129 research outputs found
Poisoning with illicit substances: toxicology for the anaesthetist
The consumption of illicit substances represents a considerable threat to the health and wellbeing of particular sectors of our communities. Hospitalisation is sometimes required for the treatment of the direct toxic effects of the drugs as well as for injuries sustained while under their influence. Although poisoning with ‘traditional‘ substances of abuse such as opioids, cocaine and cannabis still predominate in terms of numbers, the availability and use of new psychoactive substances are on the rise. These latter agents, some of which began life as failed pharmaceutical products, have enjoyed renewed status as recreational stimulants, entactogens or hallucinogens, properties that originally precluded them from legitimate use. These drugs may act by enhancing endogenous release of neurotransmitters, inhibiting their reuptake back into neurons or having direct effects on receptors, and may involve adrenergic, dopaminergic or serotonergic systems. The use of intravenous lipid emulsion for the symptomatic treatment of drug overdose has become a fertile ground for research and may hold promise as a non-specific treatment for poisoning with illicit substances. Dexmedetomidine, an α2-receptor agonist with a central sympatholytic effect, may be able to counteract the cardiovascular and central nervous system overstimulation that may accompany stimulant toxicity.postprin
Remifentanil reduces the release of biochemical markers of myocardial damage in patients undergoing on pump coronary artery bypass surgery
INTERVENTIONS: Patients randomized to the remifentanil group (n = 20) received a 1 µg/kg bolus followed by 0.5 µg/kg/min infusion for 30 minutes after induction but before sternotomy, whilst the control group (n = 20) received normal saline. Serial samples for measurement of creatine kinase (CKMB), cardiac troponin I (cTnI), ischemia modified albumin (IMA) and heart type fatty acid binding protein (hFABP) were taken at baseline, pre bypass, T = 10 minutes, 2, 6, 12, and 24 hours after cross clamp release, to assess the degree of myocardial damage. MEASUREMENTS AND MAIN RESULTS: Patients in the remifentanil group had lower levels of CKMB from T _ 2 hours to 24 hours, cTnI from T = 10 minutes to T = 12 hours, IMA from T = 10 min to T = 2 hours and h-FABP from T _ 10 minutes to T = 12 hours (p < 0.05). The time to tracheal extubation was shorter in patients in the remifentanil group. The overall length of ICU and hospital stays was not different. CONCLUSIONS: The addition of remifentanil to the anesthesia regimen reduced the degree of myocardial damage. This incremental benefit may be attributable to either to remifentanil itself or to an overall increased opioid dose, the latter may be necessary to trigger cardiac protection. © 2009 Elsevier Inc. All rights reserved.postprin
Intrathecal morphine remotely preconditions the heart via a neural pathway
Central opioid receptor activation triggers cardioprotection against ischemia reperfusion injury, independent of peripheral opioid receptor activity. Using a rodent model of myocardial ischemia reperfusion injury with infarct size as the primary outcome, we tested the hypothesis that spinal opioids confer this beneficial effect via a neural pathway. Intrathecal morphine reduced the infarct size compared with control (23% +/- 7% vs. 58% +/- 3%, respectively, P < 0.01). Prior antagonism of the autonomic pathway, and the receptors for bradykinin, calcitonin gene-related peptide, and the KATP channel, respectively, abolished this cardioprotection (54% +/- 13%, 52% +/- 10%, 56% +/- 9%, and 49% +/- 8%, respectively, P < 0.05). In a second set of experiments, we demonstrated that the increased expression of myocardial phosphorylated-Akt and endothelial nitric oxide synthase induced by intrathecal morphine was blocked by prior administration of hexamethonium. These findings support the notion that spinal opioid receptors stimulate a neural pathway that uses nonopioid neurotransmitters to confer cardioprotection from ischemia reperfusion injury. The use of intrathecal morphine for this purpose has potential clinical application, and it is already being used in the perioperative period to provide prolonged analgesia.postprin
Remifentanil post-conditioning attenuates cardiac ischemia-reperfusion injury via κ or δ opioid receptor activation
