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Relevant bibliographies by topics / Pharmacology, Epinephrine

Academic literature on the topic 'Pharmacology, Epinephrine'

Author: Grafiati

Published: 10 March 2023

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Dissertations / Theses
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Journal articles on the topic "Pharmacology, Epinephrine"

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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.

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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.

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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.

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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.

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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.

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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.

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

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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Dissertations / Theses on the topic "Pharmacology, Epinephrine"

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Wade, Spencer David DDS. "Stability of Epinephrine in a 0.9% Saline Solution." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1561489299362315.

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Nilsson, Ulrika K. "Lysophosphatidic acid : Physiological effects and structure-activity relationships." Doctoral thesis, Linköping : Univ, 2002. http://www.ep.liu.se/diss/med/07/51/index.html.

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Eriksson, Andreas. "Platelet Adhesion to Proteins in Microplates : Applications in Experimental and Clinical Research." Doctoral thesis, Linköping : Department of Medical and Health Sciences, Linköping University, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-11733.

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Johansson, Jakob. "Cardiopulmonary Resuscitation : Pharmacological Interventions for Augmentation of Cerebral Blood Flow." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4281.

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FARINI, VALENTINA. "NUTRITIONAL AND HORMONAL MODULATION OF HUMAN MELANOMA PROGRESSION." Doctoral thesis, 2013. http://hdl.handle.net/2158/806331.

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The tumoral microenvironment, also called “tumor reactive stroma”, is composed by several heterotypic cells like cancer-associated fibroblasts (CAFs), pro inflammatory cells, endothelial cells and perycites which stroma create a complex and continuative “cross-talk” made of direct cell-to-cell contacts and paracrine/exocrine signals (growth factors, cytokines, soluble factors) promoting tumor development through stimulation of cancer cells survival/proliferation, migration and metastatic ability. The mediators of chronic stress norepinephrine (NE) and epinephrine (E) exert stimulant effects on the invasion process of a number of neoplastic cells, and this effect seems to be due, at least in part, to the interaction with β-adrenoceptors (AR), which are expressed by various malignant tumours. In particular, the expression of β-AR has been studied in various human solid tumors, such as breast, colon, prostatic, ovary, nasopharyngeal and oral cancer, raising the possibility that such receptors could affect invasion and dissemination processes. My study aimed to evaluate the expression of β-AR and the influence of NE and E on the malignant behaviour of melanoma cell lines. Preliminary results assessed by immunohistochemistry on a series of human benign and malignant melanocytic lesions showed that both β1- and β2-AR were expressed in melanocytic tumors, according to neoplastic progression, being significantly more expressed in malignant than benign lesions, and, for β2-AR, significantly more present in atypical than common naevi. In vitro studies demonstrated that primary and metastatic cell lines expressed both β-AR types and were stimulated by NE and/or E to secrete higher amounts of IL-6, VEGF and IL-8, which contribute to melanoma progression, while NE enhanced motility through matrix metalloprotease-2. The pro-invasive effect of NE and E was inhibited by non-selective AR inhibitor propanolol, confirming β-AR involvement. In addition, VEGF increased the invasive spur induced by NE in A375 cell line, while IL-6 in association with NE could activate dermal fibroblasts toward a myofibroblastic phenotype, typical of tumour microenvironment. Taken together the results suggest that NE and E can dramatically affect the aggressiveness of melanoma cells and, since primary and metastatic melanomas exhibit strongly β-AR expression, could affect the course of the disease in melanoma patients too. These data support the hypothesis that the interaction of cathecolamines with β-AR could be a useful target in oncologic therapy in order to prevent melanoma metastatic progression. Beside and in synergy with signals produced by tumor micorenvironment, cancer cells are also able to completely modify their metabolic behaviour in order to sustain cancer progression. In particular, there is growing interest in defining the role of reactive stroma in the regulation of cancer cells metabolism. At this purpose, the “Warburg effect” is the best known tumor-specific alteration of common metabolic pathways, as cancer cells show increased glycolysis even in conditions of high oxygen tension (‘‘aerobic glycolysis’’), leading to high lactate production. In addition, cancer cells can use elevated amounts of glucose as a carbon source for anabolic reactions. The aim of the second part of my study is to focus on the ability of nutrients to regulate transcription factors involved in cancer cells metabolism. One of these factors is represented by hypoxia inducible factor-1α (HIF-1α). It is well established that, under hypoxic condition, HIF-1α activates target genes whose protein products mediate a switch from oxidative to glycolytic metabolism (ex. GLUT-1, LDH-A), while it is not well established yet the role of HIF-1α in regulating these complex pathways under normoxic condition. To this purpose, A375 primary melanoma cell line was cultured in normoxic condition in presence/absence of nutrients like glucose, pyruvate and lactate in order to understand how different nutrients can activate key pathways for cancer progression. Cytofluorimetric analysis demonstrate that A375 show strong dependance on glucose content of media in order to sustain survival, thereby according to a Warburg metabolic phenotype, and that nutrients alone are able to induce the expression of HIF-1α and of its target gene carbonic anidrase-IX (CA-IX), probably thorugh an increased reactive oxygen species (ROS) production. In order to further understand the role of nutrients-induced HIF-1α, we performed migration and invasion assays with Boyden chambers, respectively in absence or presence of Matrigel mimicking the extracellular matrix. Nutrients alone are also able to elicit a pro-invasive response of A375 and this effect is reverted after both treatment with Topotecan, a HIF-1α farmacological inhibitor, and HIF-1α gene silencing. Finally, data obtained so far allow us to hypothesize a novel important role of nutrients-induced HIF-1α normoxic stabilization in order to sustain cancer progression.

