Journal articles on the topic 'Clonidine Synthesis'
To see the other types of publications on this topic, follow the link: Clonidine Synthesis.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 35 journal articles for your research on the topic 'Clonidine Synthesis.'
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
Ghabbour, Hazem A., Ahmed H. Bakheit, Essam Ezzeldin, and Gamal A. E. Mostafa. "Synthesis Characterization and X-ray Structure of 2-(2,6-Dichlorophenylamino)-2-imidazoline Tetraphenylborate: Computational Study." Applied Sciences 12, no. 7 (March 31, 2022): 3568. http://dx.doi.org/10.3390/app12073568.
Full textAbstract:
The title compound tetraphenylborate salt of clonidine (Catapres®), 2-(2,6-dichlorophenylamino)-2-imidazoline tetraphenylborate (3), was prepared in 76 % yield by the reaction of 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride (clonidine hydrochloride) (1) with sodium tetraphenylborate (2) in deionized water through anion exchange reaction at ambient temperature. The structure of the title borate salt was characterized by UV, thermal analysis, mass and NMR analyses. White crystals of (3) suitable for an X-ray structural analysis were obtained by slow growing from acetonitrile. The molecular structure of the titled compound (3) was crystallized in the acetonitrile, P21/c, a = 9.151 (3) Å, b = 12.522 (3) Å, c = 25.493 (6) Å, β = 105.161 (13)° V = 2819.5 (13) Å3, Z = 4. A DFT quantum chemistry calculation method was employed to investigate the interaction mechanism of clonidine with tetraphenylborate. The stable configurations of the complexes of clonidine with tetraphenylborate with electrostatic interactions were obtained. Finally, the interaction strength and type of the complexes were studied through the reduced density gradient (RDG) function. This study provides new theoretical insight into the interaction mechanism and a guide for screening and designing the optimal clonidine and tetraphenylborate reacting to form the complex.
2
KALKOTE, U. R., K. C. BRAHME, and N. R. AYYANGAR. "ChemInform Abstract: Synthesis of New Clonidine Analogues." ChemInform 23, no. 21 (August 22, 2010): no. http://dx.doi.org/10.1002/chin.199221182.
Full text
3
Plato, Craig F., and Jeffrey L. Garvin. "α2-Adrenergic-mediated tubular NO production inhibits thick ascending limb chloride absorption." American Journal of Physiology-Renal Physiology 281, no. 4 (October 1, 2001): F679—F686. http://dx.doi.org/10.1152/ajprenal.2001.281.4.f679.
Full textAbstract:
Stimulation of α2-adrenergic receptors inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (THAL) expresses α2-receptors. We hypothesized that selective α2-receptor activation decreases NaCl absorption by cortical THALs through activation of NOS and increased production of NO. We found that the α2-receptor agonist clonidine (10 nM) decreased chloride flux ( J Cl) from 119.5 ± 15.9 to 67.4 ± 13.8 pmol · mm−1 · min−1 (43% reduction; P < 0.02), whereas removal of clonidine from the bath increased J Cl by 20%. When NOS activity was inhibited by pretreatment with 5 mM N G-nitro-l-arginine methyl ester, the inhibitory effects of clonidine on THAL J Clwere prevented (81.7 ± 10.8 vs. 71.6 ± 6.9 pmol · mm−1 · min−1). Similarly, when the NOS substrate l-arginine was deleted from the bath, addition of clonidine did not decrease THAL J Cl from control (106.9 ± 11.6 vs. 132.2 ± 21.3 pmol · mm−1 · min−1). When we blocked the α2-receptors with rauwolscine (1 μM), we found that the inhibitory effect of 10 nM clonidine on THAL J Cl was abolished, verifying that α2, rather than I1, receptors mediate the effects of clonidine in the THAL. We investigated the mechanism of NOS activation and found that intracellular calcium concentration did not increase in response to clonidine, whereas pretreatment with 150 nM wortmannin abolished the clonidine-mediated inhibition of THAL J Cl, indicating activation of phosphatidylinositol 3-kinase and the Akt pathway. We found that pretreatment of THALs with 10 μM LY-83583, an inhibitor of soluble guanylate cyclase, blocked clonidine-mediated inhibition of THAL J Cl. In conclusion, α2-receptor stimulation decreases THAL J Cl by increasing NO release and stimulating guanylate cyclase. These data suggest that α2-receptors act as physiological regulators of THAL NO synthesis, thus inhibiting chloride transport and participating in the natriuretic and diuretic effects of clonidine in vivo.
4
Alvo, M., A. M. Espinoza, V. Fernandez, and E. T. Marusic. "Alpha 2-agonists block ADH action in toad bladder and this inhibition is not modified by indomethacin." American Journal of Physiology-Renal Physiology 255, no. 1 (July 1, 1988): F74—F77. http://dx.doi.org/10.1152/ajprenal.1988.255.1.f74.
Full textAbstract:
To identify the type of alpha-adrenoceptors involved in the inhibition of the hydrosmotic effect of antidiuretic hormone (ADH) on the toad bladder, we studied the effect of different alpha-adrenergic agonists and antagonists on ADH-induced water transport. Serosal addition of epinephrine (10(-6) M) and norepinephrine (10(-6) M) in the presence of 10(-4) M propranolol significantly inhibited the hydrosmotic effect of ADH (arginine vasopressin). This inhibitory effect of the catecholamines was completely reversed by 10(-5) M yohimbine but not by prazosin. Clonidine did not block ADH-induced water transport, but guanabenz, another alpha 2-agonist, inhibited water transport in response to ADH. In bladders pretreated with indomethacin to block prostaglandin synthesis, basal water permeability was increased, and even in this condition epinephrine inhibited ADH-induced water transport. These studies indicate that alpha 2-adrenergic receptors are involved in the inhibitory effect of catecholamines on ADH-mediated water permeability in the toad bladder. However, this effect was not mimicked by clonidine, as in the case of rabbit cortical collecting tubule. The inhibitory effect of epinephrine appears to be exerted independently of prostaglandin synthesis.
