Anesthesia and Analgesia

Vogler, George A.

doi:10.1016/b978-012074903-4/50022-4

Cited by 27 publications

(18 citation statements)

References 125 publications

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“…Several studies reported that inhalational anaesthetics suppress CSD 18 19 . In this study, we still considered isoflurane anesthesia, but not pentobarbitone, which has the least action on CSD 20 , for studying genesis and propagation of CSD for the following reasons: (1) our in vivo experiment lasted almost 7 hours, whereas barbiturates usually only maintain anesthesia from several minutes to 4 hours 21 , which did not meet our requirement; (2) Isoflurane has been widely used in other studies for studying CSD 8 16 22 23 ; indeed, isoflurane provided a stable and consistent depth of anesthesia throughout the experiment and the concentration could be adjusted according to surgical and CSD recording procedures under study; whereas barbiturates generally result in uneven levels of anesthesia 21 ; (3) Under isoflurane anaesthesia, the profound inhibitory effects of MK801 on CSD magnitude and susceptibility of the cortex to CSD ( Fig. 1 ) were consistent with those reported previously 24 25 ; (4) The fact that neither genesis nor propagation of CSD was altered in the control group yet was suppressed by NVP-AAM077, suggests that the suppression of CSD was due to NR2A inhibition, rather than to isoflurane.…”

Section: Discussionmentioning

confidence: 99%

NR2A contributes to genesis and propagation of cortical spreading depression in rats

et al. 2016

Sci Rep

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Cortical spreading depression (CSD) is a transient propagating excitation of synaptic activity followed by depression, which is implicated in migraine. Increasing evidence points to an essential role of NR2A-containing NMDA receptors in CSD propagation in vitro; however, whether these receptors mediate CSD genesis in vivo requires clarification and the role of NR2A on CSD propagation is still under debate. Using in vivo CSD in rats with electrophysiology and in vitro CSD in chick retina with intrinsic optical imaging, we addressed the role of NR2A in CSD. We demonstrated that NVP-AAM077, a potent antagonist for NR2A-containing receptors, perfused through microdialysis probes, markedly reduced cortex susceptibility to CSD, but also reduced magnitude of CSD genesis in rats. Additionally, NVP-AAM077 at 0.3 nmol perfused into the contralateral ventricle, considerably suppressed the magnitude of CSD propagation wave and propagation rate in rats. This reduction in CSD propagation was also observed with TCN-201, a negative allosteric modulator selective for NR2A, at 3 μM, in the chick retina. Our data provides strong evidence that NR2A subunit contributes to CSD genesis and propagation, suggesting drugs selectively antagonizing NR2A-containing receptors might constitute a highly specific strategy treating CSD associated migraine with a likely better safety profile.

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Section: Discussionmentioning

confidence: 99%

NR2A contributes to genesis and propagation of cortical spreading depression in rats

et al. 2016

Sci Rep

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“…At the end of the experiment, all rats were anesthetized by a thiopental sodium injection (50 mg/kg) [24] and decapited. The brains were washed in ice-cold saline, and the hippocampus was prepared as 300-μm slices using Vibratome 1000 Plus for the detection of S100β protein [25].…”

Section: Methodsmentioning

confidence: 99%

Effects of Intravenous Human Umbilical Cord Blood Mesenchymal Stem Cell Therapy versus Gabapentin in Pentylenetetrazole-Induced Chronic Epilepsy in Rats

Mohammed¹,

Ewais²,

Tawfik³

et al. 2014

Pharmacology

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Aim: The identification and application of stem cells to treat central nervous system disorders represent a dramatic evolution and expansion into the realms of neurorestoration and neuroregeneration. The aim of this study was to assess the possible ameliorative effect of mesenchymal stem cells (MSCs) in comparison to gabapentin on pentylenetetrazole (PTZ)-induced epileptogenesis and its consequences. Methods: Thirty-two rats were divided into 4 equal groups; group I: saline-injected group, group II: PTZ group, which received 13 intraperitoneal (i.p.) injections of PTZ (30 mg/kg) 3 times/week, groups III and IV: groups received PTZ and were treated with i.p. gabapentin (200 mg/kg) 60 min before each PTZ injection (group III) or a single intravenous injection of 10⁶ MSCs/rat at day 22 (group IV). Results: Treatment with either gabapentin or MSCs demonstrated a significant improvement in the PTZ-induced epileptogenesis and its severe consequences, i.e. oxidative stress damage, motor and cognitive impairments. Moreover, they enhanced the GABA neurotransmitter levels. Meanwhile, MSC administration to chronic epileptic rats afforded more ameliorative effects on PTZ-induced epileptogenesis and its severe consequences in comparison to gabapentin. Conclusion: These data indicate that MSCs were superior to gabapentin in ameliorating PTZ-induced epileptogenesis and verified the potential use of MSCs in seizure control, motor and cognitive impairments, oxidative stress, and the impairing GABA level in experimentally induced epilepsy.

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“…At the end of the study, rats were anesthetized with thiopental sodium (50 mg/kg) [23] and killed by decapitation. Blood samples were collected by cardiac puncture, centrifuged at 2000 rpm for 15 min within 30 min of collection and stored at -80°C until assayed.…”

Section: Blood Glucose Determination and Sample Collectionmentioning

confidence: 99%

Comparing the Effects of Inorganic Nitrate and Allopurinol in Renovascular Complications of Metabolic Syndrome in Rats: Role of Nitric Oxide and Uric Acid

Essawy¹

2012

Acta Endo (Buc)

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A b s t r a c tIntroduction: The epidemic of metabolic syndrome is increasing worldwide and correlates with elevation in serum uric acid and marked increase in total fructose intake. Fructose raises uric acid and the latter inhibits nitric oxide bioavailability. We hypothesized that fructose-induced hyperuricemia may have a pathogenic role in metabolic syndrome and treatment of hyperuricemia or increased nitric oxide may improve it. Material and methods: Two experiments were performed. Male Sprague-Dawley rats were fed a control diet or a high-fructose diet to induce metabolic syndrome. The latter received either sodium nitrate or allopurinol for 10 weeks starting with the 1 st day of fructose to evaluate the preventive role of the drugs or after 4 weeks to evaluate their therapeutic role. Results: A high-fructose diet was associated with significant (p < 0.05) hyperuricemia (5.9 ±0.5 mg/dl), hypertension (125.2 ±7.8 mm Hg), dyslipidemia and significant decrease in tissue nitrite (27.4 ±2.01 mmol/l). Insulin resistance, as manifested by HOMAIR (20.6 ±2.2) and QUICKI (0.23 ±0.01) indices, as well as adiposity index (12.9 ±1.1) was also significantly increased (p < 0.1). Sodium nitrate or allopurinol was able to reverse these features significantly (p < 0.05) in the preventive study better than the therapeutic study. Conclusions: Fructose may have a major role in the epidemic of metabolic syndrome and obesity due to its ability to raise uric acid. Either sodium nitrate or allopurinol can prevent this pathological condition by different mechanisms of action.

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Anesthesia and Analgesia

Cited by 27 publications

References 125 publications

NR2A contributes to genesis and propagation of cortical spreading depression in rats

NR2A contributes to genesis and propagation of cortical spreading depression in rats

Effects of Intravenous Human Umbilical Cord Blood Mesenchymal Stem Cell Therapy versus Gabapentin in Pentylenetetrazole-Induced Chronic Epilepsy in Rats

Comparing the Effects of Inorganic Nitrate and Allopurinol in Renovascular Complications of Metabolic Syndrome in Rats: Role of Nitric Oxide and Uric Acid

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