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Choquette, Amélie. "Caractérisation pharmacocinétique et pharmacodynamique de la lidocaïne avec ou sans adrénaline lors d’un bloc paravertébral du plexus brachial chez le chien." Thèse, 2015. http://hdl.handle.net/1866/16143.

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Au cours des vingt dernières années, l’anesthésie régionale est devenue, autant en médecine vétérinaire qu’humaine, un outil essentiel à l’élaboration de protocoles analgésiques péri-opératoires. Parmi l’éventail de techniques mises au point en anesthésie canine, le bloc paravertébral du plexus vertébral (PBPB) et sa version modifiée sont d’un grand intérêt pour toute procédure du membre thoracique, dans sa portion proximale. Toutefois, l’essentiel des données publiées à ce jour provient d’études colorimétriques, sans évaluation clinique, et peu d’information est disponible sur les techniques de localisation nerveuse envisageables à ce site. Notre étude visait à décrire une approche échoguidée du PBPB modifié, puis à caractériser ses paramètres pharmacocinétiques et pharmacodynamiques après administration de lidocaïne (LI) ou lidocaïne adrénalinée (LA). Huit chiens ont été inclus dans un protocole prospectif, randomisé, en aveugle et croisé, réparti sur trois périodes. L’impact pharmacodynamique du bloc effectué avec LI ou LA a été évalué régulièrement pour 180 min suivant son exécution. Le traitement à l’adrénaline n’a pas démontré d’impact significatif (P = 0,845) sur la durée du bloc sensitif, tel qu’évalué par un stimulus douloureux mécanique appliqué aux dermatomes ciblés. À l’opposé, l’atteinte proprioceptive évaluée par la démarche a été trouvée prolongée (P = 0,027) et le bloc moteur mesuré par le pic de force verticale (PVF) au trot sur la plaque de force s’est avéré plus marqué (PVF réduit; P = 0,007) sous LA. À l’arrêt comme au trot, le nadir de la courbe PVF-temps a été trouvé retardé (P < 0,005) et la pente ascendante de retour aux valeurs normales adoucie (P = 0,005). Parallèlement aux évaluations cliniques, des échantillons plasmatiques ont été collectés régulièrement afin de quantifier et décrire le devenir pharmacocinétique de la lidocaïne. Parmi les trois élaborés, un modèle bi-compartimental doté d’une double absorption asynchrone d’ordre zéro a finalement été sélectionné et appliqué aux données expérimentales. Sous LA, la Cmax a été trouvée significativement diminuée (P < 0,001), les phases d’absorption prolongées [P < 0,020 (Dur1) et P < 0,001 (Dur2)] et leurs constantes réduites [P = 0,046(k01) et P < 0,001 (k02)], le tout en concordance avec les effets proprioceptifs et moteurs rapportés. Bien que l’extrapolation du dosage soit maintenant théoriquement envisageable à partir du modèle mis en lumière ici, des études supplémentaires sont encore nécessaires afin d’établir un protocole de PBPB d’intérêt clinique. L’analyse sur plaque de force pourrait alors devenir un outil de choix pour évaluer l’efficacité du bloc dans un cadre expérimental.
Over the last decade, regional anaesthesia has become a gold standard for peri-surgical management in veterinary medicine. Among the many techniques developed for analgesia in dogs, the paravertebral brachial plexus block (PBPB) is of great interest when targeting the proximal half of the thoracic limb. Yet, most available data on this technique is based on colorimetric protocols rather than clinical evaluation, and there are very few published results for PBPB execution using nerve location techniques. Through this work, we wished to