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Journal articles on the topic 'Ephedrine'

Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Ito, Kaori, Takashi Kikuchi, Kanako Ikube, Kouharu Otsuki, Kazuo Koike, and Wei Li. "LC-MS Profiling of Kakkonto and Identification of Ephedrine as a Key Component for Its Anti-Glycation Activity." Molecules 28, no. 11 (May 29, 2023): 4409. http://dx.doi.org/10.3390/molecules28114409.

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A total of 147 oral Kampo prescriptions, which are used clinically in Japan, were evaluated for their anti-glycation activity. Kakkonto demonstrated significant anti-glycation activity, prompting further analysis of its chemical constituents using LC-MS, which revealed the presence of two alkaloids, fourteen flavonoids, two but-2-enolides, five monoterpenoids, and four triterpenoid glycosides. To identify the components responsible for its anti-glycation activity, the Kakkonto extract was reacted with glyceraldehyde (GA) or methylglyoxal (MGO) and analyzed using LC-MS. In LC-MS analysis of Kakkonto reacted with GA, the peak intensity of ephedrine was attenuated, and three products from ephedrine-scavenging GA were detected. Similarly, LC-MS analysis of Kakkonto reacted with MGO revealed two products from ephedrine reacting with MGO. These results indicated that ephedrine was responsible for the observed anti-glycation activity of Kakkonto. Ephedrae herba extract, which contains ephedrine, also showed strong anti-glycation activity, further supporting ephedrine’s contribution to Kakkonto’s reactive carbonyl species’ scavenging ability and anti-glycation activity.

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Xiu, Li-Mei, Akira B. Miura, Kazuhiko Yamamoto, Takao Kobayashi, Qing-Hua Song, Hajime Kitamura, and Jong-Chol Cyong. "Pancreatic Islet Regeneration by Ephedrine in Mice with Streptozotocin-induced Diabetes." American Journal of Chinese Medicine 29, no. 03n04 (January 2001): 493–500. http://dx.doi.org/10.1142/s0192415x01000514.

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In this experiment, we investigated the effects of crude Ephedrae herba, alkaloid extract of Ephedrae herbal and 1-ephedrine, a major alkaloid component, on diabetic mice induced by streptozotocin (STZ). The alkaloid extract and 1-ephedrine showed suppression on the hyperglycemia. The suppression by Ephedrae herba of hyperglycemia may therefore be due to 1-ephedrine. Furthermore, we found that Ephedrae herba, alkaloid and 1-ephedrine promoted the regeneration of pancreas islets following atrophy induced by STZ. It is therefore suggested that Ephedrae herba may regenerate atrophied pancreatic islets, restore the secretion of insulin, and thus correct hyperglycemia.

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3

Kim, Eunjoo, Yun-Jin Lee, and Young-Woo Lim. "Narrative Review on the Safety of Mahuang and Ephedrine in the Treatment of Obesity: Focused on Liver." Nubebe Mibyeong Research Institute 5, no. 1 (May 31, 2024): 45–53. http://dx.doi.org/10.37928/kjsm.2024.5.1.45.

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Objectives The purpose of this study is to examine whether the use of Ephedrae herba and Ephedrine in obesity treatment is safe for the liver. Methods Toxicology studies and randomized controlled trials (RCTs) from systematic review (SR), meta-analysis related to Ephedrae herba or Ephedrine, which refer to liver function were collected through Pubmed and RISS databases. Results There were no findings that hepatotoxicity was induced by Ephedrae herba in the 2-week acute, 4-week subacute, and 13-week repeated administration toxicology studies. In the RCT studies of Ephedrae herba, Ephedrine, or herbal medicine including Ephedrae herba, there were no significant changes in liver function levels. Conclusions This study suggests that it is difficult to find clear evidence that Ephedrae herba and Ephedrine cause liver injury.

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4

Li, Yue-Chiun, Chia-Hung Wu, Thi Ha Le, Qingjun Yuan, Luqi Huang, Guo-Fen Chen, Mei-Lin Yang, et al. "A Modified 1H-NMR Quantification Method of Ephedrine Alkaloids in Ephedrae Herba Samples." International Journal of Molecular Sciences 24, no. 14 (July 10, 2023): 11272. http://dx.doi.org/10.3390/ijms241411272.

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A previous 1H-NMR method allowed the quantification of ephedrine alkaloids; however, there were some disadvantages. The cyclized derivatives resulted from the impurities of diethyl ether were identified and benzene was selected as the better extraction solvent. The locations of ephedrine alkaloids were confirmed with 2D NMR. Therefore, a specific 1H-NMR method has been modified for the quantification of ephedrine alkaloids. Accordingly, twenty Ephedrae Herba samples could be classified into three classes: (I) E. sinica-like species; (II) E. intermedia-like species; (III) others (lower alkaloid contents). The results indicated that ephedrine and pseudoephedrine are the major alkaloids in Ephedra plants, but the concentrations vary greatly determined by the plant species and the collection locations.

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5

Hung, Yu-Chun, Yi-Chuan Kau, Anthony M. Zizza, Thomas Edrich, David Zurakowski, Robert R. Myers, Ging Kuo Wang, and Peter Gerner. "Ephedrine Blocks Rat Sciatic Nerve In Vivo and Sodium Channels In Vitro." Anesthesiology 103, no. 6 (December 1, 2005): 1246–52. http://dx.doi.org/10.1097/00000542-200512000-00021.