5
Ayyangar, N. R., K. C. Brahme, and K. V. Srinivasan. "A Novel Synthesis of Clonidine, an Anti-Hypertensive Drug fromo-Chloronitrobenzene." Synthesis 1987, no. 01 (1987): 64–65. http://dx.doi.org/10.1055/s-1987-27847.
Full text
6
Filer, Crist N., and David G. Ahern. "Synthesis and characterization of [phenyl-3H] clonidine hydrochloride at high specific activity." Journal of Labelled Compounds and Radiopharmaceuticals 44, no. 5 (2001): 323–27. http://dx.doi.org/10.1002/jlcr.457.
Full text
7
Gales, Mark A. "Oral Antihypertensives for Hypertensive Urgencies." Annals of Pharmacotherapy 28, no. 3 (March 1994): 352–58. http://dx.doi.org/10.1177/106002809402800311.
Full textAbstract:
OBJECTIVE: To review the data describing the use of oral antihypertensive agents in the treatment of hypertensive urgencies (HU). DATA SOURCES: A MEDLINE search of the English-language literature and fan searches of papers evaluating oral antihypertensives in HUs and emergencies were conducted. STUDY SELECTION: Controlled and uncontrolled studies in humans are reviewed. Emphasis was placed on recent trials evaluating individual agents and comparative trials. DATA SYNTHESIS: Comparative trials have demonstrated that four currently available oral agents can lower blood pressure rapidly and predictably. Nifedipine, the most extensively studied, and clonidine have served traditionally as the oral agents of choice for the treatment of HUs. All the agents can lower blood pressure effectively within the first few hours after dosing, but their use also has been associated with adverse effects. Nifedipine and captopril are the two agents with the most rapid onset, within 0.5–1 hour, and may treat hypertensive emergencies as well as urgencies. Clonidine and labetalol have maximal blood pressure lowering effects at 2–4 hours. CONCLUSIONS: Captopril, clonidine, labetalol, and nifedipine are all effective agents for the treatment of HUs. Agent selection should be based on the perceived need for urgent blood pressure control, the cause of HU, and concomitant conditions. A definite benefit from acute blood pressure lowering in HUs has yet to be demonstrated, especially in asymptomatic patients. More controlled trials with less aggressive dosing regimens and placebo controls need to be performed to assess the most appropriate treatments for HUs with the fewest adverse effects.
8
Wang, Xinyan, Mable M. S. Chu, and Anderson O. L. Wong. "Signaling mechanisms for α2-adrenergic inhibition of PACAP-induced growth hormone secretion and gene expression grass carp pituitary cells." American Journal of Physiology-Endocrinology and Metabolism 292, no. 6 (June 2007): E1750—E1762. http://dx.doi.org/10.1152/ajpendo.00001.2007.
Full textAbstract:
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a potent growth hormone (GH)-releasing factor in lower vertebrates. However, its functional interactions with other GH regulators have not been fully characterized. In fish models, norepinephrine (NE) inhibits GH release at the pituitary cell level, but its effects on GH synthesis have yet to be determined. We examined adrenergic inhibition of PACAP-induced GH secretion and GH gene expression using grass carp pituitary cells as a cell model. Through activation of pituitary α2-adrenoreceptors, NE or the α2-agonist clonidine reduced both basal and PACAP-induced GH release and GH mRNA expression. In carp pituitary cells, clonidine also suppressed cAMP production and intracellular Ca2+ levels and blocked PACAP induction of these two second messenger signals. In GH3 cells transfected with a reporter carrying the grass carp GH promoter, PACAP stimulation increased GH promoter activity, and this stimulatory effect could be abolished by NE treatment. In parallel experiments, clonidine reduced GH primary transcript and GH promoter activity without affecting GH mRNA stability, and these inhibitory actions were mimicked by inhibiting adenylate cyclase (AC), blocking protein kinase A (PKA), removing extracellular Ca2+ in the culture medium, or inactivating L-type voltage-sensitive Ca2+ channels (VSCC). Since our recent studies have shown that PACAP can induce GH secretion in carp pituitary cells through cAMP/PKA- and Ca2+/calmodulin-dependent mechanisms, these results, taken together, suggest that α2-adrenergic stimulation in the carp pituitary may inhibit PACAP-induced GH release and GH gene transcription by blocking the AC/cAMP/PKA pathway and Ca2+ entry through L-type VSCC.
9
Seuwen, K., I. Magnaldo, B. K. Kobilka, M. G. Caron, J. W. Regan, R. J. Lefkowitz, and J. Pouysségur. "Alpha 2-adrenergic agonists stimulate DNA synthesis in Chinese hamster lung fibroblasts transfected with a human alpha 2-adrenergic receptor gene." Cell Regulation 1, no. 6 (May 1990): 445–51. http://dx.doi.org/10.1091/mbc.1.6.445.
