Comparative analgesic efficacy and tolerability of ketorolac tromethamine and glafenine in patients with post-operative pain

Arsac, M; Frileux, C

doi:10.1185/03007998809114238

Cited by 6 publications

(2 citation statements)

References 5 publications

(1 reference statement)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent work from Zhang’s Lab. demonstrates that PBM-treatment from 2 to 8 post-stroke in rats can effectively switch an M1 microglial phenotype to an anti-inflammatory M2 phenotype, and promotes neurogenesis ( Arsac and Frileux, 1988 ). In addition, treatment with PBM has been shown to enhance cognitive capability in normal people ( Barrett and Gonzalez-Lima, 2013 ) and healthy animals ( Gonzalez-Lima and Barrett, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Photobiomodulation Promotes Hippocampal CA1 NSC Differentiation Toward Neurons and Facilitates Cognitive Function Recovery Involving NLRP3 Inflammasome Mitigation Following Global Cerebral Ischemia

Guo

Wang

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Our recent study revealed that photobiomodulation (PBM) inhibits delayed neuronal death by preserving mitochondrial dynamics and function following global cerebral ischemia (GCI). In the current study, we clarified whether PBM exerts effective roles in endogenous neurogenesis and long-lasting neurological recovery after GCI. Adult male rats were treated with 808 nm PBM at 20 mW/cm2 irradiance for 2 min on cerebral cortex surface (irradiance ∼7.0 mW/cm2, fluence ∼0.8 J/cm2 on the hippocampus) beginning 3 days after GCI for five consecutive days. Cognitive function was evaluated using the Morris water maze. Neural stem cell (NSC) proliferation, immature neurons, and mature neurons were examined using bromodeoxyuridine (BrdU)-, doublecortin (DCX)-, and NeuN-staining, respectively. Protein expression, such as NLRP3, cleaved IL1β, GFAP, and Iba1 was detected using immunofluorescence staining, and ultrastructure of astrocyte and microglia was observed by transmission electron microscopy. The results revealed that PBM exerted a markedly neuroprotective role and improved spatial learning and memory ability at 58 days of ischemia/reperfusion (I/R) but not at 7 days of reperfusion. Mechanistic studies revealed that PBM suppressed reactive astrocytes and maintained astrocyte regeneration at 7 days of reperfusion, as well as elevated neurogenesis at 58 days of reperfusion, as evidenced by a significant decrease in the fluorescence intensity of GFAP (astrocyte marker) but unchanged the number of BrdU-GFAP colabeled cells at the early timepoint, and a robust elevation in the number of DCX-NeuN colabeled cells at the later timepoint in the PBM-treated group compared to the GCI group. Notably, PBM treatment protected the ultrastructure of astrocyte and microglia cells at 58 days but not 7 days of reperfusion in the hippocampal CA1 region. Furthermore, PBM treatment significantly attenuated the GCI-induced immunofluorescence intensity of NLRP3 (an inflammasome component), cleaved IL1β (reflecting inflammasome activation) and Iba1, as well as the colocalization of NLRP3/GFAP or cleaved IL-1β/GFAP, especially in animals subjected to I/R at 58 days. Taken together, PBM treatment performed postischemia exerted a long-lasting protective effect on astrocytes and promoted endogenous neurogenesis in the hippocampal CA1 region, which might contribute to neurological recovery after GCI.

show abstract

Section: Discussionmentioning

confidence: 99%

Photobiomodulation Promotes Hippocampal CA1 NSC Differentiation Toward Neurons and Facilitates Cognitive Function Recovery Involving NLRP3 Inflammasome Mitigation Following Global Cerebral Ischemia

Guo

Wang

et al. 2021

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…The mean score for ketorolac (2.3) was statistically significantly higher (p < 0.001) than the mean score for aspirin (2.0). Patients' evaluations of pain relief also consistently favored ketorolac over 110s PHARMACOTHERAPY SUPPLEMENT TO VOLUME 10, NUMBER 6,1990 aspirin at each visit throughout the 52-week observation period.…”

