Log in

Relevant bibliographies by topics / Pharmacology, Epinephrine / Journal articles

Journal articles on the topic 'Pharmacology, Epinephrine'

To see the other types of publications on this topic, follow the link: Pharmacology, Epinephrine.

Author: Grafiati

Published: 10 March 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Pharmacology, Epinephrine.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Anwarul Haque, Hassaan Sadiq, and Muhammad Abdullah. "Epinephrine in Paediatric Clinical Practice - Clinical Update." ANNALS OF ABBASI SHAHEED HOSPITAL AND KARACHI MEDICAL & DENTAL COLLEGE 22, no. 1 (March 31, 2017): 64–69. http://dx.doi.org/10.58397/ashkmdc.v22i1.99.

Full text

Abstract:

Epinephrine is a "friend of the doctor" because it is a life-saving drug used in the rescue of patients at difficult times when other things do not help. It is widely used in paediatric emergency and paediatric intensive care units. This short commentary on pharmacology provides a clinical update about the use of epinephrine in paediatric clinical practice. The first part of this article briefly reviews the clinical pharmacology and the second part describes the clinical indications and adverse effects of epinephrine.

APA, Harvard, Vancouver, ISO, and other styles

2

Bingemann, Theresa A., Anil Nanda, and Anne F. Russell. "Pharmacology Update: School Nurse Role and Emergency Medications for Treatment of Anaphylaxis." NASN School Nurse 36, no. 5 (June 8, 2021): 264–70. http://dx.doi.org/10.1177/1942602x211021902.

Full text

Abstract:

Anaphylaxis is a rapidly occurring allergic reaction that is potentially life threatening. Recognition of the early signs and prompt treatment of anaphylaxis is critical. School nurses are tasked with educating nonmedical school personnel on the recognition and treatment of anaphylaxis and emphasizing that epinephrine is the first line of treatment for anaphylaxis. Fortunately, there is now availability of multiple epinephrine administration devices. However, this also means that there are more devices that school nurses and nonmedical assistive personnel need to learn about to be able to administer in an emergency. Once epinephrine is administered, emergency medical services must be activated. Education regarding what to expect after the administration of epinephrine with respect to side effects and onset of action is also necessary. Though adjunctive medicines, such as antihistamines and inhalers, may also be administered after the injection of epinephrine, they should not be solely relied on in anaphylaxis. School nurses are uniquely situated for this role, as they understand the local environment in a school and can assess and reassess the needs of the faculty and staff.

APA, Harvard, Vancouver, ISO, and other styles

3

Pupo, Andre S., and Kenneth P. Minneman. "Adrenergic Pharmacology: Focus on the Central Nervous System." CNS Spectrums 6, no. 8 (August 2001): 656–62. http://dx.doi.org/10.1017/s1092852900001346.

Full text

Abstract:

ABSTRACTNorepinephrine and epinephrine are involved in the control of several important functions of the central nervous system (CNS), including sleep, arousal, mood, appetite, and autonomic outflow. Catecholamines control these functions through activation of a family of adrenergic receptors (ARs). The ARs are divided into three subfamilies (α1, α2, and β) based on their pharmacologic properties, signaling mechanisms, and structure. ARs in the CNS are targets for several therapeutic agents used in the treatment of depression, obesity, hypertension, and other diseases. Not much is known, however, about the role of specific AR sub-types in the actions of these drugs. In this paper, we provide an overview of adrenergic pharmacology in the CNS, focusing on the pharmacologic properties of subtype-selective AR agonists and antagonists, the accessibility of these drugs to the CNS, and the distribution of ARs in different areas of the brain.

APA, Harvard, Vancouver, ISO, and other styles

4

Sneader, W. "Epinephrine analogues." Drug News & Perspectives 14, no. 9 (2001): 539. http://dx.doi.org/10.1358/dnp.2001.14.9.858410.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Warren, J. B., N. Doble, N. Dalton, and P. W. Ewan. "Systemic absorption of inhaled epinephrine." Clinical Pharmacology and Therapeutics 40, no. 6 (December 1986): 673–78. http://dx.doi.org/10.1038/clpt.1986.243.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Allen, Elizabeth M., Don H. Van Boerum, Alice F. Olsen, and J. Michael Dean. "Difference Between the Measured and Ordered Dose of Catecholamine Infusions." Annals of Pharmacotherapy 29, no. 11 (November 1995): 1095–100. http://dx.doi.org/10.1177/106002809502901104.

Full text

Abstract:

Objective: To measure the actual concentrations of dopamine, dobutamine, and epinephrine in infusates prepared for patients, and to compare these concentrations with those of the dopamine HCl, dobutamine, and epinephrine HCl infusates that had been prescribed to evaluate drug preparation accuracy. Design: Prospective, unblind study. Setting: Pediatric intensive care unit in a tertiary-care teaching hospital. Participants: All dopamine, dobutamine, and epinephrine infusions ordered for patients during the 2-month study period were eligible for inclusion in the study. Measurements: Daily samples of dopamine, dobutamine, and epinephrine infusates that were prepared for 41 pediatric patients were obtained; the infusate catecholamine concentration was measured by HPLC and compared with the ordered concentration. The concentration then was multiplied by the rate of infusion to determine the catecholamine dose. Main Results: There were significant differences between the measured doses of dopamine, dobutamine, and epinephrine and the dopamine HCl, dobutamine, and epinephrine HCl doses (p = 0.0001, p = 0.039, and p = 0.0009, respectively) that had been ordered because of preparation inaccuracies. Failure to account for the HCl salt in the stock drug accounted for some, but not all, of the inaccuracy of the dopamine HCl and epinephrine HCl infusates. There was a wide interday variability in the measured catecholamine dosage in patients receiving the same dose for 3 days or more. Conclusions: There are daily fluctuations in the preparation of dopamine, dobutamine, and epinephrine infusates that could alter the amount of drug actually delivered to critically ill patients and potentially contribute to their hemodynamic instability.

APA, Harvard, Vancouver, ISO, and other styles

7

Mefford, Ivan N. "Epinephrine in mammalian brain." Progress in Neuro-Psychopharmacology and Biological Psychiatry 12, no. 4 (January 1988): 365–88. http://dx.doi.org/10.1016/0278-5846(88)90099-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Anshien, Marco, S. Rutherfoord Rose, and Brandon K. Wills. "Unintentional Epinephrine Auto-injector Injuries." American Journal of Therapeutics 26, no. 1 (2019): e110-e114. http://dx.doi.org/10.1097/mjt.0000000000000541.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

Stein, C. M., R. Nelson, H. B. He, M. Wood, and A. J. J. Wood. "Effects of Epinephrine on Norepinephrine Release." Clinical Pharmacology & Therapeutics 59, no. 2 (February 1996): 139. http://dx.doi.org/10.1038/sj.clpt.1996.55.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Oyama, Yoshimasa, Justin Blaskowsky, and Tobias Eckle. "Dose-dependent Effects of Esmolol-epinephrine Combination Therapy in Myocardial Ischemia and Reperfusion Injury." Current Pharmaceutical Design 25, no. 19 (September 13, 2019): 2199–206. http://dx.doi.org/10.2174/1381612825666190618124829.

