Lateralized Periodic Discharges During Remifentanil Infusion

2021 ◽  
pp. 155005942110106
Author(s):  
Janaarththanan Sakathevan ◽  
Karthik Somasundaram ◽  
Sandra C. Chinyere ◽  
Cristina Rodríguez-Viña ◽  
David Martín-López

Lateralized periodic discharges (LPDs) are a common electroencephalographic (EEG) pattern in the neurointensive care unit setting. LPDs are typically observed in association with acute structural lesions of the brain with different etiologies. There are no reports describing a link between the occurrence of LPDs and the administration of remifentanil. Remifentanil is a rapid-acting pure μ-opioid receptor agonist, which is indicated to provide analgesia and sedation in mechanically ventilated patients in intensive care units. We present a case of an 84-year-old man with neuroglycopenia who developed LPDs while sedated with remifentanil. We report, for the first time, a potential relationship between remifentanil and the induction of LPDs.

Author(s):  
Krishnan Ravikumar ◽  
Balasubramanian Sridhar ◽  
Nitin Pradhan ◽  
Mayur Khunt

Pain ◽  
2018 ◽  
Vol 159 (11) ◽  
pp. 2277-2284 ◽  
Author(s):  
Antonio Rodriguez-Gaztelumendi ◽  
Viola Spahn ◽  
Dominika Labuz ◽  
Halina Machelska ◽  
Christoph Stein

1999 ◽  
Vol 277 (3) ◽  
pp. C492-C500 ◽  
Author(s):  
Jian-Ming Pei ◽  
Xiao-Chun Yu ◽  
Jin-Song Bian ◽  
Tak-Ming Wong

To study the effects of κ-opioid receptor stimulation on intracellular Ca2+ concentration ([Ca2+]i) homeostasis during extracellular acidosis, we determined the effects of κ-opioid receptor stimulation on [Ca2+]iresponses during extracellular acidosis in isolated single rat ventricular myocytes, by a spectrofluorometric method. U-50488H (10–30 μM), a selective κ-opioid receptor agonist, dose dependently decreased the electrically induced [Ca2+]itransient, which results from the influx of Ca2+ and the subsequent mobilization of Ca2+ from the sarcoplasmic reticulum (SR). U-50488H (30 μM) also increased the resting [Ca2+]iand inhibited the [Ca2+]itransient induced by caffeine, which mobilizes Ca2+ from the SR, indicating that the effects of the κ-opioid receptor agonist involved mobilization of Ca2+ from its intracellular pool into the cytoplasm. The Ca2+responses to 30 μM U-50488H were abolished by 5 μM nor-binaltorphimine, a selective κ-opioid receptor antagonist, indicating that the event was mediated by the κ-opioid receptor. The effects of the agonist on [Ca2+]iand the electrically induced [Ca2+]itransient were significantly attenuated when the extracellular pH (pHe) was lowered to 6.8, which itself reduced intracellular pH (pHi) and increased [Ca2+]i. The inhibitory effects of U-50488H were restored during extracellular acidosis in the presence of 10 μM ethylisopropyl amiloride, a potent Na+/H+exchange blocker, or 0.2 mM Ni2+, a putative Na+/Ca2+exchange blocker. The observations indicate that acidosis may antagonize the effects of κ-opioid receptor stimulation via Na+/H+and Na+/Ca2+exchanges. When glucose at 50 mM, known to activate the Na+/H+exchange, was added, both the resting [Ca2+]iand pHi increased. Interestingly, the effects of U-50488H on [Ca2+]iand the electrically induced [Ca2+]itransient during superfusion with glucose were significantly attenuated; this mimicked the responses during extracellular acidosis. When a high-Ca2+ (3 mM) solution was superfused, the resting [Ca2+]iincreased; the increase was abolished by 0.2 mM Ni2+, but the pHi remained unchanged. Like the responses to superfusion with high-concentration glucose and extracellular acidosis, the responses of the [Ca2+]iand electrically induced [Ca2+]itransients to 30 μM U-50488H were also significantly attenuated. Results from the present study demonstrated for the first time that extracellular acidosis antagonizes the effects of κ-opioid receptor stimulation on the mobilization of Ca2+ from SR. Activation of both Na+/H+and Na+/Ca2+exchanges, leading to an elevation of [Ca2+]i, may be responsible for the antagonistic action of extracellular acidosis against κ-opioid receptor stimulation.


2002 ◽  
Vol 15 (02) ◽  
pp. 72-77
Author(s):  
J. L. Cook ◽  
J. R. Dodam ◽  
J. M. Kreeger ◽  
J. L. Tomlinson ◽  
K. Kuroki ◽  
...  

SummaryThe objective of this study was to evaluate the effects of [D-Ala2, Nme-Phe4, Gly5-ol] enkephalin (DAMGO), a μ-opioid receptor agonist, and β-funaltrexamine (β-FNA), a μ-opioid receptor antagonist, on the biosynthetic capabilities of canine chondrocytes cultured in the presence of interleukin-1 β (IL-1 β). Articular chondrocytes were harvested from the humeral heads of three adult dogs and cultured in a three-dimensional (3-D) gel medium made from low-melting agarose and cell culture medium. Chondrocytes in 3-D culture were exposed to IL-1 β (0 or 20 ng/ml), DAMGO (0,0.1,1.0, or 10 μM), and β-FNA (0 or 10 μM) by addition to the liquid media in all possible combinations. On days five and 15 of 3-D culture, liquid medium samples were harvested for subsequent analysis of glycosaminogly- can (GAG), prostaglandin E2 (PGE2) and matrix metalloprotease-3 (MMP-3) content. On the same days, gel plugs were also harvested and evaluated for GAG content.Incubation with IL-1 β decreased the amount of GAG in the gel plugs and caused an increase in PGE2 production on days five and 15 of 3-D culture. Treatment with DAMGO or β-FNA did not significantly modulate PGE2 production, MMP-3 production, GAG loss to the medium or GAG content of the gel plugs on either day five or 15 of 3-D culture in the presence or absence of IL-1 β. We concluded that DAMGO and β-FNA had neither protective nor detrimental effects on the biosynthetic capabilities of chondrocytes in the presence or absence of IL-1 β.


1998 ◽  
Vol 250 (3) ◽  
pp. 720-725 ◽  
Author(s):  
Mariana Spetea ◽  
Krisztina Monory ◽  
Csaba Tömböly ◽  
Géza Tóth ◽  
Eleni Tzavara ◽  
...  

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