Full textAbstract:
To test the hypothesis that agents activating receptors negatively coupled to adenylyl cyclase (AC) can stimulate cell proliferation, we have expressed a human alpha 2-adrenergic receptor (alpha 2-C10) in CCL39 cells and studied the effects of alpha 2-agonists on reinitiation of DNA synthesis in quiescent cells. We report that the alpha 2-agonists epinephrine and clonidine stimulate [3H]-thymidine incorporation in synergy with fibroblast growth factor and that the alpha 2-antagonist yohimbine efficiently inhibits this response. Epinephrine- and clonidine-stimulated DNA synthesis is completely blocked by pertussis toxin and correlates well with the inhibition of prostaglandin E1-stimulated AC. Thus, their action closely resembles the action of serotonin in the same cell system, which is mediated through 5-HT1b receptors. In fact, serotonin- and epinephrine-stimulated DNA synthesis reinitiation is not additive, suggesting that both agents act through a common pathway. Interestingly, alpha 2-agonists also induced a moderate release of inositol phosphates, indicating that alpha 2-adrenergic receptors can interact both with the AC and phospholipase C messenger system. Activation of phosphoinositide (PI) turnover by epinephrine leads to a significant stimulation of Na+/H+ exchange but is insufficient to trigger a mitogenic response in CCL39 cells, as will be discussed. We found no evidence for epinephrine-induced activation of Na+/H+ exchange by a mechanism independent of PI breakdown.Our data show that alpha 2-adrenergic receptors can play a role in the regulation of cell proliferation in an appropriate context; also, the data support the hypothesis that receptors negatively coupled to AC must be taken into account as mediators of growth factor action in fibroblasts, in particular when activated in parallel with receptor tyrosine kinases.
10
Gaida, W., R. E. Lang, K. Kraft, Th Unger, and D. Ganten. "Altered Neuropeptide Concentrations in Spontaneously Hypertensive Rats: Cause or Consequence?" Clinical Science 68, no. 1 (January 1, 1985): 35–43. http://dx.doi.org/10.1042/cs0680035.
Full textAbstract:
1. Changes in brain neuropeptide content in spontaneously hypertensive rats may be primarily related to the development of hypertension or may be secondary consequences of it. 2. We have measured brain concentrations of β-endorphin, Leu-enkephalin, arginine vasopressin (AVP) and oxytocin (OXT) in stroke-prone spontaneously hypertensive rats (SHRSP) and in age-matched normotensive Wistar Kyoto (WKY) controls, as well as in SHRSP with normalized blood pressure by chronic treatment with clonidine. Opioid peptide contents were measured in 12-, 18- and 24-week-old rats. β-Endorphin was measured in the neuro-intermediate and anterior lobes of the pituitary, the hypothalamus, midbrain and brain stem; Leu-enkephalin in the neuro-intermediate lobe of the pituitary, hypothalamus, mid-brain, brain stem, as well as in the spinal cord and adrenal glands. AVP and OXT were measured in the neuro-intermediate lobe of the pituitary, hypothalamus, brain stem and spinal cord. 3. β-Endorphin in the neuro-intermediate lobe of the pituitary was significantly higher in 12- and 18-week-old SHRSP. Adrenal gland Leu-enkephalin was lower in SHRSP as compared with the WKY. 4. OXT and AVP contents were markedly reduced in all brain regions of SHRSP except the neuro-intermediate lobe of the pituitary, where no significant changes were found. 5. In no case did long-term antihypertensive treatment with clonidine reverse the altered peptide content in the SHRSP. 6. We conclude that alterations in brain neuropeptide content in SHRSP are not secondary to hypertension. The blood pressure lowering activity of clonidine appears not to depend on major alterations of peptide concentrations. A genetic defect in the synthesis of adrenal enkephalins and hypothalamic OXT and AVP seems likely from these studies.
11
Guirguis, Erenie, Jonathan Richardson, Tara Kuhn, and Ashley Fahmy. "Treatment of Severe Alcohol Withdrawal: A Focus on Adjunctive Agents." Journal of Pharmacy Technology 33, no. 5 (June 19, 2017): 204–12. http://dx.doi.org/10.1177/8755122517714491.
Full textAbstract:
Objective:To review adjunctive treatment options for severe alcohol withdrawal. Data Sources: The search strategy included a search of Ovid MEDLINE using keywords alcohol withdrawal, severe alcohol withdrawal, AWS, delirium tremens, delirium, dexmedetomidine, propofol, anticonvulsants, clonidine, and phenobarbital and included articles dated from January 1990 to March 2017. Study Selection and Data Extraction: All English-language clinical trials and case reports assessing the efficacy of adjunctive agents in severe alcohol withdrawal were evaluated. Data Synthesis: Although first-line pharmacotherapy for alcohol withdrawal continues to be benzodiazepines, literature does not clearly define adjunctive treatment options for severe alcohol withdrawal. During severe alcohol withdrawal patients may become unable to tolerate or may become unresponsive to high-dose benzodiazepines. Large doses of benzodiazepines may also result in oversedation, respiratory insufficiency, and worsening delirium. Conclusions: Phenobarbital and dexmedetomidine are both viable adjunctive treatment options for severe alcohol withdrawal. Current evidence has shown these agents decrease the dose requirements of benzodiazepines with limited incidence of adverse reactions. Propofol may also be a viable option in mechanically ventilated patients, but its lack of clear safety and efficacy advantages over current treatment options may limit its use in practice. Clonidine, oral anticonvulsants, and ketamine require further controlled clinical trials to clearly define their role in the treatment of severe alcohol withdrawal.
12
Honey, Brooke L., Russell J. Benefield, Jamie L. Miller, and Peter N. Johnson. "α2-Receptor Agonists for Treatment and Prevention of Iatrogenic Opioid Abstinence Syndrome in Critically Ill Patients." Annals of Pharmacotherapy 43, no. 9 (August 18, 2009): 1506–11. http://dx.doi.org/10.1345/aph.1m161.