Full text

Abstract:

Background: Animal studies on cardiac arrest found that a combination of epinephrine with esmolol attenuates post-resuscitation myocardial dysfunction. Based on these findings, we hypothesized that esmololepinephrine combination therapy would be superior to a reported cardioprotective esmolol therapy alone in a mouse model of myocardial ischemia and reperfusion (IR) injury. Methods: C57BL/6J mice were subjected to 60 min of myocardial ischemia and 120 min of reperfusion. Mice received either saline, esmolol (0.4 mg/kg/h), epinephrine (0.05 mg/kg/h), or esmolol combined with epinephrine (esmolol: 0.4 mg/kg/h or 0.8 mg/kg/h and epinephrine: 0.05 mg/kg/h) during reperfusion. After reperfusion, infarct sizes in the area-at-risk and serum cardiac troponin-I levels were determined. Hemodynamic effects of drugs infused were determined by measurements of heart rate (HR) and mean arterial blood pressure (MAP) via a carotid artery catheter. Results: Esmolol during reperfusion resulted in robust cardioprotection (esmolol vs. saline: 24.3±8% vs. 40.6±3% infarct size), which was abolished by epinephrine co-administration (38.1±15% infarct size). Increasing the esmolol dose, however, was able to restore esmolol-cardioprotection in the epinephrine-esmolol (18.6±8% infarct size) co-treatment group with improved hemodynamics compared to the esmolol group (epinephrine-esmolol vs. esmolol: MAP 80 vs. 75 mmHg, HR 452 vs. 402 beats/min). Conclusion: These results confirm earlier studies on esmolol-cardioprotection from myocardial IR-injury and demonstrate that a dose optimized epinephrine-esmolol co-treatment maintains esmolol-cardioprotection with improved hemodynamics compared to esmolol treatment alone. These findings might have implications for current clinical practice in hemodynamically unstable patients suffering from myocardial ischemia.

APA, Harvard, Vancouver, ISO, and other styles

11

Gonzalez, Edgar R., Joseph P. Ornato, and Ronald L. Levine. "Vasopressor Effect of Epinephrine with and without Dopamine during Cardiopulmonary Resuscitation." Drug Intelligence & Clinical Pharmacy 22, no. 11 (November 1988): 868–72. http://dx.doi.org/10.1177/106002808802201105.

Full text

Abstract:

We prospectively studied nine prehospital cardiac arrest patients (six M, three F; aged 60 ± 8 yr) to determine the vasopressor response following incremental (1, 3, and 5 mg) doses of intravenous epinephrine given 5 minutes apart with or without dopamine 15 μg/kg/min. All patients were in ventricular fibrillation on arrival of the paramedics and were not resuscitated with standard advanced cardiac life support therapy. Cardiopulmonary resuscitation (CPR) was performed with a computerized Thumper at 60 compressions/min with a 50:50 downstroke-to-upstroke ratio. All patients were intubated and received 12 ventilations/min at a fraction of inspired oxygen of 80 percent. Radial artery pressure was monitored through a #20 gauge radial artery catheter inserted by cutdown within ten minutes after arrival at the emergency room. Five patients received epinephrine alone (group A) and four received epinephrine plus dopamine (group B). The patient's age, paramedic response time, arterial blood gases, and initial diastolic blood pressure (BP) did not differ significantly between treatment groups. Baseline systolic BP was significantly higher (p < 0.01) in group B (68 ± 10 mm Hg) than in group A (35 ± 5 mm Hg). Epinephrine produced a dose-dependent vasopressor response in group A, but not in group B. In group A, peak systolic BP following epinephrine 1, 3, and 5 mg was 57 ± 20, 69 ± 23, and 76 ± 27 mm Hg, respectively (p < 0.05 for 5 mg vs. baseline). No statistically significant difference was observed among the respective values in group B (81 ± 13, 80 ± 18, and 78 ± 19 mm Hg). In group A, peak diastolic BP following epinephrine 1, 3, and 5 mg was 24 ± 8, 28 ± 16, and 31 ± 6 mm Hg, respectively (p < 0.05 for epinephrine 5 mg vs. baseline). No statistically significant difference was observed among the respective values in group B (33 ± 10, 33 ± 11, and 34 ± 13 mm Hg). Epinephrine produces a dose-dependent vasopressor response during CPR in humans. The administration of high doses of epinephrine to patients receiving high-dose dopamine does not produce an additive vasopressor response.

APA, Harvard, Vancouver, ISO, and other styles

12

Williams, Jay H., and William S. Barnes. "Extracellular calcium and the inotropic effect of epinephrine on frog skeletal muscle." Canadian Journal of Physiology and Pharmacology 67, no. 12 (December 1, 1989): 1574–79. http://dx.doi.org/10.1139/y89-252.

Full text

Abstract:

The purpose of these experiments was to determine if extracellular calcium plays an important role in mediating the inotropic effect of epinephrine in isolated frog sartorius muscle. Initial experiments indicated that epinephrine potentiated the muscle twitch in a concentration-dependent manner with concentrations of 10 μM to 1 mM, increasing peak tension by approximately 33%. To inhibit the influx of extracellular calcium, muscles were incubated for 20 min in media containing epinephine in which calcium had been removed and replaced by magnesium or EDTA, or in experimental media containing epinephrine and the calcium channel blockers D-600 or diltiazem (5 μM). Each experimental condition was found to antagonize the effects of epinephrine such that peak twitch tensions were not significantly different from the control. When muscles were returned to normal Ringer's solution containing epinephrine, twitches exhibited progressive potentiation. Muscles were also incubated for 20 min in epinephrine without stimulation. Once stimulation was resumed, twitches were not immediately potentiated but rather gradually increased over time. These results suggest that the inotropic effects of epinephrine are influenced by the influx of extracellular calcium, an event that is dependent on muscle activation.Key words: epinephrine, skeletal muscle contraction, extracellular calcium, calcium antagonists, twitch potentiation.

APA, Harvard, Vancouver, ISO, and other styles

13

Brockman, Ronald P. "Effects of epinephrine on the net hepatic uptake of lactate, pyruvate, and glycerol in sheep." Canadian Journal of Physiology and Pharmacology 69, no. 4 (April 1, 1991): 475–79. http://dx.doi.org/10.1139/y91-071.

Full text

Abstract:

Epinephrine causes hyperglycemia in part by increasing gluconeogenesis. However, the mechanism of its gluconeogenic effects has not been studied in ruminants. This study was undertaken to examine the effect of epinephrine on the net hepatic uptake of selected glucose precursors in sheep. The major abdominal blood vessels of the sheep were catheterized in normal and alloxan diabetic sheep. Glucose production, metabolic clearance of glucose, and the hepatic removal of certain glucose precursors were determined before, during, and after epinephrine infusion. Epinephrine increased the hepatic glucose output, the concentrations of lactate and glycerol in plasma, and the net hepatic uptake and fractional hepatic extraction of lactate and glycerol. These effects were independent of changes in the concentrations of insulin and glucagon in plasma. These results show that epinephrine directly stimulates hepatic gluconeogenesis in sheep.Key words: epinephrine, hepatic gluconeogenesis, sheep.