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Background The sympathomimetic drug ephedrine has been used intrathecally as the sole local anesthetic for labor and delivery. Because ephedrine may be a useful adjuvant to local anesthetics, the authors investigated the local anesthetic properties of ephedrine in a rat sciatic nerve block model and the underlying mechanism in cultured cells stably expressing Na channels. Methods After approval of the animal protocol, the sciatic nerves of anesthetized rats were exposed by lateral incision of the thighs, 0.2 ml ephedrine at 0.25, 1, 2.5, or 5% and/or bupivacaine at 0.125% was injected, and the wound was closed. Motor and sensory/nociceptive functions were evaluated by the force achieved by pushing against a balance and the reaction to pinch, respectively. The whole cell configuration of the patch clamp technique was used to record Na currents from human embryonal kidney cells stably transfected with Nav1.4 channels. Results The nociception blockade was significantly longer than the motor blockade at test doses of 2.5 and 5% of ephedrine, or when 1% ephedrine was combined with 0.125% bupivacaine (analysis of variance with repeated measures, P < 0.001, n = 8/group). In vitro, the 50% inhibitory concentrations of ephedrine at -150 and -60 mV were 1,043 +/- 70 and 473 +/- 13 mum, respectively. High-frequency stimulation revealed a use-dependent block of 18%, similar to most local anesthetics. Conclusions Because ephedrine's properties are at least partly due to Na channel blockade, detailed histopathologic investigations are justified to determine the potential of ephedrine as an adjuvant to clinically used local anesthetics.

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6

Napolitano, Antonella, Peter R. Murgatroyd, Nick Finer, Elizabeth K. Hussey, Robert Dobbins, Steve O'Rahilly, and Derek J. R. Nunez. "Assessment of Acute and Chronic Pharmacological Effects on Energy Expenditure and Macronutrient Oxidation in Humans: Responses to Ephedrine." Journal of Obesity 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/210484.

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Evidence of active brown adipose tissue in human adults suggests that this may become a pharmacological target to induce negative energy balance. We have explored whole-body indirect calorimetry to detect the metabolic effects of thermogenic drugs through administration of ephedrine hydrochloride and have assessed ephedrine's merits as a comparator compound in the evaluation of novel thermogenic agents. Volunteers randomly given ephedrine hydrochloride 15 mg QID(n=8)or placebo(n=6)were studied at baseline and after 1-2 and 14-15 days of treatment. We demonstrate that overnight or 23-hour, 2% energy expenditure (EE) and 5% fat (FO) or CHO oxidation effects are detectable both acutely and over 14 days. Compared to placebo, ephedrine increased EE and FO rates overnight (EE 63 kJ day 2, EE 105 kJ, FO 190 kJ, day 14), but not over 23 h. We conclude that modest energy expenditure and fat oxidation responses to pharmacological interventions can be confidently detected by calorimetry in small groups. Ephedrine should provide reliable data against which to compare novel thermogenic compounds.

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7

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 713 (August 1998): 8. http://dx.doi.org/10.2165/00128415-199807130-00022.

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8

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 1356 (June 2011): 16. http://dx.doi.org/10.2165/00128415-201113560-00052.

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9

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 569 (September 1995): 7. http://dx.doi.org/10.2165/00128415-199505690-00016.

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10

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 591 (March 1996): 8. http://dx.doi.org/10.2165/00128415-199605910-00020.

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11

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 444 (March 1993): 7. http://dx.doi.org/10.2165/00128415-199304440-00024.

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12

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 652 (May 1997): 9. http://dx.doi.org/10.2165/00128415-199706520-00023.

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&NA;. "Ephedrine." Reactions Weekly &NA;, no. 675 (November 1997): 8. http://dx.doi.org/10.2165/00128415-199706750-00020.

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14

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 1409 (July 2012): 23. http://dx.doi.org/10.2165/00128415-201214090-00072.

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15

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 1198 (April 2008): 18. http://dx.doi.org/10.2165/00128415-200811980-00056.

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&NA;. "Ephedrine." Reactions Weekly &NA;, no. 1102 (May 2006): 8. http://dx.doi.org/10.2165/00128415-200611020-00023.

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&NA;. "Ephedrine." Reactions Weekly &NA;, no. 925 (October 2002): 7. http://dx.doi.org/10.2165/00128415-200209250-00019.

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18

&NA;. "Ephedrine." Reactions Weekly &NA;, no. 949 (May 2003): 11. http://dx.doi.org/10.2165/00128415-200309490-00042.

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&NA;. "Ephedrine." Reactions Weekly &NA;, no. 991 (March 2004): 8–9. http://dx.doi.org/10.2165/00128415-200409910-00022.

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&NA;. "Ephedrine." Reactions Weekly &NA;, no. 1001 (May 2004): 8. http://dx.doi.org/10.2165/00128415-200410010-00022.

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21

SHANNON, John R., Keith GOTTESDIENER, Jens JORDAN, Kong CHEN, Stacey FLATTERY, Patrick J. LARSON, Mari Rios CANDELORE, Barry GERTZ, David ROBERTSON, and Ming SUN. "Acute effect of ephedrine on 24-h energy balance." Clinical Science 96, no. 5 (April 14, 1999): 483–91. http://dx.doi.org/10.1042/cs0960483.