Full textAbstract:
Objective: To review the literature regarding the use of α2-agonists in the treatment and prevention of iatrogenic opioid abstinence syndrome (IOAS) in critically ill patients. Data Sources: Primary literature was identified through a search of MEDLINE (1950–June 2009), EMBASE (1988–June 2009), International Pharmaceutical Abstracts (1970–June 2009), and the Cochrane Library (1996–June 2009), using the names of individual α2-agonists and the following key words: children, opioid withdrawal, opioid, and adult. Relevant abstracts from the Society of Critical Care Medicine, reference citations from selected articles, and manufacturers’ product information were also reviewed. Study Selection and Data Extraction: All English-language articles identified from the data sources were evaluated. Three retrospective studies and 6 case reports/series representing 44 patients were included for analysis. Data Synthesis: Central α2-agonists are thought to minimize symptoms of IOAS by decreasing presynaptic outflow of catecholamines. Successful use of clonidine and dexmedetomidine for management of IOAS has been reported. Lofexidine, an α2-agonist not yet approved in the US, may offer similar withdrawal symptom relief but has yet to be studied in the intensive care setting. Although the quality of studies identified was limited, preliminary evidence does provide some support for the use of transdermal clonidine and injectable dexmedetomidine in the treatment and prevention of IOAS. These agents were shown to facilitate discontinuation of opioids and to minimize withdrawal symptoms with few reported adverse events. Conclusions: Central α2-agonists appear to be effective and safe second-line agents for treatment and prevention of IOAS. Further studies should be conducted to determine their role in the therapy of patients with IOAS.
13
Xu, Zemin, Chuanyao Tong, Hui-Lin Pan, Sergio E. Cerda, and James C. Eisenach. "Intravenous Morphine Increases Release of Nitric Oxide From Spinal Cord by an α-Adrenergic and Cholinergic Mechanism." Journal of Neurophysiology 78, no. 4 (October 1, 1997): 2072–78. http://dx.doi.org/10.1152/jn.1997.78.4.2072.
Full textAbstract:
Xu, Zemin, Chuanyao Tong, Hui-Lin Pan, Sergio E. Cerda, and James C. Eisenach. Intravenous morphine increases release of nitric oxide from spinal cord by an α-adrenergic and cholinergic mechanism. J. Neurophysiol. 78: 2072–2078, 1997. Systemic opioids produce analgesia in part by activating bulbospinal noradrenergic pathways. Spinally released norepinephrine (NE) has been suggested to produce analgesia in part by stimulating α2-adrenoceptors on cholinergic spinal interneurons to release acetylcholine (ACh). We hypothesized that this spinally released ACh would stimulate synthesis of nitric oxide (NO), and that spinally released NO after intravenous (IV) opioid injection thus would depend on a cascade of noradrenergic and cholinergic receptor stimulation. To test these hypotheses, IV morphine was administered to anesthetized sheep, and neurotransmitters in dorsal horn interstitial fluid were measured by microdialysis. IV morphine increased NE and ACh in dorsal horn microdialysates, and these increases were inhibited by IV naloxone or cervical spinal cord transection. IV morphine also increased dorsal horn microdialysate concentrations of nitrite, a stable metabolite of NO. Increases in NE, ACh, and nitrite were antagonized by prior intrathecal injection of the α2-adrenergic antagonist idazoxan, the muscarinic antagonist atropine, or the NO synthase inhibitor N-methyl-l-arginine (NMLA). To examine the concentration-dependent effects of spinal adrenergic stimulation, isolated rat spinal cord tissue was perfused with the α2-adrenergic agonist clonidine. Clonidine increased nitrite in the spinal cord tissue perfusate, an effect blocked by coadministration of idazoxan, atropine, and NMLA. These data support a previously hypothesized cascade of spinally released NE and ACh after systemic opioid administration. These data also suggest that spinally released NO plays a role in the analgesic effects of systemic opioids. In addition, these data imply a positive feedback whereby spinally released nitric oxide increases NE release and that has not previously been described.
14
Nakagawa, Shiori, Takayuki Ueno, Takayuki Manabe, and Kiyoshi Kawasaki. "Imidazolines increase the levels of the autophagosomal marker LC3-II in macrophage-like RAW264.7 cells." Canadian Journal of Physiology and Pharmacology 96, no. 8 (August 2018): 845–49. http://dx.doi.org/10.1139/cjpp-2018-0021.
Full textAbstract:
This study evaluated whether imidazolines can induce autophagy in the murine macrophage-like cell line RAW264.7. Idazoxan increased the content of LC3-II, an autophagosomal marker, in RAW264.7 cells. To determine whether this effect was due to the induction of its synthesis or inhibition of its degradation, idazoxan treatment was performed in the presence of bafilomycin A1, which blocks autophagosome-lysosome fusion, as well as Pepstatin A and E-64d, both of which block protein degradation in autolysosomes. An increased content of LC3-II was observed in the presence of bafilomycin A1 as well as the protease inhibitors. Furthermore, an increased number of autophagosomes was observed following idazoxan treatment using an autophagosome-specific dye. This indicated that idazoxan induced autophagy. Other imidazolines, such as efaroxan, clonidine, and 2-(2-benzofuranyl)-2-imidazoline, also increased the LC3-II content in RAW264.7 cells in the presence of bafilomycin A1. Taken together, these results indicate that some imidazolines, including idazoxan, can induce autophagy in RAW264.7 cells.
15
Fujimoto, Shimpei, Yoshiyuki Tsuura, Hitoshi Ishida, Kazuo Tsuji, Eri Mukai, Mariko Kajikawa, Yoshiyuki Hamamoto, Tomomi Takeda, Yuichiro Yamada, and Yutaka Seino. "Augmentation of basal insulin release from rat islets by preexposure to a high concentration of glucose." American Journal of Physiology-Endocrinology and Metabolism 279, no. 4 (October 1, 2000): E927—E940. http://dx.doi.org/10.1152/ajpendo.2000.279.4.e927.