APA, Harvard, Vancouver, ISO, and other styles

14

Van Matre, Edward T., Kang C. Ho, Clark Lyda, Beth A. Fullmer, Alan R. Oldland, and Tyree H. Kiser. "Extended Stability of Epinephrine Hydrochloride Injection in Polyvinyl Chloride Bags Stored in Amber Ultraviolet Light–Blocking Bags." Hospital Pharmacy 52, no. 8 (July 21, 2017): 570–73. http://dx.doi.org/10.1177/0018578717721121.

Full text

Abstract:

Objective: The objective of this study was to evaluate the stability of epinephrine hydrochloride in 0.9% sodium chloride in polyvinyl chloride bags for up to 60 days. Methods: Dilutions of epinephrine hydrochloride to concentrations of 16 and 64 µg/mL were performed under aseptic conditions. The bags were then placed into ultraviolet light–blocking bags and stored at room temperature (23°C-25°C) or under refrigeration (3°C-5°C). Three samples of each preparation and storage environment were analyzed on days 0, 30, 45, and 60. Physical stability was performed by visual examination. The pH was assessed at baseline and upon final degradation evaluation. Sterility of the samples was not assessed. Chemical stability of epinephrine hydrochloride was evaluated using high-performance liquid chromatography. To determine the stability-indicating nature of the assay, degradation 12 months following preparation was evaluated. Samples were considered stable if there was less than 10% degradation of the initial concentration. Results: Epinephrine hydrochloride diluted to 16 and 64 µg/mL with 0.9% sodium chloride injection and stored in amber ultraviolet light–blocking bags was physically stable throughout the study. No precipitation was observed. At days 30 and 45, all bags had less than 10% degradation. At day 60, all refrigerated bags had less than 10% degradation. Overall, the mean concentration of all measurements demonstrated less than 10% degradation at 60 days at room temperature and under refrigeration. Conclusion: Epinephrine hydrochloride diluted to 16 and 64 µg/mL with 0.9% sodium chloride injection in polyvinyl chloride bags stored in amber ultraviolet light–blocking bags was stable up to 45 days at room temperature and up to 60 days under refrigeration.

APA, Harvard, Vancouver, ISO, and other styles

15

Malhotra, Harinder, and Greg L. Plosker. "Cisplatin/Epinephrine Injectable Gel." Drugs & Aging 18, no. 10 (2001): 787–93. http://dx.doi.org/10.2165/00002512-200118100-00007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Markman, Maurie. "Cisplatin/Epinephrine Injectable Gel." Drugs & Aging 18, no. 10 (2001): 794–95. http://dx.doi.org/10.2165/00002512-200118100-00008.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Awada, Ahmad. "Cisplatin/Epinephrine Injectable Gel." Drugs & Aging 18, no. 10 (2001): 794–95. http://dx.doi.org/10.2165/00002512-200118100-00009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Jean, Christine, Gilles Tancrède, Suzanne Rousseau-Migneron, and André Nadeau. "Plasma epinephrine in chronically adrenodemedullated rats: lack of response to acute or chronic exercise." Canadian Journal of Physiology and Pharmacology 69, no. 8 (August 1, 1991): 1217–21. http://dx.doi.org/10.1139/y91-178.

Full text

Abstract:

Even if it is well established that epinephrine is a hormone originating from the adrenal medullae, the reappearance of circulating epinephrine has been reported in rats a few days after adrenodemedullation. To verify if the extra-adrenal tissue responsible for this epinephrine production can be stimulated, sham-operated or adrenodemedullated rats, either trained or kept sedentary, were submitted to an acute exercise stimulation test. Blood sampling was done before and after the test in precannulated rats for the determination of plasma epinephrine, norepinephrine, and corticosterone levels. Basal epinephrine levels were significantly reduced in trained and sedentary adrenodemedullated rats compared with their sham-operated counterparts. In response to exercise, there was no significant rise in epinephrine levels in both groups of adrenodemedullated rats. The norepinephrine levels in the basal state and in response to exercise were not altered by adrenodemedullation nor by physical conditioning. Basal corticosterone levels were similar between adrenodemedullated and sham-operated animals, either trained or kept sedentary. In response to exercise, corticosterone levels increased significantly in each group of rats but to a lesser extent in both groups of adrenodemedullated animals. These data indicate that the extra-adrenal epinephrine secretion that develops in the absence of adrenal medullae is not influenced by acute exercise nor by physical training.Key words: adrenodemedullation, extra-adrenal epinephrine, rat, physical training, acute exercise.

APA, Harvard, Vancouver, ISO, and other styles

19

Klausner, Mark A., Christopher Irwin, John F. Mullane, David G. Shand, Philip T. Leese, John D. Arnold, William Wollberg, Nancy B. Wagner, and Galen S. Wagner. "Effect of Cetamolol on Epinephrine-Induced Hypokalemia." Journal of Clinical Pharmacology 28, no. 8 (August 1988): 751–56. http://dx.doi.org/10.1002/j.1552-4604.1988.tb03210.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Hatton, Randy C. "Bismuth Subgallate–Epinephrine Paste in Adenotonsillectomies." Annals of Pharmacotherapy 34, no. 4 (April 2000): 522–25. http://dx.doi.org/10.1345/aph.19216.

Full text

Abstract:

OBJECTIVE: To evaluate the role of bismuth subgallate–epinephrine (BSE) paste as a hemostatic in adenotonsillectomies. DATA SOURCES: MEDLINE (January 1966–October 1999) and Current Contents (January 1997–October 1999) were searched, using bismuth subgallate, adenoidectomy, tonsillectomy, and adenotonsillectomy as search terms. A citation search was performed using Science Citation Index (January 1977–October 1999). DATA SYNTHESIS: Adenotonsillectomies are common procedures; although there are few complications, hemorrhage is a concern. Bismuth subgallate has historically been used as an astringent and hemostatic. An evaluation of studies of bismuth subgallate and BSE paste was conducted. CONCLUSIONS: There is minimal evidence to support this practice, but data suggest that epinephrine may be the active ingredient in BSE paste. BSE paste is inexpensive, poses little risk, and may decrease postoperative bleeding; therefore, it may be a reasonable hemostatic agent.

APA, Harvard, Vancouver, ISO, and other styles

21

Arimura, Hiroyuki, Zeljko J. Bosnjak, Sumio Hoka, and John P. Kampine. "Catecholamine-induced changes in vascular capacitance and sympathetic nerve activity in dogs." Canadian Journal of Physiology and Pharmacology 70, no. 7 (July 1, 1992): 1021–31. http://dx.doi.org/10.1139/y92-141.