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Ephedrine is used to help achieve weight control. Data on its true efficacy and mechanisms in altering energy balance in human subjects are limited. We aimed to determine the acute effect of ephedrine on 24-h energy expenditure, mechanical work and urinary catecholamines in a double-blind, randomized, placebo-controlled, two-period crossover study. Ten healthy volunteers were given ephedrine (50 mg) or placebo thrice daily during each of two 24-h periods (ephedrine and placebo) in a whole-room indirect calorimeter, which accurately measures minute-by-minute energy expenditure and mechanical work. Measurements were taken of 24-h energy expenditure, mechanical work, urinary catecholamines and binding of (±)ephedrine in vitro to human β1-, β2- and β3-adrenoreceptors. Twenty-four-hour energy expenditure was 3.6% greater (8965±1301 versus 8648±1347 kJ, P< 0.05) with ephedrine than with placebo, but mechanical work was not different between the ephedrine and placebo periods. Noradrenaline excretion was lower with ephedrine (0.032±0.011 μg/mg creatinine) compared with placebo (0.044±0.012 μg/mg creatinine) (P< 0.05). (±)Ephedrine is a relatively weak partial agonist of human β1- and β2-adrenoreceptors, and had no detectable activity at human β3-adrenoreceptors. Ephedrine (50 mg thrice daily) modestly increases energy expenditure in normal human subjects. A lack of binding of ephedrine to β3-adrenoreceptors and the observed decrease in urinary noradrenaline during ephedrine treatment suggest that the thermogenic effect of ephedrine results from direct β1-/β2-adrenoreceptor agonism. An indirect β3-adrenergic effect through the release of noradrenaline seems unlikely as urinary noradrenaline decreased significantly with ephedrine.

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22

Tianqi, Wu. "A Comprehensive Review of Ephedrine Analogues: Varieties, Abuse and Synthesis Methodologies." Journal of Medicine and Health Science 2, no. 1 (March 2024): 96–100. http://dx.doi.org/10.62517/jmhs.202405117.

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Ephedrine analogues include ephedrine and its derivatives, which can be categorized into natural and synthetic types depending on their sources. Natural analogues primarily originate from Ephedra plants such as ephedrine, pseudoephedrine, norephedrine, norpseudoephedrine, methylephedrine and methylpseudoephedrine. Synthetic analogues are obtained through chemical modifications to achieve specific purposes. The review delves into the abuse issues and potential hazards associated with ephedrine analogues, introduces various methods ranging from traditional extraction techniques of ephedrine analogues to modern chemical and biosynthesis technologies. This aids researchers, regulatory bodies, and the public in better understanding the sources and applications of ephedrine and its analogues, providing an important reference for subsequent research and regulation of ephedrine analogues.

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23

Mercier, Frédéric J., Edward T. Riley, Willard L. Frederickson, Sandrine Roger-Christoph, Dan Benhamou, and Sheila E. Cohen. "Phenylephrine Added to Prophylactic Ephedrine Infusion during Spinal Anesthesia for Elective Cesarean Section." Anesthesiology 95, no. 3 (September 1, 2001): 668–74. http://dx.doi.org/10.1097/00000542-200109000-00020.

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Background Because ephedrine infusion (2 mg/min) does not adequately prevent spinal hypotension during cesarean delivery, the authors investigated whether adding phenylephrine would improve its efficacy. Methods Thirty-nine parturients with American Society of Anesthesiologists physical status I-II who were scheduled for cesarean delivery received a crystalloid preload of 15 ml/kg. Spinal anesthesia was performed using 11 mg hyperbaric bupivacaine, 2.5 microg sufentanil, and 0.1 mg morphine. Maternal heart rate and systolic blood pressure were measured at frequent intervals. A vasopressor infusion was started immediately after spinal injection of either 2 mg/min ephedrine plus 10 microg/min phenylephrine or 2 mg/min ephedrine alone. Treatments were assigned randomly in a double-blind fashion. The infusion rate was adjusted according to systolic blood pressure using a predefined algorithm. Hypotension, defined as systolic blood pressure less than 100 mmHg and less than 80% of baseline, was treated with 6 mg ephedrine bolus doses. Results Hypotension occurred less frequently in the ephedrine-phenylephrine group than in the ephedrine-alone group: 37% versus 75% (P = 0.02). Ephedrine (36+/-16 mg, mean +/- SD) plus 178+/-81 microg phenylephrine was infused in former group, whereas 54+/-18 mg ephedrine was infused in the latter. Median supplemental ephedrine requirements and nausea scores (0-3) were less in the ephedrine-phenylephrine group (0 vs. 12 mg, P = 0.02; and 0 vs. 1.5, P = 0.01, respectively). Umbilical artery pH values were significantly higher in the ephedrine-phenylephrine group than in the group that received ephedrine alone (7.24 vs. 7.19). Apgar scores were similarly good in both groups. Conclusion Phenylephrine added to an infusion of ephedrine halved the incidence of hypotension and increased umbilical cord pH.

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Li, Qunxian, Jing Wu, Lixian Huang, Bo Zhao, and Qingbin Li. "Ephedrine ameliorates cerebral ischemia injury via inhibiting NOD-like receptor pyrin domain 3 inflammasome activation through the Akt/GSK3β/NRF2 pathway." Human & Experimental Toxicology 40, no. 12_suppl (October 29, 2021): S540—S552. http://dx.doi.org/10.1177/09603271211052981.

