Does caffeine improve respiratory rate during remifentanil target controlled infusion sedation? A case report in endoscopic sedation

2017 ◽  
Vol 13 (2) ◽  
pp. 125 ◽  
Author(s):  
Fabio Sbaraglia, MD ◽  
Mariella De Riso, MD ◽  
Maria Elena Riccioni, MD ◽  
Guido Costamagna, MD ◽  
Maria Sammartino, MD
Keyword(s):  
Respiratory Rate ◽  
Protective Role ◽  
Respiratory Center ◽  
Respiratory Drive ◽  
Remifentanil Infusion ◽  
Impaired Patient ◽  
Target Controlled Infusion ◽  
Therapeutic Colonoscopy ◽  
Positive Effect ◽  
Neonatal Apnea

Sedation for endoscopic procedures may be challenging when facing patients with high risk. Traditional techniques, as propofol or meperidine/midazolam administration, cannot ensure an adequate level of safety and efficacy for these patients. Remifentanil infusion is a common alternative, but the incidence of apneic events does not allow achieving safely a good level of analgesia. To overcome with this issue, the authors borrowed suggestions from other medical fields. The clinical practice has recognized a wide utility of methylxanthines (caffeine, theophylline, etc). The positive effect of caffeine on the airways function is known and in the treatment of neonatal apnea, it works as direct stimulant of central respiratory center. Furthermore, preclinical studies suggest that methylxanthines could have a protective role on the opioids inhibition of the bulbar-pontine respiratory center. As described in this report, the authors observed that, also when apnea has been induced by remifentanil, caffeine is able to restore the respiratory rate. The authors present the management of a respiratory impaired patient scheduled for a therapeutic colonoscopy. Our sedation was focused on the match between remifentanil in target controlled infusion and intravenous caffeine, like an “expresso to wake-up” the respiratory drive.

Minimizing stress with remifentanil in a patient with Takotsubo undergoing ophthalmic surgery

2016 ◽  
Vol 12 (1) ◽  
pp. 86 ◽  
Author(s):  
Sbaraglia Fabio, MD ◽  
Garra Rossella, MD ◽  
De Riso Mariella, MD ◽  
Continolo Nicola, MD ◽  
Sammartino Maria, MD
Keyword(s):  
Anxiety Disorder ◽  
Preoperative Assessment ◽  
Protective Role ◽  
Respiratory Drive ◽  
Takotsubo Syndrome ◽  
Ophthalmic Surgery ◽  
Free Condition ◽  
Relative Rarity ◽  
Positive Effect

Anesthesiological management of patients with Takotsubo syndrome (TTS) is a challenge of questions related to physiopathology, prognosis, and trigger causes. Relative rarity of this disease and lack of wide literature do not allow to state any negative or positive effect of the variety of drugs available for anesthesia. The authors report a case of a woman with a clear diagnosis of TTS and anxiety disorder, who underwent to cataract extractions at both eyes at two different times. Clinical management is described, from preoperative assessment until discharge of the patient. In both cases, surgery was successfully performed using remifentanil Target Controlled Infusion sedation in spontaneous ventilation. In this article, the authors suggest the possible cardio-protective role of remifentanil in this kind of pathology, focusing on its advantageous sedating action that guarantees a stress-free condition, while maintaining control on respiratory drive.

Dose-dependent Respiratory Depression by Remifentanil in the Rabbit Parabrachial Nucleus/Kölliker–Fuse Complex and Pre-Bötzinger Complex

2021 ◽  
Author(s):  
Barbara Palkovic ◽  
Jennifer J. Callison ◽  
Vitaliy Marchenko ◽  
Eckehard A. E. Stuth ◽  
Edward J. Zuperku ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Respiratory Depression ◽  
Receptor Agonist ◽  
Parabrachial Nucleus ◽  
Respiratory Drive ◽  
Remifentanil Infusion ◽  
Opioid Receptor Agonist ◽  
Bötzinger Complex ◽  
Dose Dependent ◽  
Partial Reversal