Background: Ischemic pre- or post-conditioning of the heart has been shown to involve opioid receptors. Remifentanil, an ultra-short-acting selective μ opioid receptor agonist in clinical use, pre-conditions the rat heart against ischemia-reperfusion injury. This study investigates whether remifentanil post-conditioning is also cardioprotective. Methods: Remifentanil post-conditioning (5-min infusion at 1, 5, 10 or 20 μg/kg/min) or ischemic post-conditioning (three cycles of a 10 s reperfusion interspersed with a 10 s ischemia) was induced in an open-chest rat heart model of ischemia and reperfusion injury, in the presence or absence of nor-binaltorphimine, naltrindole or CTOP, specific κ, δ and μ opioid receptor antagonists, respectively. The same sequence of experiments was repeated in the isolated heart model using the maximal protective dose of remifentanil from the dose-response studies. Results: Both ischemic and remifentanil post-conditioning reduced the myocardial infarct size relative to the control group in both models. This cardioprotective effect for both post-conditioning regimes was prevented by the prior administration of nor-binaltorphimine and naltrindole but not CTOP. The sole administration of the antagonists had no effect on the size of myocardial infarction. Conclusions: These results indicate that remifentanil post-conditioning protects the heart from ischemia-reperfusion injury to a similar extent as of ischemic post-conditioning. This protection involves κ and δ but not μ opioid receptor activation. This drug has great potential as a clinical post-conditioning modality as it can be given in large doses without prolonged opioid-related side effects. © 2009 The Acta Anaesthesiologica Scandinavica Foundation.postprin
Event-related potential using task-based electroencephalogram may differentiate between mild cognitive impairment and normal controls
BACKGROUND: New non-invasive biomarkers to diagnose early Alzheimer’ disease are needed. We investigated the role of event-related potential (ERP) using task-based electroencephalogram (EEG) in differentiating patients with mild cognitive problems from cognitive-normal healthy controls …published_or_final_versio
Remifentanil reduces the release of biochemical markers of myocardial damage after coronary artery bypass surgery: A randomized trial
Objective: Opioids, including remifentanil, have been demonstrated to confer cardiac protection against ischemia reperfusion injury in animals. This study evaluated whether remifentanil preconditioning is protective in first-time elective on-pump coronary artery bypass surgery patients receiving a standardized fentanyl (25 μg/kg in total) and propofol anesthetic. Design: A prospective, double blind, randomized, controlled study. Setting: University hospital; single institution. Participants: Forty patients scheduled for first-time elective, on-pump coronary artery bypass surgery for at least 3 diseased vessels. Interventions: Patients randomized to the remifentanil group (n = 20) received a 1 μg/kg bolus followed by a 0.5 μg/kg/min infusion for 30 minutes after induction but before sternotomy, while the control group (n = 20) received normal saline. Serial samples for measurement of creatine kinase (CK-MB), cardiac troponin I (cTnI), ischemia-modified albumin (IMA) and heart-type fatty-acid-binding protein (hFABP) were taken at baseline, prebypass, T = 10 minutes, 2, 6, 12, and 24 hours after cross-clamp release, to assess the degree of myocardial damage. Measurements and Main Results: Patients in the remifentanil group had lower levels of CK-MB from T = 2 hours to 24 hours, cTnI from T = 10 minutes to T = 12 hours, IMA from T = 10 minutes to T = 2 hours and h-FABP from T = 10 minutes to T = 12 hours (p < 0.05). The time to tracheal extubation was shorter in patients in the remifentanil group. The overall lengths of ICU and hospital stays were not different. Conclusions: The addition of remifentanil to the anesthesia regimen reduced the degree of myocardial damage. This incremental benefit may be attributable either to remifentanil itself or to an overall increased opioid dose, the latter may be necessary to trigger cardiac protection. © 2010 Elsevier Inc. All rights reserved.postprin
Effectiveness and safety of erythropoiesis-stimulating agent use in the perioperative period
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