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Ischemic stroke is a leading cause of death and long-term disability worldwide. The aim of this study is to explore the potential function of ephedrine in ischemic stroke and the underlying molecular mechanism. A middle cerebral artery occlusion (MCAO) rat model was established. The potential effects of ephedrine on MCAO rats and LPS-stimulated BV2 microglial cells were evaluated. Ephedrine reduced the infarct volume, cell apoptosis, brain water content, neurological score, and proinflammatory cytokines (TNF-α and IL-1β) production in MCAO rats. Ephedrine treatment also suppressed TNF-α and IL-1β production and NOD-like receptor pyrin domain 3 (NLRP3) inflammasome activation in BV2 microglial cells. The expression of NLRP3, caspase-1, and IL-1β was suppressed by ephedrine. Moreover, ephedrine treatment increased the phosphorylation of Akt and GSK3β and nuclear NRF2 levels in LPS-treated BV2 microglial cells. Meanwhile, LY294002 attenuated the inhibitory effects of ephedrine on NLRP3 inflammasome activation and TNF-α and IL-1β production. In addition, the level of pAkt was increased, while NLRP3, caspase-1, and IL-1β were decreased by ephedrine treatment in MCAO rats. In conclusion, ephedrine ameliorated cerebral ischemia injury via inhibiting NLRP3 inflammasome activation through the Akt/GSK3β/NRF2 pathway. Our results revealed a potential role of ephedrine in ischemic stroke treatment.

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Moon, Sohyeon, and Hee Jung Baik. "Aminophylline and Ephedrine, but Not Flumazenil, Inhibit the Activity of the Excitatory Amino Acid Transporter 3 Expressed in Xenopus Oocytes and Reverse the Increased Activity by Propofol." BioMed Research International 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/6817932.

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We investigated the effects of flumazenil, aminophylline, and ephedrine on the excitatory amino acid transporter type 3 (EAAT3) activity and the interaction with propofol. EAAT3 was expressed in the Xenopus oocytes. L-Glutamate-induced membrane currents were measured using the two-electrode voltage clamp at various drug concentrations. Oocytes were preincubated with protein kinase C- (PKC-) activator, or inhibitor, and phosphatidylinositol 3-kinase (PI3K) inhibitor. To study the interaction with propofol, oocytes were exposed to propofol, propofol + aminophylline, or ephedrine. Aminophylline and ephedrine significantly decreased EAAT3 activity. Aminophylline (95 μM) and ephedrine (1.19 μM) significantly decreased Vmax, but not Km of EAAT3, for glutamate. The phorbol 12-myristate-13-acetate-induced increase in EAAT3 activity was abolished by aminophylline or ephedrine. The decreased EAAT3 activities by PKC inhibitors (staurosporine, chelerythrine) and PI3K inhibitor (wortmannin) were not significantly different from those by aminophylline or ephedrine, as well as those by PKC inhibitors or PI3K inhibitor + aminophylline or ephedrine. The enhanced EAAT3 activities induced by propofol were significantly abolished by aminophylline or ephedrine. Aminophylline and ephedrine inhibit EAAT3 activity via PKC and PI3K pathways and abolish the increased EAAT3 activity by propofol. Our results indicate a novel site of action for aminophylline and ephedrine.

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26

Pravalika, P., G. Jephthah, A. Raja Reddy, and T. Rama Rao. "METHOD DEVELOPMENT AND VALIDATION OF UV SPECTROSCOPY FOR THE ESTIMATION OF EPHEDRINE HYDROCHLORIDE IN BULK AND PHARMACEUTICAL FORMULATION." Journal of Advanced Scientific Research 14, no. 10 (November 30, 2023): 1–4. http://dx.doi.org/10.55218/jasr.2023141001.

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Development and validation of simple, rapid, accurate, precise and sensitive UV-Spectrophotometric method for the estimation of Ephedrine hydrochloride in bulk drug and Injection dosage form was performed in the current research. Quantitative determination of Ephedrine hydrochloride was done using distilled water as a solvent. λmax of Ephedrine hydrochloride in distilled water was measured at 270 nm. Linearity range for Ephedrine hydrochloride was 2-10 μg/mL and coefficient of correlation for Ephedrine hydrochloride was 0.999. Accuracy was performed and the percentage recovery of Ephedrine hydrochloride was found to be in the range of 98.6-99.17. The % relative standard deviation (RSD) for precision was less than 2%, LOD & LOQ was 0.079 μg/mL and 0.24 μg/mL respectively. The results suggest that method can be employed for routine analysis of Ephedrine hydrochloride in bulk drug and in pharmaceutical Dosage form.

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BLAU, JEFFREY J. "EPHEDRINE NEPHROLITHIASIS ASSOCIATED WITH CHRONIC EPHEDRINE ABUSE." Journal of Urology 160, no. 3 Part 1 (September 1998): 825. http://dx.doi.org/10.1016/s0022-5347(01)62796-4.

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Ngan Kee, Warwick D., Kim S. Khaw, Perpetua E. Tan, Floria F. Ng, and Manoj K. Karmakar. "Placental Transfer and Fetal Metabolic Effects of Phenylephrine and Ephedrine during Spinal Anesthesia for Cesarean Delivery." Anesthesiology 111, no. 3 (September 1, 2009): 506–12. http://dx.doi.org/10.1097/aln.0b013e3181b160a3.

