5 research outputs found
Monitoring the tissue perfusion during hemorrhagic shock and resuscitation: tissue-to-arterial carbon dioxide partial pressure gradient in a pig model
[Background] Despite much evidence supporting the monitoring of the divergence of transcutaneous partial pressure of carbon dioxide (tcPCO_2) from arterial partial pressure carbon dioxide (artPCO_2) as an indicator of the shock status, data are limited on the relationships of the gradient between tcPCO_2 and artPCO_2 (tc-artPCO_2) with the systemic oxygen metabolism and hemodynamic parameters. Our study aimed to test the hypothesis that tc-artPCO_2 can detect inadequate tissue perfusion during hemorrhagic shock and resuscitation. [Methods] This prospective animal study was performed using female pigs at a university-based experimental laboratory. Progressive massive hemorrhagic shock was induced in mechanically ventilated pigs by stepwise blood withdrawal. All animals were then resuscitated by transfusing the stored blood in stages. A transcutaneous monitor was attached to their ears to measure tcPCO_2. A pulmonary artery catheter (PAC) and pulse index continuous cardiac output (PiCCO) were used to monitor cardiac output (CO) and several hemodynamic parameters. The relationships of tc-artPCO_2 with the study parameters and systemic oxygen delivery (DO2) were analyzed. [Results] Hemorrhage and blood transfusion precisely impacted hemodynamic and laboratory data as expected. The tc-artPCO_2 level markedly increased as CO decreased. There were significant correlations of tc-artPCO_2 with DO2 and COs (DO2: r = − 0.83, CO by PAC: r = − 0.79; CO by PiCCO: r = − 0.74; all P < 0.0001). The critical level of oxygen delivery (DO2crit) was 11.72 mL/kg/min according to transcutaneous partial pressure of oxygen (threshold of 30 mmHg). Receiver operating characteristic curve analyses revealed that the value of tc-artPCO_2 for discrimination of DO2crit was highest with an area under the curve (AUC) of 0.94, followed by shock index (AUC = 0.78; P < 0.04 vs tc-artPCO_2), and lactate (AUC = 0.65; P < 0.001 vs tc-artPCO_2). [Conclusions] Our observations suggest the less-invasive tc-artPCO_2 monitoring can sensitively detect inadequate systemic oxygen supply during hemorrhagic shock. Further evaluations are required in different forms of shock in other large animal models and in humans to assess its usefulness, safety, and ability to predict outcomes in critical illnesses
Monitoring the tissue perfusion during hemorrhagic shock and resuscitation: tissue-to-arterial carbon dioxide partial pressure gradient in a pig model
Large-Scale Simulation of Electromagnetic Wave Propagation Using Meshless Time Domain Method With Parallel Processing
Monocyte-derived dendritic cells perform hemophagocytosis to fine-tune excessive immune responses
SummaryBecause immune responses simultaneously defend and injure the host, the immune system must be finely regulated to ensure the host’s survival. Here, we have shown that when injected with high Toll-like receptor ligand doses or infected with lymphocytic choriomeningitis virus (LCMV) clone 13, which has a high viral turnover, inflammatory monocyte-derived dendritic cells (Mo-DCs) engulfed apoptotic erythroid cells. In this process, called hemophagocytosis, phosphatidylserine (PS) served as an “eat-me” signal. Type I interferons were necessary for both PS exposure on erythroid cells and the expression of PS receptors in the Mo-DCs. Importantly, hemophagocytosis was required for interleukin-10 (IL-10) production from Mo-DCs. Blocking hemophagocytosis or Mo-DC-derived IL-10 significantly increased cytotoxic T cell lymphocyte activity, tissue damage, and mortality in virus-infected hosts, suggesting that hemophagocytosis moderates immune responses to ensure the host’s survival in vivo. This sheds light on the physiological relevance of hemophagocytosis in severe inflammatory and infectious diseases