Abstract
Monitoring of the mitochondrial NADH redox state (an indicator of intracellular oxygen levels) together with microcirculatory blood flow (TBF) and with oxygenation (HbO2) could serve as a preferred approach to evaluate tissue O2 balance or viability. We hypothesize that in the presence of reduced oxygen delivery and extraction, blood flow will be redistributed in order to protect the most vital organs by increasing their regional blood flow, while O2 delivery to the less vital organs will diminish. Thus, the NADH redox state of less vital organs could serve as an indicator of overall O2 imbalance as well as an endpoint of resuscitation. We have therefore developed an optical device embedded in a Foley catheter to provide real-time data on the NADH redox state, TBF and HbO2 in critically ill patients. The CritiView is a computerized optical device that integrates hardware and software in order to provide real-time information of tissue viability [1]. A modified three-way Foley catheter that contains a fiberoptic probe connects the CritiView to the mucosal side of the urethral wall. We have used this device in five female pigs that underwent graded hemorrhage, and in four patients who were monitored during aortic abdominal aneurysm operations. These preliminary swine model and human studies confirm the feasibility of collecting information about mitochondrial function from the urethral wall. The main effects of graded hemorrhage started when the blood volume decreased by 30%. At 40% blood loss, minimal levels of TBF and HbO2 were correlated to the maximal NADH levels. The values of the three parameters returned to baseline after retransfusion of the shed blood. Aortic clamping in patients led to a significant decrease in TBF and HbO2 while NADH levels increased. After aortic declamping, the parameters recovered to normal values. Our preliminary results show that the CritiView may be a useful tool for the detection of O2 imbalance and the development of an emergency metabolic state in nonvital tissues.
Highlights
To clarify the relation between ATP and prostaglandinE2 (PGE2) in the immunologic system, we investigated the acute and chronic effects of PGE2 on activation of purinergic signaling in monocytes by measuring the ATP-induced elevation of intracellularCa2+ ([Ca]i) in fura-2-loaded THP-1 monocytes
IFNγ plays a critical role in host defense by promoting Th1 phenotype and bacterial clearance
Low IFNγ levels are were washed, loaded with fura-2-AM, and transferred into a quartz associated with the Th2 phenotype consistent with critical illness cuvette and placed in the thermostat-regulated sample chamber of anergy [2]
Summary
To clarify the relation between ATP and prostaglandinE2 (PGE2) in the immunologic system, we investigated the acute and chronic effects of PGE2 on activation of purinergic signaling in monocytes by measuring the ATP-induced elevation of intracellularCa2+ ([Ca]i) in fura-2-loaded THP-1 monocytes. Several experimental studies suggest that thrombolysis therapy acts directly on thrombi or emboli and enhances microcirculatory reperfusion In this retrospective study we investigated the extent of blood coagulation and fibrin formation via the plasma D-dimer level, an indicator of endogenous fibrinolytic activity, in patients who underwent inhospital and out-of-hospital cardiac arrest from nontraumatic causes. Methods MEDLINE, EMBASE, CINAHL, and the Cochrane Library were searched, and studies were included if they reported on ICU patients > 16 years old who were evaluated for CINMA clinically and electrophysiologically, and they contained sufficient data to quantitatively measure the association between CINMA and clinically relevant exposures and/or outcomes. Our aim was to evaluate the role of the cardiac markers NT-proBNP, Troponin T (TnT) and myoglobin as predictors of inhospital and 6-month all-cause mortality in patients admitted to a general adult ICU with severe sepsis/septic shock. Aging is associated with decreased cardiopulmonary and renal reserve as well as the development of progressive organ failure
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