Background Recent studies showed partial reversal of opioid-induced respiratory depression in the pre-Bötzinger complex and the parabrachial nucleus/Kölliker–Fuse complex. The hypothesis for this study was that opioid antagonism in the parabrachial nucleus/Kölliker–Fuse complex plus pre-Bötzinger complex completely reverses respiratory depression from clinically relevant opioid concentrations. Methods Experiments were performed in 48 adult, artificially ventilated, decerebrate rabbits. The authors decreased baseline respiratory rate ~50% with intravenous, “analgesic” remifentanil infusion or produced apnea with remifentanil boluses and investigated the reversal with naloxone microinjections (1 mM, 700 nl) into the Kölliker–Fuse nucleus, parabrachial nucleus, and pre-Bötzinger complex. In another group of animals, naloxone was injected only into the pre-Bötzinger complex to determine whether prior parabrachial nucleus/Kölliker–Fuse complex injection impacted the naloxone effect. Last, the µ-opioid receptor agonist [d-Ala,2N-MePhe,4Gly-ol]-enkephalin (100 μM, 700 nl) was injected into the parabrachial nucleus/Kölliker–Fuse complex. The data are presented as medians (25 to 75%). Results Remifentanil infusion reduced the respiratory rate from 36 (31 to 40) to 16 (15 to 21) breaths/min. Naloxone microinjections into the bilateral Kölliker–Fuse nucleus, parabrachial nucleus, and pre-Bötzinger complex increased the rate to 17 (16 to 22, n = 19, P = 0.005), 23 (19 to 29, n = 19, P < 0.001), and 25 (22 to 28) breaths/min (n = 11, P < 0.001), respectively. Naloxone injection into the parabrachial nucleus/Kölliker–Fuse complex prevented apnea in 12 of 17 animals, increasing the respiratory rate to 10 (0 to 12) breaths/min (P < 0.001); subsequent pre-Bötzinger complex injection prevented apnea in all animals (13 [10 to 19] breaths/min, n = 12, P = 0.002). Naloxone injection into the pre-Bötzinger complex alone increased the respiratory rate to 21 (15 to 26) breaths/min during analgesic concentrations (n = 10, P = 0.008) but not during apnea (0 [0 to 0] breaths/min, n = 9, P = 0.500). [d-Ala,2N-MePhe,4Gly-ol]-enkephalin injection into the parabrachial nucleus/Kölliker–Fuse complex decreased respiratory rate to 3 (2 to 6) breaths/min. Conclusions Opioid reversal in the parabrachial nucleus/Kölliker–Fuse complex plus pre-Bötzinger complex only partially reversed respiratory depression from analgesic and even less from “apneic” opioid doses. The lack of recovery pointed to opioid-induced depression of respiratory drive that determines the activity of these areas. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Patient-ventilator interaction during acute hypercapnia: pressure-support vs. proportional-assist ventilation

1996 ◽  
Vol 81 (1) ◽  
pp. 426-436 ◽  
Author(s):  
V. M. Ranieri ◽  
R. Giuliani ◽  
L. Mascia ◽  
S. Grasso ◽  
V. Petruzzelli ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Dead Space ◽  
Pressure Support ◽  
Esophageal Pressure ◽  
Respiratory Drive ◽  
Resistive Load ◽  
Proportional Assist Ventilation ◽  
Pressure Time ◽  
Pressure Time Product ◽  
Stimulation Of

The objective of this study was to compare patient-ventilator interaction during pressure-support ventilation (PSV) and proportional-assist ventilation (PAV) in the course of increased ventilatory requirement obtained by adding a dead space in 12 patients on weaning from mechanical ventilation. With PSV, the level of unloading was provided by setting the inspiratory pressure at 20 and 10 cmH2O, whereas with PAV the level of unloading was at 80 and 40% of the elastic and resistive load. Hypercapnia increased (P < 0.001) tidal swing of esophageal pressure and pressure-time product per breath at both levels of PSV and PAV. During PSV, application of dead space increased ventilation (VE) during PSV (67 +/- 4 and 145 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001). This was due to a relevant increase in respiratory rate (48 +/- 4 and 103 +/- 5% during 20 and 10 cmH2O PSV, respectively, P < 0.001), whereas the increase in tidal volume (VT) played a small role (13 +/- 1 and 21 +/- 2% during 20 and 10 cmH2O PSV, respectively, P < 0.001). With PAV, the increase in VE consequent to hypercapnia (27 +/- 3 and 64 +/- 4% during 80 and 40% PAV, respectively, P < 0.001) was related to the increase in VT (32 +/- 1 and 66 +/- 2% during 80 and 40% PAV, respectively, P < 0.001), respiratory rate remaining unchanged. The increase in pressure-time product per minute and per liter consequent to acute hypercapnia and the sense of breathlessness were significantly (P < 0.001) higher during PSV than during PAV. Our data show that, after hypercapnic stimulation of the respiratory drive, the capability to increase VE through changes in VT modulated by variations in inspiratory muscle effort is preserved only during PAV; the compensatory strategy used to increase VE during PSV requires greater muscle effort and causes more pronounced patient discomfort than during PAV.