Full text

Abstract:

The effects of three catecholamines, dopamine, epinephrine, and dobutamine, on the systemic circulation, especially on systemic vascular capacitance, were studied using cardiopulmonary bypass in dogs anesthetized with pentobarbital. Venous outflow was divided into three compartments: splanchnic, renal, and other; changes in systemic blood volume (SBV) were calculated from the changes in total venous outflow. To examine the contribution of sympathetic discharge to these vascular responses, sympathetic efferent nerve activity (SENA) from the ventral ansa subclavian nerve was recorded simultaneously. Experiments were done under three conditions: control, after baroreceptor deafferentation, and after hexamethonium injection with low and high doses of each catecholamine. During control and after baroreceptor deafferentation, dopamine- and epinephrine-induced changes in SBV were less than those after hexamethonium, and not significant except with low dose epinephrine. After hexamethonium, dopamine (200 μg/kg), epinephrine (10 μg/kg), and dobutamine (100 μg/kg) reduced SBV by 10.6 ± 3.4, 13.1 ± 1.7, and 1.9 ± 0.3 mL/kg, respectively. Splanchnic outflow increased significantly with dopamine and epinephrine after hexamethonium. High dose dopamine and epinephrine significantly suppressed SENA to 38 ± 9 and 15 ± 6% of baseline, respectively. Low dose dopamine decreased arterial pressure and SENA. This suppression in SENA was attenuated but still observed after baroreceptor deafferentation. Dobutamine reduced SBV, but had no effect on SENA. These results suggest that dopamine and epinephrine primarily decrease SBV by venoconstriction in the splanchnic region, however, these effects are greatly modified by basal sympathetic discharge and changes in SENA and vascular tone.Key words: catecholamines, dopamine, epinephrine, dobutamine, vascular capacitance, venoconstriction.

APA, Harvard, Vancouver, ISO, and other styles

22

Kitamura, Rie, Hideo Hirakata, Hiroto Okuda, Masami Sato, Hiroshi Toda, Kumi Nakamura, Yoshio Hatano, Nobukata Urabe, and Kazuhiko Fukuda. "Thiopental enhances human platelet aggregation by increasing arachidonic acid release." Canadian Journal of Physiology and Pharmacology 79, no. 10 (October 1, 2001): 854–60. http://dx.doi.org/10.1139/y01-066.

Full text

Abstract:

Conflicting results have been reported regarding the effect of thiopental on aggregation and cytosolic calcium levels in platelets. The present study attempted to clarify these phenomena. Using platelet-rich plasma or washed suspensions, platelet aggregation, thromboxane (TX) B2 formation, arachidonic acid (AA) release, and cytosolic free calcium concentrations ([Ca2+]i) were measured in the presence or absence of thiopental (30300 µM). Platelet activation was induced by adenosine diphosphate (ADP, 0.515 µM), epinephrine (0.120 µM) arachidonic acid (0.51.5 mM), or (+)-9,11-epithia-11,12-methano-TXA2 (STA2, 30500 nM). Measurements of primary aggregation were performed in the presence of indomethacin (10 µM). Low concentrations of ADP and epinephrine, which did not induce secondary aggregation in a control study, induced strong secondary aggregation in the presence of thiopental ([Formula: see text]100 µM). Thiopental ([Formula: see text]100 µM) also increased the TXB2 formation induced by ADP and epinephrine. Thiopental (300 µM) increased ADP- and epinephrine-induced 3H-AA release. Thiopental (300 µM) also augmented the ADP- and epinephrine-induced increases in [Ca2+]i in the presence of indomethacin. Thiopental appears to enhance ADP- and epinephrine-induced secondary platelet aggregation by increasing AA release during primary aggregation, possibly by the activation of phospholipase A2.Key words: barbiturates, anesthetics, eicosanoids, phospholipase.

APA, Harvard, Vancouver, ISO, and other styles

23

Wexels, Jan C., Eivind S. P. Myhre, and Ole D. Mjøs. "Effects of hypo- and hyper-capnia on myocardial blood flow and metabolism during epinephrine infusion in the dog." Canadian Journal of Physiology and Pharmacology 64, no. 1 (January 1, 1986): 44–49. http://dx.doi.org/10.1139/y86-006.

Full text

Abstract:

We have previously demonstrated a 40% increase in myocardial blood flow (MBF) during hypercapnia but no significant decrease of MBF during hypocapnia. The present study was undertaken to evaluate if epinephrine infusion, which increases both myocardial oxygen consumption [Formula: see text] and myocardial performance, might influence the effects of hypocapnia and hypercapnia on MBF. Induction of hypocapnia was performed by hyperventilation in closed-chest dogs anesthetized with pentobarbital. By adding carbon dioxide to the inspiratory gas, normocapnia and hypercapnia were created. Epinephrine infusion (0.8 μg∙kg−1∙min−1) increased MBF and cardiac output (CO) by 90 and 140%, respectively, while [Formula: see text] was increased by 45%. Epinephrine had a direct coronary vasodilating effect in excess of myocardial needs evidenced by increased oxygen content of the coronary sinus blood. During epinephrine infusion, induction of hypocapnia effected no change of MBF, while myocardial oxygen extraction increased significantly. Although oxygen saturation [Formula: see text] and [Formula: see text] in the coronary sinus blood decreased, these values remained well above those observed with hypocapnia without epinephrine infusion, thereby excluding impaired oxygen supply to the heart. Hypercapnia induced an increase of MBF by nearly 40% despite the coronary vasodilatation already induced by epinephrine infusion.

APA, Harvard, Vancouver, ISO, and other styles

24

Byrd, James C., Maria Hadjiconstantinou, and David Cavalla. "Epinephrine synthesis in the PC12 pheochromocytoma cell line." European Journal of Pharmacology 127, no. 1-2 (August 1986): 139–42. http://dx.doi.org/10.1016/0014-2999(86)90216-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Sternberg, Debra B., Donna Korol, Gary D. Novack, and James L. McGaugh. "Epinephrine-induced memory facilitation: attenuation by adrenoceptor antagonists." European Journal of Pharmacology 129, no. 1-2 (September 1986): 189–93. http://dx.doi.org/10.1016/0014-2999(86)90353-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Toller, Wolfgang, Gerald Wölkart, Christian Stranz, Helfried Metzler, and Friedrich Brunner. "Contractile action of levosimendan and epinephrine during acidosis." European Journal of Pharmacology 507, no. 1-3 (January 2005): 199–209. http://dx.doi.org/10.1016/j.ejphar.2004.11.049.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Wang, Huazhen, Naiqin Han, Nana Xu, Qingjiao Wu, Xiaoqing Dong, and Zhen Han. "Efficacy of combined nebulized aerosol inhalation and pulmicort respules in the treatment of emergency pediatric laryngitis, and its effect on adverse reactions." Tropical Journal of Pharmaceutical Research 21, no. 6 (August 10, 2022): 1317–22. http://dx.doi.org/10.4314/tjpr.v21i6.26.