Full textAbstract:
We have found that preexposure to an elevated concentration of glucose reversibly induces an enhancement of basal insulin release from rat pancreatic islets dependent on glucose metabolism. This basal insulin release augmented by priming was not suppressed by reduction of the intracellular ATP or Ca2+ concentration, because even in the absence of ATP at low Ca2+, the augmentation was not abolished from primed electrically permeabilized islets. Moreover, it was not inhibited by an α-adrenergic antagonist, clonidine. A threshold level of GTP is required to induce these effects, because together with adenine, mycophenolic acid, a cytosolic GTP synthesis inhibitor, completely abolished the enhancement of basal insulin release due to the glucose-induced priming without affecting the glucose-induced increment in ATP content and ATP-to-ADP ratio. In addition, a GDP analog significantly suppressed the enhanced insulin release due to priming from permeabilized islets in the absence of ATP at low Ca2+, suggesting that the GTP-sensitive site may play a role in the augmentation of basal insulin release due to the glucose-induced priming effect.
16
Fulas, Oli Abate, André Laferrière, Ghada Ayoub, Dayaker Gandrath, Cristina Mottillo, Hatem M. Titi, Robin S. Stein, Tomislav Friščić, and Terence J. Coderre. "Drug-Nutraceutical Co-Crystal and Salts for Making New and Improved Bi-Functional Analgesics." Pharmaceutics 12, no. 12 (November 26, 2020): 1144. http://dx.doi.org/10.3390/pharmaceutics12121144.
Full textAbstract:
The discovery and development of effective analgesics is greatly lagging behind the steadily rising prevalence of chronic pain. Currently prescribed analgesics for chronic pain are lacking in efficacy mainly due to their narrowly-targeted mechanism of action. Driving neuronal hyperexcitability that underlies symptoms of chronic pain are multiple non-neuronal processes, among which are tissue hypoxia and oxidative stress. Here we demonstrate the design, synthesis, and activity of new multi-component bi-functional analgesic crystalline solids, co-crystals, and salts, based on pairing of vasodilatory anti-hypoxic drugs pentoxifylline, clonidine and linsidomine with antioxidant nutraceuticals protocatechuic acid, α-lipoic acid, and caffeic acid. After validation, chemical and structural characterization of these novel salts and co-crystals, topical formulations of the products were tested in a rat model of complex regional pain syndrome. Analgesic effects achieved with the salts and co-crystal exceeded the efficacy and/or potency of constituent compounds indicating that more effective, advanced analgesics can readily be developed by careful pairing of compounds that simultaneously target multiple neural and non-neural processes driving chronic pain.
17
Hilleman, Daniel E., and Umesh V. Banakar. "Issues in Contemporary Drug Delivery." Journal of Pharmacy Technology 8, no. 5 (September 1992): 203–11. http://dx.doi.org/10.1177/875512259200800509.
Full textAbstract:
Objective: To identify and discuss the clinical utility of new delivery systems and formulations of cardiac drugs. Data Sources: Studies describing or evaluating new drug delivery systems for cardiac drugs were identified through a MEDLINE literature search. Study Selection: All studies describing or evaluating new delivery systems for cardiac drugs were reviewed. Data Extraction: Data were abstracted and evaluated by each author independently. Data Synthesis: The most common oral sustained-release formulations include the wax-matrix system, the gastrointestinal therapeutic system (GITS), and the spheroidal oral drug absorption system (SODAS). The wax-matrix delivery system is limited by the occurrence of “dose-dumping.” In a low-pH setting, the wax-matrix formulation may dissolve too rapidly, liberating the entire dose in a short period of time. The clinical relevance of this phenomenon is unknown. The GITS and SODAS formulations are less likely to be affected by pH and food. Nitroglycerin is available by many routes of administration. The topical patch forms are convenient to use, but are associated with the development of tolerance. A buccal formulation incorporates a relatively short onset of effect with a three- or four-times-daily dosing regimen. Although tolerance is less of a problem with buccal nitroglycerin than with topical nitrates, this formulation is less convenient to use because of buccal irritation and interference with eating and talking. A new spray formulation of nitroglycerin offers longer shelf-life storage stability and an easier mode of administration. The spray canister is stable for three years compared with 12 weeks for an opened bottle of sublingual nitroglycerin tablets. Sublingual administration of oral cardiac drugs offers the potential for a more rapid onset of effects. Although nifedipine is often given sublingually, objective data indicate that it is not absorbed buccally but rather in the stomach. It appears that the chew-and-swallow route is most appropriate for nifedipine. Captopril is absorbed sublingually but its efficacy has not been demonstrated. Transdermal clonidine improves compliance and is associated with fewer adverse effects than oral clonidine. Transdermal formulations of beta-blockers are currently being evaluated. Conclusions: Further advancements in the development of novel delivery systems for cardiac drugs are expected in the future.
18
CELLA, SILVANO G., VITTORIO LOCATELLI, VITO DE GENNARO, CRISTINA PELLINI, CARLO PINTOR, and EUGENIO E. MÜLLER. "In VivoStudies with Growth Hormone (GH)-Releasing Factor and Clonidine in Rat Pups: Ontogenetic Development of their Effect on GH Release and Synthesis*." Endocrinology 119, no. 3 (September 1986): 1164–70. http://dx.doi.org/10.1210/endo-119-3-1164.