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Background Use of ephedrine in obstetric patients is associated with depression of fetal acid-base status. The authors hypothesized that the mechanism underlying this is transfer of ephedrine across the placenta and stimulation of metabolism in the fetus. Methods A total of 104 women having elective Cesarean delivery under spinal anesthesia randomly received infusion of phenylephrine (100 microg/ml) or ephedrine (8 mg/ml) titrated to maintain systolic blood pressure near baseline. At delivery, maternal arterial, umbilical arterial, and umbilical venous blood samples were taken for measurement of blood gases and plasma concentrations of phenylephrine, ephedrine, lactate, glucose, epinephrine, and norepinephrine. Results In the ephedrine group, umbilical arterial and umbilical venous pH and base excess were lower, whereas umbilical arterial and umbilical venous plasma concentrations of lactate, glucose, epinephrine, and norepinephrine were greater. Umbilical arterial Pco2 and umbilical venous Po2 were greater in the ephedrine group. Placental transfer was greater for ephedrine (median umbilical venous/maternal arterial plasma concentration ratio 1.13 vs. 0.17). The umbilical arterial/umbilical venous plasma concentration ratio was greater for ephedrine (median 0.83 vs. 0.71). Conclusions Ephedrine crosses the placenta to a greater extent and undergoes less early metabolism and/or redistribution in the fetus compared with phenylephrine. The associated increased fetal concentrations of lactate, glucose, and catecholamines support the hypothesis that depression of fetal pH and base excess with ephedrine is related to metabolic effects secondary to stimulation of fetal beta-adrenergic receptors. Despite historical evidence suggesting uteroplacental blood flow may be better maintained with ephedrine, the overall effect of the vasopressors on fetal oxygen supply and demand balance may favor phenylephrine.

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Chen, Dan, Feng Ma, Xiao-hui Liu, Rui Cao, and Xiong-Zhi Wu. "ANTI-TUMOR EFFECTS OF EPHEDRINE AND ANISODAMINE ON SKBR3 HUMAN BREAST CANCER CELL LINE." African Journal of Traditional, Complementary and Alternative Medicines 13, no. 1 (December 3, 2015): 25–32. http://dx.doi.org/10.21010/ajtcam.v13i1.4.

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Background: To investigate the effects of ephedrine and anisodamine on the proliferation of human breast cancer. Materials and Methods: SKBR3 cell was treated with or without ephedrine and / or anisodamine, respectively. The trypan blue exclusion assay was used to determine cell numbers. Flow cytometry was used to assess cell cycle distribution and apoptosis. The concentration of cAMP and cyclin D1 was analyzed by enzyme-linked immunosorbent assay. Western blot was used to measure PKA. Results: Ephedrine and anisodamine inhibited cell proliferation and arrested SKBR3 cells at G0/G1 phases. Ephedrine and anisodamine increased the level of CD1 in SKBR3 cells. Furthermore, significant change in intracellular cAMP concentration was found in SKBR3 cells treated with ephedrine and anisodamine. The phosphorylation of PKA substrate was not activated after 48 hours of treatment with ephedrine and anisodamine. Conclusion: Ephedrine and anisodamine inhibit the proliferation of SKBR3 cells via a significantly change of intracellular cAMP concentration.

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Wen, S., and T. Liao. "Ephedrine causes liver toxicity in SD rats via oxidative stress and inflammatory responses." Human & Experimental Toxicology 40, no. 1 (July 30, 2020): 16–24. http://dx.doi.org/10.1177/0960327120943938.

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Ephedrine abuse has spread in many parts of the world and severely threatens human health. The mechanism of ephedrine-induced toxicity still remains unclear. This study was performed to investigate the effects of ephedrine treatment on the liver and explore the underlying mechanisms. Sprague Dawley rats were divided into saline and ephedrine groups. Rats were treated with ephedrine at 20 mg/kg or 40 mg/kg ( n = 10) by oral gavage daily for 7 days. Pathological changes were examined by hematoxylin and eosin staining and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling assay. Enzyme-linked immunosorbent assays were used to measure the liver functional markers, oxidative stress markers, and inflammatory cytokines. Real-time polymerase chain reaction and Western blot were used to measure gene and protein expression, respectively. Our data showed that ephedrine treatment increased hepatocellular cell apoptosis and impaired liver function. Moreover, ephedrine treatment increased oxidative stress and inflammatory responses, which may be due to the increase of transforming growth factor β (TGF-β)/Smad3 expression. Our study demonstrated that short-term treatment of ephedrine caused liver toxicity in rats through regulating TGF-β/Smad pathway.

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Guimarães, A. E., M. T. T. Pacheco, L. Silveira Jr., D. Barsottini, J. Duarte, A. B. Villaverde, and R. A. Zângaro. "Near Infrared Raman Spectroscopy (NIRS): A technique for doping control." Spectroscopy 20, no. 4 (2006): 185–94. http://dx.doi.org/10.1155/2006/328210.