Full text

Abstract:

Purpose: To determine the efficacy of combined use of nebulized epinephrine inhalation and pulmicortrespules in the treatment of emergency pediatric laryngitis and, its impact on the incidence of adverse reactions.Methods: A total of 100 cases of pediatric laryngitis admitted in The People’s Hospital of Zhangqiu District between December 2018 and December 2020 were randomly assigned (1:1) to receive either pulmicort respules (control group) or pulmicort respules plus nebulized epinephrine inhalation treatment (study group). Outcome measures included level of effectiveness and adverse reactions.Results: Pulmicort respules plus nebulized epinephrine inhalation treatment was associated with shorter remission time for dyspnea, wheeze, croup, and hoarseness versus pulmicort respules. The combination treatment produced higher total effectiveness of 96 % than pulmicort respules with total effectiveness of 82 % (p < 0.05). After treatment, both groups had decreased serum levels of interleukin-8 (IL-8), IL-6, C-reactive protein (CRP), and tumor necrosis factor (TNF)-α, with markedly lower levels in the group given nebulized epinephrine inhalation in combination with pulmicort respules (p < 0.05). Compared with patients given pulmicort respules only, those given combination treatments had a significantly shorter hospitalization time and a lower incidence of adverse reactions (4 vs 8 %; p < 0.05).Conclusion: Nebulized epinephrine inhalation in combination with pulmicort respules has high safety in the treatment of emergency pediatric laryngitis, and it significantly reduces clinical symptoms, inflammatory response, and hospital stay. However, further clinical trials are required prior to its use in clinical practice.

APA, Harvard, Vancouver, ISO, and other styles

28

Bocking, A. D., S. E. White, S. Kent, L. Fraher, V. K. M. Man, H. Rundle, and S. B. Hooper. "Effect of prolonged catecholamine infusion on heart rate, blood pressure, breathing, and growth in fetal sheep." Canadian Journal of Physiology and Pharmacology 73, no. 12 (December 1, 1995): 1750–58. http://dx.doi.org/10.1139/y95-239.

Full text

Abstract:

Norepinephrine and epinephrine were infused into fetal sheep for 24 h to compare the effects on fetal heart rate, blood pressure, breathing movements, and tissue growth with those of prolonged reductions in uterine blood flow. Norepinephrine concentrations increased (p < 0.01) from 871 ± 71 to 6831 ± 1090 pg/mL (2 h) with norepinephrine infusion, and epinephrine concentrations increased from 310 ± 95 to 1424 ± 288 pg/mL (2 h) with epinephrine infusion. Fetal pH decreased (p < 0.01) from 7.37 ± 0.01 to 7.29 ± 0.02 at 0.5 h of the norepinephrine infusion and returned to control values by 2 h, whereas fetal lactate concentrations increased (p < 0.05) from 1.6 ± 0.2 to 4.6 ± 1.0 mmol/L at 2 h and remained elevated for 12 h. Lactate concentrations also increased with epinephrine infusion. Fetal heart rate increased (p < 0.05) from 176 ± 5 to 246 ± 6 and 220 ± 6 beats/min in the 1st h of norepinephrine and epinephrine infusions, respectively, with a subsequent decline. Fetal blood pressure increased (p < 0.05) from 43 ± 3 and 40 ± 2 to 53 ± 3 and 47 ± 2 mmHg (1 mmHg = 133.3 Pa) during the 1st h of norepinephrine and epinephrine infusions, respectively, remaining elevated for 24 h. Fetal body weights were not different between the groups of animals, although liver/body weight ratio was less (p < 0.05) in epinephrine-infused fetuses (0.030 ± 0.001) compared with vehicle-infused animals (0.036 ± 0.002). There was no change in DNA synthesis rate in any of the fetal organs, despite changes in organ-specific DNA and protein content. Our results indicate that the changes in fetal cardiovascular and behavioural function, as well as tissue growth, that occur with prolonged reductions in uterine blood flow are not mediated solely by elevated circulating catecholamine concentrations.Key words: fetal physiology, catecholamines, pregnancy.

APA, Harvard, Vancouver, ISO, and other styles

29

Yamaguchi, Nobuharu, Richard Briand, and Martine Brassard. "Direct evidence that an increase in aortic norepinephrine level in response to insulin-induced hypoglycemia is due to increased adrenal norepinephrine output." Canadian Journal of Physiology and Pharmacology 67, no. 5 (May 1, 1989): 499–505. http://dx.doi.org/10.1139/y89-079.

Full text

Abstract:

This study reports on the major source of circulating norepinephrine that is known to increase, progressively, during sustained hypoglycemia induced by intravenous insulin administration. Plasma concentrations of epinephrine, norepinephrine, and dopamine were simultaneously determined for adrenal venous and aortic blood in dogs anesthetized with sodium pentobarbital. The model used allowed us to perform a functional adrenalectomy (ADRX), while continuously monitoring the adrenal medullary secretory function. Under basal conditions, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine were 0.169 ± 0.074, 0.067 ± 0.023, and 0.011 ± 0.003, respectively. Plasma concentrations (ng/mL) of aortic epinephrine, norepinephrine, and dopamine were 0.132 ± 0.047, 0.268 ± 0.034, and 0.034 ± 0.009. Following insulin injection (0.15 IU/kg, i.v.), the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased gradually (p < 0.05), reaching the values of 0.918 ± 0.200, 0.365 ± 0.058, and 0.034 ± 0.007 30 min after insulin administration. Similarly, aortic epinephrine, norepinephrine, and dopamine concentrations (ng/mL) increased significantly (p < 0.05) to 0.702 ± 0.144, 0.526 ± 0.093, and 0.066 ± 0.024. The aortic glucose concentration (mg/dL) was diminished from 81.8 ± 4.1 to 36.9 ± 3.4 (p < 0.01). After taking the blood sample at 30 min following insulin administration, ADRX was immediately performed. Five minutes after the onset of ADRX, the net output (μg/min) of adrenal epinephrine, norepinephrine, and dopamine increased further to 1.707 ± 0.374 (p < 0.05), 0.668 ± 0.139 (p < 0.05), and 0.052 ± 0.017. By contrast, aortic epinephrine, norepinephrine, and dopamine concentrations rapidly diminished (p < 0.05) to their initial control levels reaching 0.051 ± 0.014, 0.252 ± 0.023, and 0.031 ± 0.005 ng/mL, 5 min after ADRX. The present results indicate that during the early phase of insulin-induced hypoglycemia, circulating norepinephrine in aortic blood significantly increases due, primarily, to the enhanced adrenal norepinephrine output.Key words: insulin, plasma norepinephrine, adrenal catecholamines, functional adrenalectomy, hypoglycemia.

APA, Harvard, Vancouver, ISO, and other styles

30

Rubin, Ronald P. "Hermann (Hugh) Blaschko (1900–1993): His fundamental contributions to biochemical pharmacology and clinical medicine." Journal of Medical Biography 27, no. 3 (March 8, 2019): 179–83. http://dx.doi.org/10.1177/0967772017703091.