Full text
19
Maunder, E. M. W., A. V. Pillay, and A. D. Care. "Endocrine control of plasma concentrations of calcium-binding protein in the pig." Journal of Endocrinology 115, no. 1 (October 1987): 121–28. http://dx.doi.org/10.1677/joe.0.1150121.
Full textAbstract:
ABSTRACT The aetiology of the rise in plasma calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP), following insulin-induced hypoglycaemia, was studied in the pig. ACTH led to a rise in plasma concentrations of both CaBP and cortisol. Metyrapone, which blocks cortisol synthesis, abolished the increases in plasma concentrations of CaBP and cortisol normally observed in response to insulin-induced hypoglycaemia. However, there was no significant rise in plasma concentrations of CaBP in response to pharmacological or physiological doses of cortisol. Injection of clonidine, an α2-adrenergic agonist, led to a rise in plasma concentrations of CaBP, whereas phenylephrine, an α1-adrenergic agonist, tended to exert an inhibitory effect. Also, administration of phentolamine (an α-adrenergic blocker) before injection of insulin abolished the usual increase in plasma concentrations of CaBP, whereas propranolol (a β-adrenergic blocker) enhanced the normal increase in plasma concentrations of CaBP in response to insulin-induced hypoglycaemia. Isoproterenol, a β-adrenergic agonist, was without effect on plasma CaBP. Neither GH nor glucagon appear to be involved in the rise in plasma CaBP following insulin-induced hypoglycaemia. Although atropine abolished the effect of acute hypoglycaemia on plasma CaBP, carbamylcholine was without effect on plasma CaBP concentration. It is concluded that the increases in plasma CaBP induced by either ACTH or α2-adrenergic stimulation may be interrelated since the administration of ACTH can lead to raised plasma concentrations of catecholamines. J. Endocr. (1987) 115, 121–128
20
Johnson, D. A., and J. E. Cortez. "Chronic Treatment with Beta Adrenergic Agonists and Antagonists Alters the Composition of Proteins in Rat Parotid Saliva." Journal of Dental Research 67, no. 8 (August 1988): 1103–8. http://dx.doi.org/10.1177/00220345880670080801.
Full textAbstract:
This investigation was undertaken to determine the role of β-adrenergic receptors in the regulation of the protein composition of rat parotid saliva. Chronic treatment of rats with dobutamine, a β1-adrenergic agonist, resulted in changes in parotid saliva volume, protein concentration, and composition which were essentially the same as those changes which occurred following chronic treatment with isoproterenol, a non-specific β-adrenergic agonist. Chronic treatment with the β2-adrenergic agonist, terbutaline, had no effect on parotid saliva volume, protein concentration, or composition. Chronic treatment of rats with a β1-adrenergic antagonist, metoprolol, had different effects on saliva dependent on the manner by which the drug was delivered. Twice-daily injections of metoprolol led to a decrease in flow rate, but protein concentration and composition were unaltered. When metoprolol was delivered by surgically implanted osmotic mini pumps, neither the flow of parotid saliva nor its concentration of protein was altered; however, there was a reduction in the proportion of proline-rich proteins in saliva. Comparable changes in parotid saliva protein composition occurred when the mini pumps delivered propranolol, a non-specific β-adrenergic antagonist. Chronic treatment of rats with an α2-adrenergic agonist (clonidine) or antagonist (yohimbine) was without effect on parotid saliva flow rate, protein concentration, or composition. These findings suggest that the synthesis of proline-rich proteins is regulated, in part, by β-adrenergic receptor stimulation, and primarily by the β1-receptor subtype.
21
Lassi, Dângela Layne Silva, André Malbergier, André Brooking Negrão, Lígia Florio, João P. De Aquino, and João Maurício Castaldelli-Maia. "Pharmacological Treatments for Cocaine Craving: What Is the Way Forward? A Systematic Review." Brain Sciences 12, no. 11 (November 14, 2022): 1546. http://dx.doi.org/10.3390/brainsci12111546.
Full textAbstract:
Background: cocaine craving is a core feature of cocaine use disorder and remains a critical challenge for abstinence and relapse prevention. This review summarizes the anti-craving efficacy of pharmacotherapies tested for cocaine use disorder, in the context of randomized-controlled clinical trials. Objectives: we assessed the databases of the U.S. National Library of Medicine, Google Scholar, and PsycINFO, without date restrictions up to August 2022, to identify relevant studies. Study eligibility criteria, participants, and interventions: we included double-blinded randomized-controlled trials investigating pharmacotherapies for cocaine craving and/or cocaine use disorder whose outcomes included cocaine craving. Study appraisal and synthesis methods: Two authors screened studies’ titles and abstracts for inclusion, and both read all the included studies. We systematically gathered information on the following aspects of each study: title; author(s); year of publication; sample size; mean age; sample characteristics; study set-ting; whether participants were treatment-seeking; study design; craving measures; study interventions; drop-out rates; and other relevant outcomes. Results: Overall, we appraised 130 clinical trials, including 8137 participants. We further considered the drugs from the studies that scored equal to or greater than six points in the quality assessment. There was a correlation between craving and cocaine use outcomes (self-reports, timeline follow-back or urinary benzoylecgonine) in the vast majority of studies. In the short-term treatment, acute phenylalanine-tyrosine depletion, clonidine, fenfluramine, meta-chlorophenylpiperazine (m-CPP) and mecamylamine presented promising effects. In the long term, amphetamine, biperiden, carbamazepine, lisdexamfetamine, lorcaserin, methamphetamine, mirtazapine, pioglitazone, progesterone, guanfacine, levodopa, nefazodone presented promising anti-craving effects. Unfortunately, the highly tested medications were not successful in most of the trials, as follows: propranolol in the short term; amantadine, aripiprazole, bromocriptine, citicoline, ketamine, modafinil, olanzapine, topiramate in the long term. The remaining 52 medications had no positive anti-craving outcomes. Limitations: Our review was limited by high heterogeneity of craving assessments across the studies and by a great range of pharmacotherapies. Further, the majority of the studies considered abstinence and retention in treatment as the main outcomes, whereas craving was a secondary outcome and some of the studies evaluated patients with cocaine use disorder with comorbidities such as opioid or alcohol use disorder, schizophrenia, bipolar disorder or attention deficit hyperactivity. Lastly, most of the studies also included non-pharmacological treatments, such as counseling or psychotherapy Conclusions: There is a direct association between craving and cocaine use, underscoring craving as an important treatment target for promoting abstinence among persons with cocaine use disorder. Clonidine, fenfluramine and m-CPP showed to be promising medications for cocaine craving in the short-term treatment, and amphetamine, biperiden, carbamazepine, lisdexamfetamine, lorcaserin, methamphetamine, mirtazapine, pioglitazone, progesterone, guanfacine, levodopa, nefazodone in the long-term treatment.