scholarly journals TNFR1 and TNFR2 Signaling Interplay in Cardiac Myocytes

2007 ◽  
Vol 282 (49) ◽  
pp. 35564-35573 ◽  
Author(s):  
Nicole Defer ◽  
Anie Azroyan ◽  
Françoise Pecker ◽  
Catherine Pavoine
Keyword(s):  
Cardiac Myocytes ◽  
Protective Role ◽  
Limiting Factor ◽  
Receptor Subtypes ◽  
Ros Production ◽  
Altered Cell ◽  
Factor Α ◽  
Positive Effect ◽  
Fractional Shortening

Tumor necrosis factor α (TNFα) plays a major role in chronic heart failure, signaling through two different receptor subtypes, TNFR1 and TNFR2. Our aim was to further delineate the functional role and signaling pathways related to TNFR1 and TNFR2 in cardiac myocytes. In cardiac myocytes isolated from control rats, TNFα induced ROS production, exerted a dual positive and negative action on [Ca2+] transient and cell fractional shortening, and altered cell survival. Neutralizing anti-TNFR2 antibodies exacerbated TNFα responses on ROS production and cell death, arguing for a major protective role of the TNFR2 pathway. Treatment with either neutralizing anti-TNFR1 antibodies or the glutathione precursor, N-acetylcysteine (NAC), favored the emergence of TNFR2 signaling that mediated a positive effect of TNFα on [Ca2+] transient and cell fractional shortening. The positive effect of TNFα relied on TNFR2-dependent activation of the cPLA2 activity, independently of serine 505 phosphorylation of the enzyme. Together with cPLA2 redistribution and AA release, TNFα induced a time-dependent phosphorylation of ERK, MSK1, PKCζ, CaMKII, and phospholamban on the threonine 17 residue. Taken together, our results characterized a TNFR2-dependent signaling and illustrated the close interplay between TNFR1 and TNFR2 pathways in cardiac myocytes. Although apparently predominant, TNFR1-dependent responses were under the yoke of TNFR2, acting as a critical limiting factor. In vivo NAC treatment proved to be a unique tool to selectively neutralize TNFR1-mediated effects of TNFα while releasing TNFR2 pathways.

scholarly journals Nutrients Bioaccessibility and Anti-inflammatory Features of Fermented Bee Pollen: A Comprehensive Investigation

2021 ◽  
Vol 12 ◽  
Author(s):  
Pasquale Filannino ◽  
Raffaella Di Cagno ◽  
Olimpia Vincentini ◽  
Daniela Pinto ◽  
Andrea Polo ◽  
...  
Keyword(s):  
Colon Adenocarcinoma ◽  
Human Keratinocytes ◽  
Protective Role ◽  
Protective Effects ◽  
Adenocarcinoma Cell Line ◽  
Inflammatory Stimuli ◽  
Keratinocyte Cell ◽  
Functional Features ◽  
Positive Effect

We compared raw bee-collected pollen (Raw-BCP), spontaneously fermented BCP (Unstarted-BCP), and BCP fermented with selected microbial starters (Started-BCP) to deepen whether fermentation may favorably affect the nutrients bioaccessibility and functional features of BCP. Under in vitro gastrointestinal batches, the highest serum-availability of phenolic compounds was found in Started-BCP, highlighting the positive effect exerted by selected microbial starters. The same effect was not found in spontaneously fermented BCP. In colon adenocarcinoma cell line-2 (Caco-2) cells stressed by a pro-inflammatory stimulus, the treatment with Started-BCP halted the increase of pro-inflammatory mediator’s level. Started-BCP counteracted efficiently the deleterious effects of inflammatory stimuli on the integrity of the Caco-2 cells monolayer and its barrier function. Started-BCP successfully counteracted the H2O2-induced intracellular accumulation of reactive oxygen species (ROS) in Caco-2 cells. A protective role against lipopolysaccharide (LPS)-induced inflammation was exerted by Started-BCP in human keratinocytes. The same protective effects on Caco-2 and keratinocyte cell lines were negligible after treatments with Raw-BCP or Unstarted-BCP.

Simplifying the measurement of neural respiratory drive index: parasternal electromyogram to measure respiratory rate

2020 ◽  
Author(s):  
Grace McDowell ◽  
Rebecca Dcruz ◽  
Nicholas Hart ◽  
Patrick Murphy ◽  
Christopher Carlin
Keyword(s):  
Respiratory Rate ◽  
Respiratory Drive

scholarly journals Evaluation of Glycosylated PTGS2 in Colorectal Cancer for NSAIDS-Based Adjuvant Therapy

