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It is a commonly held view that information flow between widely separated regions of the cerebral cortex is a necessary component in the generation of wakefulness (also termed "connected" consciousness). This study therefore hypothesized that loss of wakefulness caused by propofol anesthesia should be associated with loss of information flow, as estimated by the effective connectivity in the scalp electroencephalogram (EEG) signal.
Novel analgesics that do not suppress the respiratory drive are urgently needed. Glutamate signaling through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors plays important roles in central pain circuits. AMPAkines augment AMPA receptor function and have been shown to stimulate the respiratory drive to oppose opioid-induced hypoventilation. However, their role in chronic pain states remains unknown.
Postliver transplantation acute kidney injury (AKI) severely affects patient survival, whereas the mechanism is unclear and effective therapy is lacking. The authors postulated that reperfusion induced enhancement of connexin32 (Cx32) gap junction plays a critical role in mediating postliver transplantation AKI and that pretreatment/precondition with the anesthetic propofol, known to inhibit gap junction, can confer effective protection.
The wakeful brain can easily access and coordinate a large repertoire of different states-dynamics suggestive of "criticality." Anesthesia causes loss of criticality at the level of electroencephalogram waveforms, but the criticality of brain network connectivity is less well studied. The authors hypothesized that propofol anesthesia is associated with abrupt and divergent changes in brain network connectivity for different frequencies and time scales-characteristic of a phase transition, a signature of loss of criticality.
The effects of high-dose fentanyl-oxygen anesthesia (100 micrograms/kg) on myocardial blood flow (argon washin), myocardial oxygen consumption, myocardial lactate balance, and cardiovascular dynamics were studied in nine patients undergoing three-vessel coronary artery bypass operations. All patients had been on maintenance doses of a beta-receptor blocker (pindolol). Except for pindolol all medication had been discontinued 48 hours prior to the study. Measurements were performed in the awake state, after 10 micrograms/kg fentanyl, after 100 micrograms/kg fentanyl, and during sternotomy. Moderate doses of fentanyl (10 micrograms/kg) produced minimal changes in myocardial blood flow, myocardial oxygen consumption, and cardiovascular dynamics; myocardial oxygen balance as well maintained. Large doses of fentanyl (100 micrograms/kg) produced a 16 per cent decrease in mean aortic pressure, cardiac index did not change significantly, while stroke volume index decreased by 23 per cent. Myocardial oxygen consumption decreased by 14 per cent and myocardial blood flow by 10 per cent. Myocardial lactate production was observed in five patients, indicating myocardial ischemia. During sternotomy arterial pressure and heart rate increased 8 per cent and 29 per cent, respectively, resulting in an increase in myocardial work, as reflected by a 38 per cent increase in myocardial oxygen consumption and by a 54 per cent increase in myocardial blood flow. Myocardial lactate production was observed in seven of nine patients. Our data demonstrate that in patients on maintenance doses of beta-receptor blockers, large doses of fentanyl as the sole "anesthetic" produce incomplete anesthesia and fail to protect the myocardium from ischemia due to noxious stimuli during coronary artery surgery.
The exact mechanisms that underlie the pathological processes of myocardial ischemia in humans are unclear. Cardiopulmonary bypass with cardioplegic arrest allows the authors to examine the whole transcriptional profile of human left ventricular myocardium at baseline and after exposure to cold cardioplegia-induced ischemia as a human ischemia model.
Exercise is often prescribed as a therapy for chronic pain. Short-term exercise briefly increases the production of endogenous analgesics, leading to transient antinociception. In limited studies, exercise produced sustained increases in endogenous opioids, sustained analgesia, or diminished measures of chronic pain. This study tests the hypothesis that regular aerobic exercise leads to sustained reversal of neuropathic pain by activating endogenous opioid-mediated pain modulatory systems.
Anesthetic cardioprotection reduces myocardial infarct size after ischemia-reperfusion injury. Currently, the role of microRNA in this process remains unknown. MicroRNAs are short, noncoding nucleotide sequences that negatively regulate gene expression through degradation or suppression of messenger RNA. In this study, the authors uncovered the functional role of microRNA-21 (miR-21) up-regulation after anesthetic exposure.
Continuous nerve block with ropivacaine is commonly performed after repair surgery for traumatic peripheral nerve injuries. After peripheral nerve injury, tetrodotoxin-resistant voltage-gated sodium channel Nav1.8 is upregulated and contributes to macrophage inflammation. This study investigated whether ropivacaine promotes peripheral nerve regeneration through Nav1.8-mediated macrophage signaling.
The catabolism of the essential amino acid tryptophan to kynurenine is emerging as a potential key pathway involved in post-cardiac arrest brain injury. The aim of this study was to evaluate the effects of the modulation of kynurenine pathway on cardiac arrest outcome through genetic deletion of the rate-limiting enzyme of the pathway, indoleamine 2,3-dioxygenase.
Limited information exists on the effects of temporary functional deafferentation (TFD) on brain activity after peripheral nerve block (PNB) in healthy humans. Increasingly, resting-state functional connectivity (RSFC) is being used to study brain activity and organization. The purpose of this study was to test the hypothesis that TFD through PNB will influence changes in RSFC plasticity in central sensorimotor functional brain networks in healthy human participants.
Positive end-expiratory pressure (PEEP) benefits in acute respiratory distress syndrome are driven by lung dynamic strain reduction. This depends on the variable extent of alveolar recruitment. The recruitment-to-inflation ratio estimates recruitability across a 10-cm H2O PEEP range through a simplified maneuver. Whether recruitability is uniform or not across this range is unknown. The hypotheses of this study are that the recruitment-to-inflation ratio represents an accurate estimate of PEEP-induced changes in dynamic strain, but may show nonuniform behavior across the conventionally tested PEEP range (15 to 5 cm H2O).
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