22
Rouch, Alexander J., and Lúcia H. Kudo. "Role of PGE2 in α2-induced inhibition of AVP- and cAMP-stimulated H2O, Na+, and urea transport in rat IMCD." American Journal of Physiology-Renal Physiology 279, no. 2 (August 1, 2000): F294—F301. http://dx.doi.org/10.1152/ajprenal.2000.279.2.f294.
Full textAbstract:
PGE2 inhibits osmotic water permeability ( P f) in the rat inner medullary collecting duct (IMCD) via cellular events occurring after the stimulation of cAMP, i.e., post-cAMP-dependent events. The α2-agonists also inhibit P f in the rat IMCD via post-cAMP-dependent events. The purpose of this study was to determine whether PGE2 plays a role in α2-mediated inhibition of P f, Na+, and urea transport in the rat IMCD. Isolated terminal IMCDs from Wistar rats were perfused to measure, in separate experiments, P f, lumen-to-bath22Na+ transport ( J lb), and urea permeability ( P u). Transport was stimulated with 220 pM arginine vasopressin (AVP) or 0.1 mM 8-(4-chlorophenylthio)-cAMP (CPT-cAMP). Indomethacin was used to inhibit endogenous prostaglandin synthesis, and the α2-agonists clonidine, oxymetazoline, and dexmedetomidine were used to test the role of PGE2 in the α2-mediated mechanism that inhibits transport. All agents were added to the bath. Indomethacin at 5 μM significantly elevated CPT-cAMP-stimulated P f, J lb, and P u, and subsequent addition of 100 nM PGE2 reduced these transport parameters. Indomethacin reversed α2 inhibition of CPT-cAMP-stimulated P f, J lb, and P u, and subsequent addition of PGE2 reduced transport in each case. Indomethacin partially reversed α2 inhibition of AVP-stimulated P f, J lb, and P u, and PGE2 reduced transport back to the α2-inhibited level. These results indicate that PGE2 is a second messenger involved in the mechanism of transport inhibition mediated by α2-adrenoceptors via post-cAMP-dependent events in the rat IMCD.
23
Saphier, D. "Electrophysiology and neuropharmacology of noradrenergic projections to rat PVN magnocellular neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 5 (May 1, 1993): R891—R902. http://dx.doi.org/10.1152/ajpregu.1993.264.5.r891.
Full textAbstract:
Responses of electrophysiologically identified tuberohypophysial paraventricular nucleus (PVN) neurons were examined following electrical stimulation of the A1, A2, A6, and C2 catecholaminergic cell groups and of the ventral noradrenergic ascending bundle (VNAB). A1, A2, and A6 stimulation evoked primarily excitatory responses from the cells recorded, but C2 stimulation yielded a greater proportion of inhibitory responses. VNAB stimulation at low frequencies (0.5/5 Hz) excited the majority of cells tested, but high-frequency (50 Hz) trains of stimulation reversed the direction of response to inhibition for approximately half of the cells excited by single-shock stimulation. Only 5-Hz stimulation had any affect on blood pressure, causing a slight increase. Treatment with alpha-methylparatyrosine, to inhibit (nor) epinephrine synthesis, reduced the proportion of excitatory responses and prevented the response reversals following 50-Hz VNAB stimulation. Treatment with 6-hydroxydopamine also reduced the proportion of cells excited by VNAB stimulation. Iontophoresis of either norepinephrine or the alpha 1-adrenoceptor agonist l-phenylephrine increased the activity of most cells tested whilst the alpha 1-antagonist ergotamine reduced the activity of most cells tested and prevented excitation elicited by VNAB stimulation. The alpha 2-agonist clonidine excited all cells tested. The beta-antagonist propranolol increased the activity of the majority of cells and prevented inhibitory responses following 50-Hz VNAB stimulation. The results confirm a role for brain stem projections in regulating PVN neuronal activity and demonstrate for the first time that the VNAB provides excitatory input to the PVN, primarily regulated by alpha 1-adrenoceptors. The effects of propranolol on spontaneous activity, and on the inhibitory responses following high-frequency VNAB stimulation, indicate the presence of an inhibitory counterbalancing beta-adrenoceptor mechanism.
24
Tallet, J., N. M. Munoz, R. Fried, and A. R. Leff. "Endogenous modulation of alpha-adrenergic contraction in canine tracheal muscle." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 464–71. http://dx.doi.org/10.1152/jappl.1986.61.2.464.