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This paper reports the application of near-infrared Raman spectroscopy to detect ephedrine in biological medium. At present time, the doping control for ephedrine in athletes uses the urinalysis by the gas chromatography/mass spectrometry, with main disadvantage the need of collecting urine and the time delay to obtain results. This work aims to develop a noninvasive technique that will allow to evaluate the concentration of the ephedrine in a real time diagnosis. A Raman system composed by a Ti:Saphire laser pumped by an Argon laser was used, operating at the wavelength of 785 nm, with a laser power of 70 mW at sample position. Raman scattered photons were collected by a f/l.8 spectrometer and a N2-cooled CCD detector. Ephedrine Raman peaks at 1002 and 1603 cm−1were studied, opening possibility for the identification and quantification of ephedrine. Raman spectra of ephedrine with different concentrations in human urine were taken, and the intensity of the ephedrine peak at 1002 cm−1was measured as a function of its concentration. It was also studied the Raman spectrum of an urine sample from a Wistar rat, after a subcutaneous inoculation of an ephedrine solution in physiologic serum, at the concentration of 5 mg/ml. It was found that Raman spectroscopy could detect ephedrine in urine at concentrations lower than the doping limit legally permitted by the International Olympic Committee.

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Cooper, David W., Mark Carpenter, Paul Mowbray, William R. Desira, David M. Ryall, and Manmohan S. Kokri. "Fetal and Maternal Effects of Phenylephrine and Ephedrine during Spinal Anesthesia for Cesarean Delivery." Anesthesiology 97, no. 6 (December 1, 2002): 1582–90. http://dx.doi.org/10.1097/00000542-200212000-00034.

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Background In our routine practice, we observed a reduced incidence of fetal acidosis (umbilical artery pH < 7.20) at cesarean delivery during spinal anesthesia when a combination of phenylephrine and ephedrine was used as first line vasopressor therapy, compared with using ephedrine alone. Methods The study was randomized and double blind. It compared phenylephrine 100 microg/ml (phenylephrine group), ephedrine 3 mg/ml (ephedrine group), and phenylephrine 50 microg/ml combined with ephedrine 1.5 mg/ml (combination group), given by infusion, to maintain maternal systolic arterial pressure at baseline during spinal anesthesia for elective cesarean delivery. Results Fetal acidosis was less frequent in the phenylephrine group (1 of 48) (P = 0.004) and less frequent in the combination group (1 of 47) (P = 0.005) than in the ephedrine group (10 of 48). The mean systolic arterial pressure was similar for the three groups: Phenylephrine group median 98% (IQR 94-103) of baseline, ephedrine group 100% (96-106) and combination group 101% (97-108) (P = 0.11). The mean heart rate was higher in the ephedrine group (median 107% [IQR 99-118] of baseline) than in the phenylephrine group (88% [82-98]) (P < 0.0001), or the combination group (96% [86-102]) (P < 0.0001). Nausea and vomiting were less frequent in the phenylephrine group (nausea 17%, vomiting 0%) than in the ephedrine group (nausea 66%, vomiting 36%) (P < 0.0001), or the combination group (nausea 55%, vomiting 18%) (P < 0.0001). Conclusions Giving phenylephrine alone by infusion at cesarean delivery was associated with a lower incidence of fetal acidosis and maternal nausea and vomiting than giving ephedrine alone. There was no advantage to combining phenylephrine and ephedrine because it increased nausea and vomiting, and it did not further improve fetal blood gas values, compared with giving phenylephrine alone.

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FARIDI, MANZOOR AHMED, and IRBAZ BIN RIAZ. "SPINAL ANAESTHESIA FOR CESAREAN DELIVERY." Professional Medical Journal 17, no. 04 (December 10, 2010): 648–53. http://dx.doi.org/10.29309/tpmj/2010.17.04.3015.

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Objective: To determine the effective dose of intravenous ephedrine for the prevention of hypotension during spinal anesthesia for cesarean delivery. Design: A randomized, double-blinded dose finding study. Place and Duration: The study was carried out in Combined Military Hospital Gujranwala from March 2009 to March 2010. Methodology: Total patients were 80 full term women who were randomly allocated into four groups and were given Ringer lactate 10 ml per kg body weight intravenously. One minute after the spinal injection, patients were given saline control or ephedrine 0.1mg per kg body weight, 0.25mg per kg body weight, or 0.4mg per kg body weight for 30 seconds. The study period started at the time of spinal injection and continued for 15 minutes. Systolic arterial pressure and heart rate were recorded at 1-minintervals. Side effects like hypotension, hypertension, tachycardia, bradycardia, nausea and vomiting were also recorded. Total rescue ephedrine and total dose of used ephedrine in all groups were measured. Neonates were assessed by APGAR score. Results: There was less incidence of hypotension in the ephedrine 0.4mg per kg body weight and 0.25 mg per kg body weight group as compared with ephedrine 0.1mgper kg body weight and the control group, 5(25%),13(65%) vs. 16(80%), 18 (90%) respectively. Systolic arterial pressure (SAP) in the first 15 min after the spinal injection was statistically significant greater in the 0.4mg per kg body weight group compared with other groups (P <0.001). Reactive hypertension occurred in 9(45%) in the 0.4mg per kg group, compared with control group, 0(0%), ephedrine 0.1 mg, 1(5%) andephedrine 0.25 mg 3(15%) patients. The Heart rate in the first 15 minutes in the ephedrine 0.4mg per kg body weight and 0.25 mg per kg body weight group was statistically significant higher than those of ephedrine 0.1mg per kg body weight and control group (P<0.001). The incidence of tachycardia was more in ephedrine 0.4 mg per kg body weight and 0.25 mg per kg body weight groups as compared to ephedrine 0.1mg perkg body weight and the control group, 9 (45%), 6 (30%) vs. 3 (15%), 2 (10%) respectively. There were significant decrease in total doses of rescue ephedrine required in the ephedrine0.4mg per kg body weight group as compared to other three groups. Total doses of used ephedrine in all groups were similar. Conclusion: We conclude that although ephedrine 0.25 mg per kg body weight reduces the hypotension but the smallest effective dose of ephedrine to reduce the incidence of hypotension significantly was 0.4mg per kg body weight.