Full text

Abstract:

Hermann (Hugh) Blaschko was a biochemical pharmacologist best known for discovering how adrenaline (epinephrine), noradrenaline (norepinephrine), and dopamine were synthesized, stored, and metabolized in adrenomedullary cells and sympathetic nerves. Blaschko’s work not only supported the validity of the concept of neurochemical synaptic transmission but he also made fundamental contributions to the development of drugs used in clinical medicine to treat diseases such as depression, hypertension, and Parkinson's Disease.

APA, Harvard, Vancouver, ISO, and other styles

31

Péronnet, F., G. Boudreau, J. de Champlain, and R. A. Nadeau. "Effect of increases in myocardial epinephrine content on epinephrine release from the dog heart." Canadian Journal of Physiology and Pharmacology 71, no. 12 (December 1, 1993): 884–88. http://dx.doi.org/10.1139/y93-134.

Full text

Abstract:

The effect of short-term (10 min) and prolonged (180 min) epinephrine (E) infusion (92.5 ng∙kg−1∙min−1) on E content of the myocardium and on the subsequent release of E from the heart during stimulation of the left stellate ganglion (4 and 10 Hz, 4 V, 2 ms, 1 min) was studied in anesthetized dogs. The E content in the free wall of the left ventricle significantly increased 1.7- and 4.2-fold following short-term and prolonged E infusion, respectively, compared with a control group infused with saline. Tissue norepinephrine (NE) content was not modified by E infusion. The plasma E concentration gradient across the heart indicated a significant release of E during electrical stimulation of the left stellate ganglion, which was related to the amount of E stored in the tissue (e.g., control, 126 ± 60; 10-min infusion, 279 ± 105; 180-min infusion, 1487 ± 287 pg∙mL−1; at 10 Hz). NE release from the heart also tended to increase with the amount of E stored in the myocardium and released upon electrical stimulation of the left stellate ganglion, although the difference did not reach statistical significance. These results provide further direct evidence that blood-borne E can be taken up and stored in sympathetic nerve endings and can be released as a cotransmitter with NE. Locally released E could favor NE release.Key words: norepinephrine, sympathetic system, neuronal uptake, desipramine, cotransmitter, β2 facilitation.

APA, Harvard, Vancouver, ISO, and other styles

32

Koshman, Sheri L., Peter J. Zed, and Riyad B. Abu-Laban. "Vasopressin in Cardiac Arrest." Annals of Pharmacotherapy 39, no. 10 (October 2005): 1687–92. http://dx.doi.org/10.1345/aph.1g187.

Full text

Abstract:

Objective: To review the efficacy and safety of vasopressin in cardiac arrest. Data Sources: MEDLINE, EMBASE, and PubMed were searched (all to June 2005) for full-text English-language publications describing trials in humans. Search terms were vasopressin, epinephrine, adrenaline, heart arrest, cardiac arrest, and clinical trial. Study Selection and Data Extraction: Prospective, randomized, controlled trials that evaluated efficacy or safety endpoints of vasopressin in the management of cardiac arrest were included. Efficacy outcomes included return of spontaneous circulation, successful resuscitation, survival to hospital admission, 2hour survival, and survival to hospital discharge. Safety outcomes were as defined by each trial. Data Synthesis: Three prospective trials were identified and included in this review. Vasopressin does not appear to offer any therapeutic advantage compared with epinephrine in the treatment of both in-hospital and out-of-hospital cardiac arrest, regardless of the presenting arrest rhythm. Although there is a suggestion that vasopressin may be effective in treatment of asystole, the evidence for this arises from a subgroup analysis that should be viewed as hypothesis generating. There are limited data describing the safety of vasopressin in cardiac arrest. CONCLUSIONS: The current evidence for the use of vasopressin in cardiac arrest is indeterminate. Given the similarly equivocal evidence of efficacy for epinephrine, either drug could be considered the first-line agent in cardiac arrest. Placebo-controlled studies with appropriate statistical power are warranted to evaluate meaningful clinical outcomes, such as survival to hospital discharge. Further evaluation of the role of vasopressin in asystolic cardiac arrest and its use in combination with epinephrine is also justified.

APA, Harvard, Vancouver, ISO, and other styles

33

Seva, Kazuhiko, Shingo Sasaki, Izumi Miki, and Shigeru Motoniura. "Alteration of epinephrine and norepinephrine levels in myocardial interstitium of papillary muscle by infusion of high levels of epinephrine or norepinephrine." Japanese Journal of Pharmacology 73 (1997): 266. http://dx.doi.org/10.1016/s0021-5198(19)45564-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

Wilson, John X., Khaled J. Saleh, E. Davindra Armogan, and Ewa J. Jaworska. "Catecholamine and blood pressure regulation by gonadotropin-releasing hormone analogs in amphibians." Canadian Journal of Physiology and Pharmacology 65, no. 12 (December 1, 1987): 2379–85. http://dx.doi.org/10.1139/y87-377.

Full text

Abstract:

Analogs of gonadotropin-releasing hormone (GnRH) occur in the brain, plasma, and sympathoadrenal system of anuran amphibians. The present experiments studied the effects of GnRH and [Trp7, Leu8]-GnRH on plasma catecholamines and cardiovascular function in conscious adult bullfrogs (Rana catesbeiana) and cane toads (Bufo marinus). Both GnRH analogs elicited dose-dependent (0.1–1 nmol∙kg−1) increases in arterial norepinephrine, epinephrine, and blood pressure levels when injected intravenously into toads. In bullfrogs, [Trp7, Leu8]-GnRH (1 nmol∙kg−1) increased arterial norepinephrine concentration approximately 10-fold without affecting the concentrations of norepinephrine sulfate, norepinephrine glucuronide, epinephrine, epinephrine sulfate, or epinephrine glucuronide. The noradrenergic response of bullfrogs to [Trp7, Leu8]-GnRH was specific to the neurohormone because it could be inhibited by [D-pGlu1, D-Phe2, D-Trp3,6]-GnRH. The sympathomimetic activities of the GnRH analogs did not depend on changes in temperature, which occur seasonally in natural habitats, because similar noradrenergic responses were observed at 4 and 22 °C. GnRH and [Trp7, Leu8]-GnRH (0.01–10 nmol∙kg−1) did not raise arterial blood pressure in bullfrogs despite their pressor actions in toads. This interspecific difference was remarkable because cardiovascular responses to norepinephrine, angiotensin II, and vasotocin in bullfrogs were similar to those in toads. The parallels between catecholamine and blood pressure responses suggest that epinephrine is the principal mediator of the blood pressure response to native GnRH analogs in toads. In bullfrogs, [Trp7, Leu8]-GnRH mobilizes norepinephrine but not epinephrine, and the noradrenergic effect is insufficient to raise blood pressure. These observations are consistent with a physiological role for native GnRH analogs in the regulation of the sympathoadrenal system in anuran amphibians.

