Stress conditions such as sepsis, trauma, burn, fracture, and major surgery are associated with hypermetabolism and hypercatabolism. Protein is mobilized for energy and uptake of amino acids by muscle tissue is decreased in stress conditions. The metabolic response to stress causes movement of amino acids (predominantly alanine and glutamine) from peripheral reserves to metabolically active tissues. Glutamine is a conditionally essential amino acid during stress. Glutamine plays a role in maintenance of intestinal immune function and reinforcement of wound repair. Supplementation of parenteral glutamine (0.3~0.5 g/kg/day) as a component of nutrition support may improve clinical outcomes in appropriate patients. In patients with multiorgan failure, supplementation with a high dose of glutamine (>0.5 g/kg/day) in the acute phase of critical illness is not recommended. In stress conditions, provision of adequate protein is essential and glutamine supplementation should be considered in patients without specific contraindications.
Alanine ; Amino Acids ; Burns ; Critical Illness ; Glutamine* ; Humans ; Metabolism* ; Sepsis ; Wounds and Injuries

OBJECTIVETo observe the effects of exogenous adrenomedullin (ADM) on endogenous expression of ADM in the kidney and hypothalamus of rats early after mechanical renal trauma.

METHODSAdult Wistar rats were randomized into 4 groups (n=32), namely the control group, renal impact trauma group, preventive ADM injection group, and therapeutic ADM injection group. In the latter two groups, ADM (0.1 nmol/kg) was administrated by intraperitoneal injection 10 min before and 10 min after renal trauma. The rats were executed at 1, 6, 12, and 24 h after the trauma to examine the expression of ADM in the kidney and hypothalamus.

RESULTSIn preventive ADM injection group, the renal expression of ADM increased significantly at 1 h after the trauma (P<0.05) and tended to further increase with time till 24 h when its expression recovered the normal level. In the therapeutic ADM injection group, strong renal ADM positivity was found at 1 and 6 h after the injury (P<0.05) followed by gradual decrease till recovering the normal level at 24 h. Low renal ADM expression was detected, which was the strongest at 1 and 12 h (P<0.05) and became normal at 24 h. The time course of ADM expression in the hypothalamus was similar to that in the kidney in the therapeutic ADM injection group, and in the preventive injection group, the strongest ADM expression in the hypothalamus occurred at 6 and 24 h, and the lowest expression occurred at 12 h (P<0.05). The trauma group showed significantly decreased ADM expression in the hypothalamus compared with the control group (P<0.05).

CONCLUSIONThe hypothalamic ADM expression can upregulate renal ADM expression. ADM maintains the relative stability of the internal environment and physiological activity by local and systemic positive and negative feedback mechanisms.

Adrenomedullin ; metabolism ; pharmacology ; Animals ; Female ; Hypothalamus ; drug effects ; metabolism ; Kidney ; drug effects ; injuries ; metabolism ; Male ; Rats ; Rats, Wistar ; Wounds and Injuries ; metabolism

OBJECTIVETo explore the effect and action mechanism of moxibustion on healing of cutaneous wound in rats.

METHODSTwenty-four SD rats were selected and made into linear full-thickness skin injury model. With randomized digital table, rats were randomly divided into a treatment group and a model group, 12 cases in each one. Then according to treatment time, each group was again divided into a 1d group, a 3d group and a 7d group, 4 cases in each one. The moxibustion at injured skin was applied in the treatment group, 30 min per time, once a day. Hematoxylineosin (HE) staining method was adapted to measure growth status of capillary and number of vascular endothelial cell; immunohistochemical method was used to measure the expression of vascular endothelial growth factor (VEGF).

RESULTSThe wound healing indices in the treatment 7d group were higher than those in the model 7d group on both the 4th day and 8th day after treatment (both P < 0.05). The number of capillary in the treatment 1d group and 3d group was higher than that in the model 1 d and 3 d groups (both 1 < 0.05). The number of capillary in the treatment 7d group was lower than that in the model 7d group (P < 0.05). The number of vascular endothelial cell in the treatment 3d group was higher than that in the model 3d group (P < 0.05). The number of vascular endothelial cell in the treatment 7d group was lower than that in the model 7d group (P < 0.05). The difference of number of vascular endothelial cell between the treatment 1d group and model 1d group was not significant (P > 0.05). Positive cells accumulated score of V EGF expression in the treatment 3d group was higher than that in the model 3d group (P < 0.05). Positive cells accumulated score of VEGF expression in the treatment 7d group was lower than that in the model 7d group (P < 0.05). The difference of positive cells accumulated score of VEGF expression between the treatment 1d group and model 1d group was not significant (P > 0.05).