describe an ultrasound-guided approach of the PBPB and characterize its pharmacokinetic/ pharmacodynamic parameters when executed with either lidocaine alone (LI) or combined to adrenaline (LA). Eight dogs were included in a prospective, randomised, blinded, crossover protocol performed over three distinct periods. Pharmacodynamic impact of LI and LA was compared for 180 minutes after block administration. No significant difference (P = 0.845) was noted between treatments regarding length of the sensitive block, as evaluated regularly through a mechanical painful stimulus applied to selected dermatomes. On the opposite, gait examination showed a longer proprioceptive deficit using LA (P = 0.027). Motor block measured with dynamic force plate analysis showed a lower peak vertical force with LA than LI (P = 0.007). For both dynamic and static evaluations, nadir was clearly delayed (P < 0.005) and the ascending slope back to baseline significantly softened (P = 0.005) in the LA group. Throughout block execution and evaluation, blood samples were collected regularly in order to quantify and describe lidocaine kinetics. Models where developed and compared. A two-compartment model with dual zero-order absorption processes was selected as the best fit for our experimental data. Cmax proved to be significantly reduced with LA (P < 0.001), thus reducing potential toxicity. Absorption phase was prolonged [P < 0.020 (Dur1) and P < 0.001 (Dur2)] and zero-order absorption constant rates lowered [P = 0.046(k01) and P < 0.001 (k02)] following adrenaline addition, in accordance with the previously noted prolonged gait and motor effects. Though dosage extrapolation is now possible using the model developed and tested here, further studies would be needed to establish a PBPB protocol of more clinical interest. Then, force plate analysis could become a key tool for block quality assessment, as both dynamic and static measurements proved to be the reliable ways to collect ground reaction force (GRF) data.

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Book chapters on the topic "Pharmacology, Epinephrine"

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Bylund, David B. "Epinephrine." In xPharm: The Comprehensive Pharmacology Reference, 1–5. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61695-2.

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Duncan, Christopher M., and Paula A. Craigo. "Pharmacology of Neural Blockade." In Mayo Clinic Atlas of Regional Anesthesia and Ultrasound-Guided Nerve Blockade, 19–24. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199743032.003.0002.

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Chapter 2 reviews the mechanism of action for local anesthetics. Clinical features such as potency, onset of action, duration, and dose are discussed. Drug metabolism, toxicity (local and systemic), and its treatment are included. The chapter concludes with additional information on adjuvant medications (eg, epinephrine, clonidine) used to extend or enhance the clinical effects of local anesthetics.

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Ziegler, Michael G., Brian P. Kennedy, and Frederick W. Houts. "Extra-Adrenal Nonneuronal Epinephrine and Phenylethanolamine-N-Methyltransferase." In Advances in Pharmacology, 843–46. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60878-9.

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Ainsworth, Sean. "A." In Neonatal Formulary, edited by Sean Ainsworth, 55–126. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198840787.003.0014.