APA, Harvard, Vancouver, ISO, and other styles

35

Perks, A. M., and S. Cassin. "The effects of arginine vasopressin and epinephrine on lung liquid production in fetal goats." Canadian Journal of Physiology and Pharmacology 67, no. 5 (May 1, 1989): 491–98. http://dx.doi.org/10.1139/y89-078.

Full text

Abstract:

The effects of arginine vasopressin (AVP) and epinephrine on lung liquid secretion were investigated in 67 acute fetal goats (116 days of gestation to term) with intact umbilical cords after caesarean section. Secretion was measured by an impermeant tracer technique. AVP was infused intravenously (1.6–39.2 mU/(kg∙min); 2 h) into 26 fetuses. All fetuses below 130 days of gestation, except one, showed no response. All above 133 days reduced secretion, or turned to reabsorption, except at the lowest infusion rate. The effect persisted, and usually increased postinfusion. Expansion of the lungs with saline did not change the response. The percentage reductions were linearly related to the logarithm of the infusion rate (threshold, 1.42 mU/(kg∙min)). The absolute reductions were linearly related to fetal weight. Epinephrine was infused intravenously (0.30–6.72 μg/(kg∙min); 1–2 h) into 12 fetuses. All fetuses (118 days to term) reduced secretion or reabsorbed by the second hour. At the highest infusion rate, reabsorption was immediate; at the lowest, secretion increased slightly, then fell significantly in the second hour. Epinephrine acted at levels considered physiological at delivery in the sheep. AVP appears to act at plasma levels found in most vaginal deliveries; it may augment epinephrine-induced reabsorption during stress, and help long-term removal of lung fluid.Key words: fetal goats, lung liquid, arginine vasopressin, epinephrine.

APA, Harvard, Vancouver, ISO, and other styles

36

Sneader, W. "The discovery and synthesis of epinephrine." Drug News & Perspectives 14, no. 8 (2001): 491. http://dx.doi.org/10.1358/dnp.2001.14.8.858417.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Landry, Jean-François, Jean-Pierre Després, Denis Prud'homme, Benoît Lamarche, Angelo Tremblay, André Nadeau, and Claude Bouchard. "A study of some potential correlates of the hypotensive effects of prolonged submaximal exercise in normotensive men." Canadian Journal of Physiology and Pharmacology 70, no. 1 (January 1, 1992): 53–59. http://dx.doi.org/10.1139/y92-008.

Full text

Abstract:

This study was undertaken (1) to examine the relation of plasma catecholamine and insulin levels to the blood pressure response during and after submaximal exercise, (2) to verify whether the blood pressure response to an epinephrine infusion is associated with the blood pressure response to a prolonged submaximal exercise, and (3) to study some potential correlates of the hypotensive effect of prolonged aerobic exercise. Nine normotensive young men (mean age 22.0 ± 1.4 years) were subjected to a 1-h epinephrine infusion protocol and a 1-h submaximal exercise test on a cycle ergometer. The two tests were performed 1 week apart. The physiological and hormonal responses observed during the submaximal exercise test were generally greater than those observed during the epinephrine infusion test. Blood pressure responses in both tests showed no significant association with changes in plasma insulin levels. Changes in plasma norepinephrine concentration were positively correlated with changes in systolic blood pressure during the submaximal exercise test but not during the epinephrine infusion. Results also showed that the blood pressure response to epinephrine infusion was not correlated with the blood pressure response to submaximal exercise. However, post-exercise and post-infusion systolic blood pressure responses (differences between "post-test" and "resting" values) were significantly associated (r = 0.81, p < 0.01). In addition, a significant hypotensive effect of submaximal exercise was observed for both systolic and diastolic blood pressure. However, the individual differences observed in the hypotensive effect of aerobic exercise appeared to be more related to variations in vascular sensitivity than to exercise-induced variations in plasma insulin and catecholamine levels, at least in this sample of healthy normotensive young men.Key words: blood pressure, exercise, catecholamines, insulin, epinephrine infusion.

APA, Harvard, Vancouver, ISO, and other styles

38

Harrington, Keith J., Robert G. Allen, and Jay W. Dewald. "Renal vascular effects of epinephrine infusion in the halothane-anesthetized piglet." Canadian Journal of Physiology and Pharmacology 72, no. 4 (April 1, 1994): 394–96. http://dx.doi.org/10.1139/y94-057.

Full text

Abstract:

The objective of this study was to determine the dose–response effects of epinephrine, given by systemic intravenous infusion to the halothane-anesthetized newborn piglet, on renal blood flow, mean arterial blood pressure, and renal vascular resistance. Seven newborn piglets were acutely instrumented. A transit-time ultrasound flow probe was placed around the renal artery and a femoral arterial catheter was placed for blood pressure monitoring. Epinephrine was infused in doubling doses from 0.2 to 3.2 μg∙kg−1∙min−1. Mean arterial blood pressure increased from 54 mmHg (1 mmHg = 133.3 Pa) to an average of 96 mmHg at 3.2 μg∙kg−1∙min−1 of epinephrine. Renal blood flow increased from 165 mL∙min−1∙100 g−1 at baseline to 185 mL∙min−1∙100 g−1 at a dose of 0.2 μg∙kg−1∙min−1 and increased further at 0.4 and 0.8 μg∙kg−1∙min−1 to reach 261 mL∙min−1∙100 g−1. Renal blood flow began to fall at a dose of 3.2 μg∙kg−1∙min−1, remaining however, significantly above baseline (211 mL∙min−1∙100 g−1). Consequently, calculated renal vascular resistance fell as the dose was increased from 0.2 to 0.8 μg∙kg−1∙min−1 and then rose again at 1.6 and 3.2 μg∙kg−1∙min−1, being significantly above baseline at 3.2 μg∙kg−1∙min−1. These results demonstrate that epinephrine when given by systemic infusion to the halothane-anesthetized newborn pig is a renal vasodilator at low doses and causes renal vasoconstriction at moderate to high doses. Renal blood flow remained above baseline at all doses tested, and thus, within the dosage range tested, epinephrine infusion should not cause renal ischemia.Key words: epinephrine, kidney blood flow, piglet, renal vascular resistance.