Section: Efficacymentioning

confidence: 91%

Comparison of Long‐Term Safety of Ketorolac Tromethamine and Aspirin in the Treatment of Chronic Pain

Rubin,

Yee,

Ruoff

1990

Pharmacotherapy

View full text Add to dashboard Cite

A double‐blind, randomized trail was conducted in 823 patients who required longterm analgesic therapy for chronic pain such as that caused by osteoarthritis, fibromyopathies or fibromyalgias, other nonarticular chronic soft tissue pain syndromes, or headaches. The safety and analgesic efficacy of ketorolac tromethamine 10 mg 4 times a day as needed was compared with that of aspirin 650 mg 4 times a day as needed. The primary emphasis of this 52‐week study was on evaluating the safety of the drugs. Patients returned to the clinics at 2, 5, 10, 15, 20, 28, 36, 44, and 52 weeks for assessments of safety and efficacy. Both patients' and investigators' evaluations of overall efficacy and safety favored ketorolac over aspirin. The probability of early withdrawal from the study was significantly higher with aspirin than with ketorolac, primarily because of lack of efficacy. Early withdrawal for safety‐related reasons alone was similar for those taking aspirin and ketorolac.

show abstract

Activation of mesocorticolimbic reward circuits for assessment of relief of ongoing pain: A potential biomarker of efficacy

Xie

Patwardhan

et al. 2014

Pain

View full text Add to dashboard Cite

Preclinical assessment of pain has increasingly explored operant methods that may allow behavioral assessment of ongoing pain. In animals with incisional injury, peripheral nerve block produces conditioned place preference (CPP) and activates the mesolimbic dopaminergic reward pathway. We hypothesized that activation of this circuit could serve as a neurochemical output measure of relief of ongoing pain. Medications commonly used clinically including gabapentin and non-steroidal anti-inflammatory drugs (NSAIDs) were evaluated in models of post-surgical (one day following incision) or neuropathic (14 days following spinal nerve ligation, SNL) pain to determine if the clinical efficacy profile of these drugs in these pain conditions was reflected by extracellular dopamine (DA) release in the nucleus accumbens (NAc) shell. Microdialysis was performed in awake rats. Basal DA levels were not significantly different between experimental groups and no significant treatment effects were seen in sham-operated animals. Consistent with clinical observation, spinal clonidine produced CPP and produced a dose-related increase in net NAc DA release in SNL rats. Gabapentin, commonly used to treat neuropathic pain produced increased NAc DA in rats with SNL, but not in animals with incisional, injury. In contrast, ketorolac or naproxen produced increased NAc DA in animals with incisional, but not neuropathic, pain. Increased extracellular NAc DA release was consistent with CPP and observed selectively with treatments commonly used clinically for post-surgical or neuropathic pain. Evaluation of NAc DA efflux in animal pain models may represent an objective neurochemical assay that may serve as a biomarker of efficacy for novel pain-relieving mechanisms.

show abstract

Comparative analgesic efficacy and tolerability of ketorolac tromethamine and glafenine in patients with post-operative pain

Cited by 6 publications

References 5 publications

Photobiomodulation Promotes Hippocampal CA1 NSC Differentiation Toward Neurons and Facilitates Cognitive Function Recovery Involving NLRP3 Inflammasome Mitigation Following Global Cerebral Ischemia

Photobiomodulation Promotes Hippocampal CA1 NSC Differentiation Toward Neurons and Facilitates Cognitive Function Recovery Involving NLRP3 Inflammasome Mitigation Following Global Cerebral Ischemia

Comparison of Long‐Term Safety of Ketorolac Tromethamine and Aspirin in the Treatment of Chronic Pain

Activation of mesocorticolimbic reward circuits for assessment of relief of ongoing pain: A potential biomarker of efficacy

Contact Info

Product

Resources

About