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This chapter presents information on neonatal drugs that begin with A, including use, pharmacology, adverse effects, fetal and infant implications of maternal treatment, treatment, and supply of Abacavir, Acetylcysteine (N-acetylcysteine), Aciclovir = Acyclovir (USAN), Adenosine, Adrenaline = Epinephrine (rINN), Albendazole, Alginate compounds (Gaviscon®), Alimemazine (trimeprazine— former BAN and USAN), Alteplase (tissue-type plasminogen activator [rt-PA]), Amikacin, Amiodarone, Amlodipine, Amodiaquine with artesunate, Amoxicillin = Amoxycillin (former BAN), Amphotericin B, Ampicillin, Anti-vascular endothelial growth factors (for ROP), Arginine (L-arginine), Artemether with lumefantrine, Aspirin = acetylsalicylic acid (INN), Atosiban, Atracurium, Atropine, and Azithromycin

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Blakely, Randy D., and Subramaniam Apparsundaram. "Structural Diversity in the Catecholamine Transporter Gene Family: Molecular Cloning and Characterization of an L-Epinephrine Transporter from Bullfrog Sympathetic Ganglia." In Advances in Pharmacology, 206–10. Elsevier, 1997. http://dx.doi.org/10.1016/s1054-3589(08)60729-2.

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Conference papers on the topic "Pharmacology, Epinephrine"

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Tsomartova, Dibakhan, Nataliya Yaglova, Sergey Obernikhin, Svetlana Nazimova, and Valentin Vasilyevich Yaglov. "ALTERED CYTOPHYSIOLOGY OF EPINEPHRINE-PRODUCING CELLS IN RATS AFTER CHRONIC EXPOSURE TO LOW DOSES OF DDT." In NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.12.

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Chronic low-dose exposure to dichlorodiphenyltrichloroethane does not diminish epinephrine production since epinephrine-secreting adrenal cells significantly intensify mitochondrial ac-tivity to restore epinephrine secretion.

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Timokhina, Ekaterina Petrovna, Nataliya Valentinovna Yaglova, Sergey Stanislavovich Obernikhin, Valentin Vasilyevich Yaglov, Svetlana Vladimirovna Nazimova, and Dibakhan Aslanbekovna Tsomartova. "SENSITIVITY OF CATHEHOLAMINE-PRODUCING STRUCTURES TO DISRUPTIVE ACTION OF DDT." In International conference New technologies in medicine, biology, pharmacology and ecology (NT +M&Ec ' 2020). Institute of information technology, 2020. http://dx.doi.org/10.47501/978-5-6044060-0-7.11.

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The results of the research revealed that norepinephrine-produsing formations demonstrate higher sensitivity to low-dose exposure to endocrine disrupting chemical DDT than epinephrine-producing ones. Differences in sensitivity to endocrine disruption remains unchanged whatever onset of exposure is prenatal or postnatal period of ontogeny.

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Kindel, G., and J. Fareed. "MODULATORY EFFECT OF SERINE PROTEASES AND RELATED ENZYMES ON ISOLATED SMOOTH MUSCLE PREPARATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644602.

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Thrombin and related proteases produce varying pharmacologic responses in animal models. To more specifically study the in vivo actions of thrombin and related proteases, we have used isolated tissue preparations of the rabbit aortic strip (RAS), isolated guinea pig ileum (GPI) and isolated rat uterus (RU). Standard tissue-agonist regimens include epinephrine, thromboxane B2 with RAS; bradykinin, acetylcholine, histamine and serotonin with GPI; and acetylcholine, bradykinin and angiotensin with RU. The smooth muscle modulant action of numerous proteinases were screened in these regimens by bracketing the median dose response of the individual agonists. Protease complexes such as serum (rabbit, human and guinea pig), activated and nonactivated prothrombin complex concentrates and pancreatin were shown to produce varying but similar contractile responses as obtained by the standard agonists. Sera produced a dose-dependent contraction of the RAS, GPI and RU preparations. Various forms of thrombin produced different degrees of contraction of RAS accompanied by a desensitization process. On a molar basis the order of contractile activity ranged α > β>γ > nitro > DIP. All thrombins were found to augment the epinephrine and thromboxane B2 induced contraction of the RAS. Bovine and human factor Xa produced marked dilatation of the RAS but did not have any effect on the GPI and RU preparations. These results suggest that proteases exert direct musculotropic actions on smooth muscles. This should be taken into consideration in the pathophysiology of vascular spasms.

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