APA, Harvard, Vancouver, ISO, and other styles

39

Furusho, Nobuhiro, Michiko Inoue, Kazuhiro Suzuki, Keiko Ishiwa, Yoko Funaki, Marumi Yamamoto, Masako Morikawa, and Minoru Tsuboi. "Study to the mechanism of Epinephrine-induced platelet aggregation." Japanese Journal of Pharmacology 49 (1989): 148. http://dx.doi.org/10.1016/s0021-5198(19)56289-8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Nishioeda, Y., M. Tsushima, I. Ninomiya, and T. Omae. "The effects on atropine of the kinetics of epinephrine." European Journal of Pharmacology 183, no. 6 (July 1990): 2291–92. http://dx.doi.org/10.1016/0014-2999(90)93842-e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

41

Cooney, Mary M., C. H. Conaway, and Ivan N. Mefford. "Epinephrine, norepinephrine and dopamine concentrations in amphibian brain." Comparative Biochemistry and Physiology Part C: Comparative Pharmacology 82, no. 2 (January 1985): 395–97. http://dx.doi.org/10.1016/0742-8413(85)90180-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Smits, P., G. Pieters, and T. Thien. "The role of epinephrine in the circulatory effects of coffee." Clinical Pharmacology and Therapeutics 40, no. 4 (October 1986): 431–37. http://dx.doi.org/10.1038/clpt.1986.203.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Adameova, Adriana, Vijayan Elimban, Paul K. Ganguly, and Naranjan S. Dhalla. "β-1 adrenoceptors and AT1 receptors may not be involved in catecholamine-induced lethal arrhythmias." Canadian Journal of Physiology and Pharmacology 97, no. 6 (June 2019): 570–76. http://dx.doi.org/10.1139/cjpp-2018-0531.

Full text

Abstract:

An excessive amount of catecholamines produce arrhythmias, but the exact mechanisms of this action are not fully understood. For this purpose, Sprague–Dawley rats were treated with or without atenolol, a β1-adrenoceptor blocker (20 mg/kg per day), for 15 days followed by injections of epinephrine for cumulative doses of 4 to 128 μg/kg. Another group of animals were pretreated with losartan, an angiotensin receptor (AT1) blocker (20 mg/kg per day), for comparison. Control animals received saline. Varying degrees of ventricular arrhythmias were seen upon increasing the dose of epinephrine, but the incidence and duration of the rhythm abnormalities as well as the number of episodes and severity of arrhythmias were not affected by treating the animals with atenolol or losartan. The levels of both epinephrine and norepinephrine were increased in the atenolol-treated rats but were unchanged in the losartan-treated animals after the last injection of epinephrine; the severity of arrhythmias did not correlate with the circulating catecholamine levels. These results indicate that both β1-adrenoceptors and AT1 receptors may not be involved in the pathogenesis of catecholamine-induced arrhythmias and support the view that other mechanisms, such as the oxidation products of catecholamines, may play a crucial role in the occurrence of lethal arrhythmias.

APA, Harvard, Vancouver, ISO, and other styles

44

Peyko, Vincent, Victor Cohen, Samantha P. Jellinek-Cohen, and Michelle Pearl-Davis. "Evaluation and treatment of accidental autoinjection of epinephrine." American Journal of Health-System Pharmacy 70, no. 9 (May 1, 2013): 778–81. http://dx.doi.org/10.2146/ajhp120316.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Takeuchi, Naoko, Jun Yamada, Yumi Sugimoto, Ikuko Kimura, and Kazuyoshi Horisaka. "Antagonistic effects of serotonin on epinephrine-induced hyperglycemia in mice." Japanese Journal of Pharmacology 49 (1989): 184. http://dx.doi.org/10.1016/s0021-5198(19)56389-2.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Martin, Anne-Céline, Diane Zlotnik, Guillaume Porta Bonete, Elodie Baron, Benoît Decouture, Tiphaine Belleville-Rolland, Bernard Le Bonniec, et al. "Epinephrine restores platelet functions inhibited by ticagrelor: A mechanistic approach." European Journal of Pharmacology 866 (January 2020): 172798. http://dx.doi.org/10.1016/j.ejphar.2019.172798.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Yadid, G., M. B. H. Youdim, and O. Zinder. "Preferential release of epinephrine by glycine from adrenal chromaffin cells." European Journal of Pharmacology 221, no. 2-3 (October 1992): 389–91. http://dx.doi.org/10.1016/0014-2999(92)90729-n.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Alves, Ester, Nikolay Lukoyanov, Paula Serrão, Daniel Moura, and Mónica Moreira-Rodrigues. "Epinephrine increases contextual learning through activation of peripheral β2-adrenoceptors." Psychopharmacology 233, no. 11 (March 2, 2016): 2099–108. http://dx.doi.org/10.1007/s00213-016-4254-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

49

BONNEY, CHARLES H., KWOK-WAI LAM, and DONALD FONG. "Ocular Hyperuricosis in the Rabbit Following Hyperuricemia and Topical Epinephrine." Journal of Ocular Pharmacology and Therapeutics 2, no. 1 (January 1986): 55–58. http://dx.doi.org/10.1089/jop.1986.2.55.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Popov, N. S., D. A. Gavrilenko, V. Yu Balabanyan, M. B. Petrova, S. A. Donskov, I. B. Atadzhanov, and N. A. Shatokhina. "Quantitative determination of monoamine neurotransmitters in rat brain homogenates using HPLC-MS/MS." Pharmacokinetics and Pharmacodynamics, no. 4 (January 18, 2023): 33–42. http://dx.doi.org/10.37489/2587-7836-2022-4-33-42.

Full text

Abstract:

Relevance. Evaluation of the effect of drugs on neurotransmitter processes is an important component of pharmacodynamic studies. The quantitative determination of monoamine neurotransmitters in the brain structures of laboratory animals is an urgent task of pharmacology and physiology.Purpose of the study. Development of a method for the quantitative determination of serotonin, dopamine, norepinephrine, histamine and epinephrine in rat brain homogenates using HPLC-MS/MS.Methods. The isolation of neurotransmitters from the brain of rats was carried out by homogenizing the biomaterial with acetonitrile and hydrochloric acid. The extraction was purified by liquid-liquid extraction with chloroform and isopropanol. Monoamines were detected using an AB Sciex QTrap 3200MD mass spectrometer, chromatography was performed using an Agilent Technologies 1260 Infinity II HPLC. Methanol and deionized water were used as eluent.Results. Sample preparation consisted of centrifugation of the resulting homogenate, drying of the supernatant in a stream of nitrogen, dissolution of the precipitate in the mobile phase, and purification of the solution using a mixture of chloroform and isopropanol. An Agilent InfinityLab Poroshell 120 EC-C18 4.6×100 mm, 2.7 μm analytical column was used to separate monoamine neurotransmitters. The total time of the chromatographic analysis was 12 minutes, the retention time of norepinephrine, epinephrine, dopamine, serotonin, histamine was 2.8; 3.2; 5.4; 7.9; and 2.2 minutes, respectively. The analytical range of the technique was 25.0–5000.0 ng/g for epinephrine, histamine, and dopamine; 5.0–5000.0 ng/g for serotonin and 50.0–5000.0 for norepinephrine. To test the technique, we analyzed monoamine neurotransmitters in the striatum of intact Wistar rats.Conclusion. The developed bioanalytical HPLC-MS/MS method for the quantitative determination of monoamine neurotransmitters in the rat brain fully complies with the validation requirements. The metrological characteristics of the technique make it possible to estimate the content of norepinephrine, epinephrine, dopamine, serotonin, and histamine in the brain structures of rats with high accuracy.

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!