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Ducros, Laurent, Philippe Bonnin, Bernard P. Cholley, Eric Vicaut, Moncef Benayed, Denis Jacob, and Didier Payen. "Increasing Maternal Blood Pressure with Ephedrine Increases Uterine Artery Blood Flow Velocity during Uterine Contraction." Anesthesiology 96, no. 3 (March 1, 2002): 612–16. http://dx.doi.org/10.1097/00000542-200203000-00017.

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Background During labor, ephedrine is widely used to prevent or to treat maternal arterial hypotension and restore uterine perfusion pressure to avoid intrapartum fetal asphyxia. However, the effects of ephedrine on uterine blood flow have not been studied during uterine contractions. The purpose of the study was to assess the effects of ephedrine on uterine artery velocities and resistance index using the Doppler technique during the active phase of labor. Methods Ten normotensive, healthy parturients with uncomplicated pregnancies at term received intravenous ephedrine during labor to increase mean arterial pressure up to a maximum of 20% above their baseline pressure. Peak systolic and end-diastolic Doppler flow velocities and resistance indices were measured in the uterine artery before and immediately after administration of bolus intravenous ephedrine and after ephedrine washout. Umbilical and fetal middle cerebral arterial resistance indices and fetal heart rate were also calculated. Results After ephedrine administration, mean arterial pressure increased by 17 +/- 4%. End-diastolic flow velocity in the uterine artery at peak amplitude of uterine contraction was restored to 74% of the value observed in the absence of contraction. The systolic velocity was totally restored, and the uterine resistance index was significantly decreased, compared with the values in the absence of contraction. Between uterine contractions, ephedrine induced similar but less marked effects. Fetal hemodynamic parameters were not altered by ephedrine administration. Conclusions Bolus administration of intravenous ephedrine reversed the dramatic decrease in diastolic uteroplacental blood flow velocity and the increase in resistance index during uterine contraction, without altering fetal hemodynamic parameters. This suggests that the increase in uterine perfusion pressure during labor could in part restore uterine blood flow to the placenta during uterine contraction.

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CHOHEDRI, ABDUL-HAMEED, SHAHRBANO SHAHBAZI, L. KHOJESTE, and Elahe Alahyari. "EPHEDRINE FOR PREVENTION HYPOTENSION." Professional Medical Journal 14, no. 04 (October 12, 2007): 610–15. http://dx.doi.org/10.29309/tpmj/2007.14.04.4817.

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Background/Aim:. To ameliorate post spinal anesthesia hypotensionin patients undergoing cesarean section. To compare the incidence of maternal hypotension associated withspinal anesthesia for cesarean section when intravenous (IV), intramuscular (IM) or oral prophylactic boluses ofephedrine were used. Design: Prospective randomized double blind study. Setting: Department of anesthesiology,Zainibiae Hospital, Shiraz University, Iran. Period: From: June 2004 to November 2005. Materials and Methods:60 ASA grade I-II pregnant mothers were enrolled. Spinal anesthesia was performed using 60-70 mg of 5% solutionof lidocaine. The patients were divided into three equal groups (n=20). Oral and IM ephedrine (25 mg) wasadministered to the first two groups 30 to 60 minutes before induction of anesthesia (Group A and B, respectively). Inthe last 20 patients, IV Ephedrine (25 mg) was administered immediately after induction of spinal anesthesia (GroupC). Maternal blood pressure and pulse rate was checked every 2 minutes. Hypotension was promptly treated with 10-mg ephedrine boluses. Results: Both IM and IV prophylactic doses of ephedrine significantly decreased the incidenceof hypotension, compared to oral prophylactic dose of ephedrine [4/20 and 0/20 in the IM and IV ephedrine groups,respectively vs. 9/20 in the oral ephedrine group (p < 0.05)]. Conclusion: Oral prophylactic dose of ephedrine is noteffective in preventing hypotension in pregnant women undergoing cesarean section with spinal anesthesia. Therefore,we only recommend a single bolus of IV ephedrine with a dose of 25mg.

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Yoo, Hee-Jeong, Ha-Young Yoon, Jeong Yee, and Hye-Sun Gwak. "Effects of Ephedrine-Containing Products on Weight Loss and Lipid Profiles: A Systematic Review and Meta-Analysis of Randomized Controlled Trials." Pharmaceuticals 14, no. 11 (November 22, 2021): 1198. http://dx.doi.org/10.3390/ph14111198.