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 683
Author(s):  
Roberta Venè ◽  
Delfina Costa ◽  
Raffaella Augugliaro ◽  
Sebastiano Carlone ◽  
Stefano Scabini ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Interleukin 1 ◽  
Cost Benefit ◽  
Protective Role ◽  
Macrophage Population ◽  
M1 Macrophage ◽  
Luminal Area ◽  
Prostaglandin Endoperoxide Synthase ◽  
Positive Effect

Observational/retrospective studies indicate that prostaglandin-endoperoxide synthase-2 (PTGS2) inhibitors could positively affect colorectal cancer (CRC) patients’ survival after diagnosis. To obtain an acceptable cost/benefit balance, the inclusion of PTGS2 inhibitors in the adjuvant setting needs a selective criterion. We quantified the 72 kDa, CRC-associated, glycosylated form of PTGS2 in 100 frozen CRC specimens and evaluated PTGS2 localization by IHC in the same tumors, scoring tumor epithelial-derived and stroma-derived fractions. We also investigated the involvement of interleukin-1 beta (IL1β) in PTGS2 induction, both in vitro and in CRC lysates. Finally, we used overall survival (OS) as a criterion for patient selection. Glycosylated PTGS2 can be quantified with high sensibility in tissue lysates, but the expression in both tumor and stromal cells limits its use for predictive purposes. Immunohistochemistry (IHC) analysis indicates that stromal PTGS2 expression could exert a protective role on patient OS. Stromal PTGS2 was prevalently expressed by cancer-associated fibroblasts exerting a barrier function near the gut lumen, and it apparently favored the antitumor M1 macrophage population. IL1β was directly linked to gPTGS2 expression both in vitro and in tumors, but its activity was apparently prevalent on the stromal cell population. We suggest that stromal PTGS2 could exert a positive effect on patients OS when expressed in the luminal area of the tumor.

THE EFFECTS OF SARIN AND ATROPINE ON THE RESPIRATORY CENTER AND NEUROMUSCULAR JUNCTIONS OF THE RAT

1959 ◽  
Vol 37 (5) ◽  
pp. 651-660 ◽  
Author(s):  
W. C. Stewart
Keyword(s):  
Respiratory Rate ◽  
Large Dose ◽  
Gastrocnemius Muscle ◽  
Neuromuscular Junctions ◽  
Respiratory Arrest ◽  
Diaphragm Muscle ◽  
Respiratory Center ◽  
Nerve Supply ◽  
Higher Doses ◽  
Stimulation Of

Records were made of the contractions of a slip of diaphragm muscle which was isolated from the circulation of the rat, while the nerve supply was preserved. Simultaneous records were also made of the contractions of the opposite (circulated) hemidiaphragm, of respiratory rate, of the Hering-Breuer reflex, and of contractions of the gastrocnemius muscle in response to stimulation of the sciatic nerve.Low doses of sarin caused immediate respiratory arrest, purely central in origin; respiration was restored to normal at once when a large dose of atropine was given. When atropine was injected before sarin, much higher doses of sarin were required to depress the respiration, and now the respiratory paralysis took place at the neuromuscular junctions in the diaphragm, the respiratory center remaining relatively unaffected. It was concluded that respiratory paralysis by sarin could be purely central, purely peripheral, or both central and peripheral, depending on the doses of sarin and atropine employed.

scholarly journals (192) Effect of Controlled Atmosphere in Postharvest Life of `Elliot' Blueberry

HortScience ◽  
2006 ◽  
Vol 41 (4) ◽  
pp. 1044A-1044 ◽  
Author(s):  
Luis Luchsinger ◽  
Alvaro Villalobos ◽  
Antonio Lizana
Keyword(s):  
Weight Loss ◽  
Relative Humidity ◽  
Respiratory Rate ◽  
Vaccinium Corymbosum ◽  
Soluble Solids ◽  
Controlled Atmosphere ◽  
Titrable Acidity ◽  
Postharvest Life ◽  
Positive Effect

Postharvest response to high CO2 controlled atmosphere (CA) was studied in the blueberry (Vaccinium corymbosum L.) cultivar Elliot. Fruit was stored at 0 °C, 90% relative humidity and 15%, 18%, and 21% of CO2 and 5% of O2 and in air (0.03% CO2 and 21% O2). Evaluations were performed after 30 and 60 days of storage and an aditional period of 3 and 6 days at 10 °C (ripening period). Parameters meassured were: color (lightness, hue, and chroma), firmness, soluble solids (SS), titrable acidity (TA), SS/TA ratio, pH, weight loss, decay, physiological disorders, and appearance. The CA caused a positive effect, preserving the quality of the fruit in storage, by decreasing the respiratory rate and decay incidence. The 15% CO2 controlled atmosphere presented the best firmness and lowest decay. Acceptable conditions of quality were kept for 60 days of storage.

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