CONCLUSIONMoxibustion could improve the healing of skin wound in rats, which could be related with regulating vascular endothelial cell and VEGF in wound tissue at different time.

Animals ; Endothelial Cells ; metabolism ; Female ; Humans ; Male ; Moxibustion ; Rats ; Rats, Sprague-Dawley ; Skin ; injuries ; metabolism ; Vascular Endothelial Growth Factor A ; genetics ; metabolism ; Wounds and Injuries ; genetics ; metabolism ; therapy

OBJECTIVE: To investigate the expression of M3 subtype of muscarinic receptors (M3R) during the incised wound healing of the skin in mice and the characteristics of its time-dependent. METHODS: The change of M3R in skin incised wound was detected by immunohistochemical staining and Western blot. RESULTS: M3R-positive cells were detected in epidermis, hair follicle, sebaceous glands, sweat glands, dermomuscular layer in normal mouse skin. Expression of M3R was mainly detectable in polymorphonuclear cells (PMNs) in the wound specimens aged from 6h to 12h after injury. Afterwards, the M3R-positive cells were mostly mononuclear cells (MNCs) and fibroblastic cells (FBCs) at 1 d to 3d post-injury, whereas the M3R-positive cells were mostly FBCs aged from 5 d to 14d. Morphometrically, the ratio of the M3R-positive cells increased aged from 6h to 12h after injury, with a peak at 12h. The ratios kept a high relatively level aged from 1 d to 5 d, but significantly that lowered as compared with aged 12h after injury. The ratio reached the peak at 7 d again after injury, and then decreased gradually. The M3R protein also revealed a time-dependent tendency with double peaks at 12h and 7 d after injury as detected by Western blotting. CONCLUSION M3R is time-dependently expression in PMNs, MNCs and FBCs suggesting that it may play roles during the skin incised wound healing, and M3R may be used as a marker for wound age determination.
Animals ; Blotting, Western ; Fibroblasts/metabolism* ; Immunohistochemistry ; Male ; Mice ; Monocytes/metabolism* ; Neutrophils/metabolism* ; Receptor, Muscarinic M3/metabolism* ; Skin/metabolism* ; Time Factors ; Wound Healing ; Wounds and Injuries/metabolism*

In order to investigate the correlation between traumatic servity and blood cAMP and cGMP levels in the patients with acute trauma and its clinical significance, 120 cases of trauma were randomly selected and divided into 4 groups (n = 30 in each group): mildly traumatic group (ISS < or = 9), moderately traumatic group (ISS = 10-16), severely traumatic group (ISS = 17-25) and dangerously traumatic group (> 25). The cAMP and cGMP levels were assayed in sera, leucocytes and platelets respectively in 6 h and 24 h after trauma. The results showed that cAMP and cGMP levels were elevated significantly in sera and platelets (P < 0.05 or P < 0.01), meanwhile cGMP levels in leucocytes (P < 0.05). It was concluded that cAMP and cGMP might play an important role in traumatic stress, participate in the cellular signal transducation and promote the immune function of leucocytes and the coagulation founction of platelets. Serum cAMP and cGMP levels were upregulated correspondingly as ISS increased, and positively correlated to the traumatic severity.
Blood Platelets/metabolism ; Cyclic AMP/*blood ; Cyclic GMP/*blood ; *Injury Severity Score ; Leukocytes/metabolism ; Wounds and Injuries/*blood

OBJECTIVE: To explore the effect of nitric oxide (NO) on the gene expression of hepatic TNF-α and IL-1β by crush injury of rat's soft tissues. METHODS: Rats were randomly divided into sham group, crush group, crush+aminoguanidine (AG) group, and crush+L-arginine (L-Arg) group. Activities of ALT and AST as well as NO level in serum were measured. Gene expressions of TNF-α and IL-1β were detected with RT-PCR. RESULTS: Obvious increase in TNF-α and IL-1β mRNA expression was detected in the crush group compared with the sham group (P<0.05). After pretreated L-Arg, expressions of TNF-α and IL-1β mRNA were markedly increased (P<0.05). After pretreated AG, those indices obviously decreased (P<0.05). Activities of ALT and AST enhanced and NO level increased in the crush group compared with the sham group (P<0.05). Pretreatment with L-Arg or AG led to substantial increased or reduced activities of ALT and AST as well as NO levels, respectively. CONCLUSION Endogenous NO mediated TNF-α, IL-1β mRNA up expression in liver induced by increased production of NO after crush injury of rat's soft tissues.
Animals ; Gene Expression ; Interleukin-1beta/metabolism* ; Liver ; Nitric Oxide/physiology* ; RNA, Messenger ; Rats ; Tumor Necrosis Factor-alpha/metabolism* ; Wounds and Injuries