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Ephedrine, the main active ingredient of mahuang, may lead to weight loss; however, it can also induce cardiovascular side effects. As ephedrine use remains controversial, this study aimed to systematically review previous studies on ephedrine-containing products and perform meta-analysis of the existing evidence on weight, blood pressure (BP), heart rate, and lipid change effects of ephedrine-containing products. We searched for placebo-controlled randomized studies in PubMed, Web of Science, and EMBASE until July 2021 using the following search terms: (ephedr* OR mahuang) AND (“weight loss” OR obes* OR overweight). Mean differences (MDs) and 95% confidence intervals (CIs) were calculated to evaluate the effects of ephedrine-containing products on weight, BP, heart rate, and lipid profiles. A total of 10 articles were included. Compared with the placebo group, the ephedrine-containing product group was associated with greater weight loss, with an MD of −1.97 kg (95% CI: −2.38, −1.57). In the ephedrine-containing product group, the mean heart rate was 5.76 beats/min higher than in the placebo group (95% CI: 3.42, 8.10), whereas intergroup differences in systolic and diastolic BP were not statistically significant. The ephedrine-containing product group had a significantly higher mean high-density lipoprotein cholesterol level (MD: 2.74 mg/dL; 95% CI: 0.94, 4.55), lower mean low-density lipoprotein cholesterol level (MD: −5.98 mg/dL; 95% CI: −10.97, −0.99), and lower mean triglyceride level (MD: −11.25 mg/dL; 95% CI: −21.83, −0.68) than the placebo group. Compared with placebo, the ephedrine-containing products showed better effects on weight loss and lipid profiles, whereas they caused increased heart rate. The ephedrine-containing products may be beneficial to obese or overweight patients; however, close monitoring is needed, especially heart rate monitoring.

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Li, Jun, Barbara A. French, Paul Fu, Fawzia Bardag-Gorce, and Samuel W. French. "Mechanism of the alcohol cyclic pattern: role of catecholamines." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 2 (August 2003): G442—G448. http://dx.doi.org/10.1152/ajpgi.00093.2003.

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The cause of the urinary alcohol level (UAL) cycle in rats fed ethanol at a constant rate has been shown to involve the hypothalamic-pituitary thyroid axis. Because the effect of thyroid hormone on the metabolic rate is augmented by catecholamines, the role of catecholamines was investigated by using the intragastric ethanol feeding model of alcoholic liver disease in which the UAL cycles over a 6- to 10-day period. The diet was supplemented with ephedrine and caffeine to test the hypothesis that the UAL cycle involves catecholamines. The UAL was followed to see whether the cycle was ablated by catecholamine supplements. Ethanol fed alone increased the blood levels of catecholamines significantly more than did ephedrine fed alone. However, blood catecholamine levels were significantly higher when ethanol was fed with ephedrine compared with the sum of ethanol and ephedrine fed alone. This indicated that the effect of ethanol and ephedrine were synergistic. The UAL cycle was completely ablated in the ethanol + ephedrine-fed rats. These rats tolerated a much higher dose of ethanol, indicating that they metabolized alcohol faster due to an increase in metabolic rate caused by ephedrine. In the ethanol + ephedrine-fed rats the liver pathology included significantly higher alanine amino transferase (ALT) in the blood and centrilobular ischemic necrosis in the liver. Necrosis was not present in the rats fed ephedrine alone. In conclusion, catecholamine supplements prevented the UAL cycle by increasing the metabolic rate to the point at which fluctuations in the metabolic rate caused by alcohol were prevented.

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&NA;. "Ephedrine abuse." Reactions Weekly &NA;, no. 1132 (December 2006): 8–9. http://dx.doi.org/10.2165/00128415-200611320-00022.

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&NA;. "Ephedrine/phenylephrine." Reactions Weekly &NA;, no. 1373 (October 2011): 14–15. http://dx.doi.org/10.2165/00128415-201113730-00047.

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&NA;. "Ephedrine abuse." Reactions Weekly &NA;, no. 465 (August 1993): 7. http://dx.doi.org/10.2165/00128415-199304650-00028.

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&NA;. "Ephedrine/pseudoephedrine." Reactions Weekly &NA;, no. 650 (May 1997): 8. http://dx.doi.org/10.2165/00128415-199706500-00023.

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&NA;. "Ephedrine abuse." Reactions Weekly &NA;, no. 671 (October 1997): 9. http://dx.doi.org/10.2165/00128415-199706710-00020.

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&NA;. "Ephedrine overdose." Reactions Weekly &NA;, no. 418 (September 1992): 7. http://dx.doi.org/10.2165/00128415-199204180-00021.

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&NA;. "Ephedrine/metaraminol." Reactions Weekly &NA;, no. 1258 (June 2009): 15. http://dx.doi.org/10.2165/00128415-200912580-00050.

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&NA;. "Ephedrine/epinephrine." Reactions Weekly &NA;, no. 1239 (February 2009): 14. http://dx.doi.org/10.2165/00128415-200912390-00038.

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&NA;. "Ephedrine abuse." Reactions Weekly &NA;, no. 1255 (June 2009): 16. http://dx.doi.org/10.2165/00128415-200912550-00044.

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&NA;. "Ephedrine/xanthines." Reactions Weekly &NA;, no. 337 (February 1991): 5. http://dx.doi.org/10.2165/00128415-199103370-00027.

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&NA;. "Caffeine/ephedrine." Reactions Weekly &NA;, no. 1315 (August 2010): 16. http://dx.doi.org/10.2165/00128415-201013150-00047.

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&NA;. "Ephedrine abuse." Reactions Weekly &NA;, no. 1318 (September 2010): 20. http://dx.doi.org/10.2165/00128415-201013180-00064.

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&NA;. "Ephedrine overdose." Reactions Weekly &NA;, no. 1006 (June 2004): 9. http://dx.doi.org/10.2165/00128415-200410060-00021.

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