Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is the primary cause of mortality in sepsis, with its core pathophysiological mechanism being severe ischemia and hypoxia in critical units—composed of microcirculation and the mitochondria of functional cells—resulting from disruptions in blood flow and oxygen flow following a dysregulated host response. Due to the systemically convergent yet clinically heterogeneous nature of the host response, current understanding and management strategies for hemodynamics remain inconsistent, often leading to inadequate resuscitation or overtreatment. To improve the quality of care, based on a systematic review of the "blood flow-oxygen flow" theory, an expert panel emphasizes reevaluating septic shock from an integrated perspective of blood flow and oxygen flow, and has formulated the Expert Consensus on Blood Flow and Oxygen Delivery Phenotyping and Clinical Management of Septic Shock (2025). The consensus proposes that clinical typing of blood flow-oxygen flow should comprehensively consider cardiac function, vascular tone, oxygen flow utilization status in critical units, and disease trajectory, while optimizing subtype identification by integrating host response phenotypes and artificial intelligence technologies. It advocates establishing a continuous assessment system through multi-site oxygen flow monitoring for organ perfusion, peripheral perfusion monitoring, and critical care ultrasound. Under the framework of the "critical care triangle", the consensus promotes the implementation of individualized, bundled management strategies, providing guidance for multiple management points to restore blood flow-oxygen flow matching, reduce the risk of organ failure, and decrease patient mortality.

Objective To investigate the feasibility of inducing rat bone marrow mesenchymal stem cells ( BMSCs ) into myocardial cells by angiotensin II ( Ang II ) and the approach of applying the induced BMSCs to construct myocardial tissue in vitro. Methods BMSCs from rats were isolated and cultured. The third generation of BMSCs were incubated in complete culture medium, in which 0.1 μmol/L Ang II was added, for 24 h. The BMSCs were switched to complete medium and cultured. The control group was cultured by complete medium without Ang II . The protein cTnT and β-MHC were tested by immunofluorescence staining and the structure of induced cells was observed by transmission electron microscopy. The bovine pericardiums were managed by the detergent-enzyme digestion method. The induced BMSCs were planted onto the acellular bovine pericardium and cultured for 3 d before being tested. Results The cells of induced group were induced into cardiomyocytes by Ang II, which could express cTnT andβ-MHC, while cells in the control group couldn't. The result of electron microscopy showed that desmosome could be observed in the induction group. The surface of acellular bovine pericardiums was detected by scanning electron microscopy and no cells remaining on the surface except 2 μm-aperture were observed in the acellular bovine pericardiums. The induced BMSCs adhered to acellular bovine pericardium and grew well. Conclusions BMSCs can be induced into cardiomyocyte in vitro and express cTnT and β-MHC. The cells can adhere well on the surface and the inside of acellular bovine pericardium. BMSCs have the potential to form engineered cardiac muscle tissue with blood vessel.

BACKGROUND: Preliminary study has proved that the bone marrow-derived mesenchymal stem cells (MSCs) in a rat emphysema model produced by use of trypsin alone can "homing" to the lesioned lung tissues, and participate in the formation of pulmonary arteries to promote lung tissue repair. Basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) play equally a powerful role in promoting angiogenesis. OBJECTIVE: To observe the influence of bFGF, VEGF and MSCs in regeneration of pulmonary capillary and pathological repair of pulmonary emphysema rats. METHODS: Except normal control group, the remaining 5 groups of rats were exposed to tobacco smoke and received a single intratracheally instillation of porcine pancreatic elastase to induce emphysema models. Following successful modeling, rats of bFGF group were intratracheally injected with 400 U bFGF and rats of VEGF group with 2 μg VEGF, once a week for three times. MSCs group was injected 1 mL suspension of 4×10~9/L MSCs into tail vein. MSCs+VEGF group was injected MSCs into tail vein and intratracheally injected VEGF (2 ug, three times) at the same time. Model control and normal control groups were intratracheally injected with equal volume of sodium chloride. Four weeks after treatment, arterial blood gas analysis was performed to observe pathological and morphological changes of lung tissues. CD34~+ expression in lung tissues was determined using immunohistochemistry method. RESULTS AND CONCLUSION: Compared with model control group, PaO_2 values dramatically increased in VEGF group (P <0.05), while other indices remained unchanged (P > 0.05); there were no obvious changes in each index in other groups (P >0.05). Gross and microscopic observations showed that, lung was smooth, pale pink, and elastic in normal control group, with uniform size of pulmonary alveoli on cross-section; pathological changes of chronic obstructive pulmonary emphysema existed in model control group, but improved in other 4 groups. Compared with model control group, mean pulmonary alveoli number and CD34~+ relative positive area dramatically increased in bFGF, VEGF, MSCs, MSCs+VEGF groups (P < 0.05), mean linear intercept and mean alveoli area were significantly reduced (P < 0.05). No significant difference was observed in each index among these 4 groups (P > 0.05). bFGF, VEGF and MSCs could improved the pathology of pulmonary emphysema models produced by tobacco smoking and intratracheally instillation of porcine pancreatic elastase. The possible mechanism of recovering the pulmonary emphysema is the proliferation of pulmonary capillary and enlargement of pulmonary artery, improved blood flow in the lung, improved ventilation/perfusion shunt, reduced pulmonary alveolus size and volume of the lung through self-compensation.

OBJECTIVE: To seek the bionic material myocardial extracellular matrix in the myocardial tissue engineering for the cultured myocardial cells and to provide a reliable scaffold.METHODS: A computer-based online search of CNKI and PubMed database to search articles published between January 1996 and August 2007 on scaffold material of tissue engineering.RESULTS: Natural biological scaffold materials with good biocompatibility and mechanical properties are ideal choice in the cardiac tissue engineering rapid prototyping technology. Natural biological materials such as collagen, chitosan have poor mechanical properties and plasticity, but good biocompatibility, which can be used for rapid prototyping of cardiac stents. The scaffolds which are prepared by the technology such as three-dimensional printing, laser sintering, three-dimensional pressing,selective laser sintering rapid prototyping technology on have the advantages such as high porosity, high surface area volume ratio,completely transparent among the holes, controllable macro-shape, porosity, and independent control of aperture.CONCLUSION: Through the use of dispersion/accumulation forming principle, surface modification of traditional biological materials in cardiac tissue engineering using computers and other high-tech nano-polymer technology is expected to provide ideal myocardial scaffolds.