Full textAbstract:
We studied the effect of passive stretch on the contraction of canine tracheal smooth muscle (TSM) to alpha-adrenergic agonists and acetylcholine (ACh) in 211 epithelium-free TSM strips from 42 dogs in vitro. Passive stretch at a resting tension of 100 g/cm2 caused a time-dependent decrease in the contractile response to alpha-adrenergic agonists after beta-adrenergic blockade with propranolol. Initial contraction elicited by 10(-3) M phenylephrine (PE) and clonidine (CLO) decreased at 2 h by 31 and 100%, respectively. Decrease in alpha-adrenergic contractility did not result from tachyphylaxis; no contraction was elicited by PE or CLO given for the first time after 4-h passive stretch at 100 g/cm2. The TSM response to ACh was unchanged over the same time in the same strips. When TSM strips were incubated at zero resting tension for 6 h, some attenuation of the alpha-adrenergic contractile still occurred but was not substantial. Similarly, when strips were incubated with 10(-6) M indomethacin (INDO) or 10(-5) M mefenamic acid (MEF) at 100 g/cm2 resting tension, time-dependent attenuation of the response to PE and CLO was reduced for at least 6 h, and initial contraction elicited by PE was augmented. Response of TSM to ACh was not affected by prostaglandin synthetase inhibition with INDO. We conclude that passive stretch of canine TSM in vitro leads to decreased responsiveness to alpha-adrenergic stimulation that can be prevented with INDO or MEF. These data are consistent with the synthesis of an inhibitory eicosanoid in epithelium-free canine TSM that may be activated by mechanical deformation of the muscle.
25
Lima, Luis, Victor Arce, Jesús A. F. Tresguerres, and Jesús Devesa. "Clonidine Potentiates the Growth Hormone (GH) Response to GH-Releasing Hormone in Norepinephrine Synthesis-Inhibited Rats: Evidence for an Alpha-2-Adrenergic Control of Hypothalamic Release of Somatostatin." Neuroendocrinology 57, no. 6 (1993): 1155–60. http://dx.doi.org/10.1159/000126482.
Full text
26
Araújo, Jimmy de Oliveira, Cristiane de Cássia Bergamaschi, Luciane Cruz Lopes, Caio Chaves Guimarães, Natalia Karol de Andrade, Juliana Cama Ramacciato, and Rogério Heládio Lopes Motta. "Effectiveness and safety of oral sedation in adult patients undergoing dental procedures: a systematic review." BMJ Open 11, no. 1 (January 2021): e043363. http://dx.doi.org/10.1136/bmjopen-2020-043363.
Full textAbstract:
ObjectivesIt can be challenging to manage patients who are anxious during dental procedures. There is a lack of evidence regarding the effectiveness and safety of oral sedation in adults. This study evaluated the effectiveness and safety of oral sedation in patients undergoing dental procedures.DesignSystematic review.MethodsRandomised clinical trials (RCTs) compared the oral use of benzodiazepines and other medications with a placebo or other oral agents in adult patients. A search of the Cochrane (CENTRAL), MEDLINE (via Ovid), EMBASE (via Ovid) and Cumulative Index to Nursing and Allied Health Literature (via Ovid) databases was conducted, without any restrictions on language or date of publication. The primary outcomes included the adverse effects and anxiety level. The secondary outcomes included sedation, satisfaction with the treatment, heart rate, respiratory rate, blood pressure and oxygen saturation. Reviewers, independently and in pairs, assessed each citation for eligibility, performed the data extraction and assessed the risk of bias. A narrative synthesis of the data was provided.ResultsA number of RCTs (n=327 patients) assessed the use of benzodiazepines (n=9) and herbal medicines (n=3). We found good satisfaction with treatment after the use of midazolam 7.5 mg or clonidine 150 µg and reduced anxiety with alprazolam (0.5 and 0.75 mg). Midazolam 15 mg promoted greater anxiety reduction than Passiflora incarnata L. 260 mg, while Valeriana officinalis 100 mg and Erythrina mulungu 500 mg were more effective than a placebo. More patients reported adverse effects with midazolam 15 mg. Diazepam 15 mg and V. officinalis 100 mg promoted less change in the heart rate and blood pressure than a placebo.ConclusionsGiven the limitations of the findings due to the quality of the included studies and the different comparisons made between interventions, further RCTs are required to confirm the effectiveness and safety of oral sedation in dentistry.PROSPERO registration numberCRD42017057142.
27
Eiland, Lea S., Lauren S. Jenkins, and Spencer H. Durham. "Pediatric Migraine: Pharmacologic Agents for Prophylaxis." Annals of Pharmacotherapy 41, no. 7-8 (July 2007): 1181–90. http://dx.doi.org/10.1345/aph.1k049.
Full textAbstract:
Objective: To identify and evaluate the data regarding medication use for migraine prophylaxis in the pediatric population. Data Sources: Literature was obtained through searches in PubMed (Mid 1950s–March 2007), Iowa Drug Information Service/Web (1966–February 2007), International Pharmaceutical Abstracts (1970–Pebruary 2007), and the Cochrane Library. The terms migraine, prophylaxis, child, and children were used and cross referenced with all drug names. Reference citations from publications identified were also reviewed and included. Study Selection and Data Extraction: Only trials that evaluated migraine headaches in the pediatric population were included. Trials including adolescent and adult populations are briefly listed, but not reviewed. Trials involving nonprescription medication were also included in the evaluation. Due to the limited information, all clinical trials, retrospective reviews, and abstracts evaluated were included in this review. Data Synthesis: Few controlled clinical trials regarding prophylaxis therapy are available. Currently, no medications are approved by the Food and Drug Administration for prophylaxis of migraines in children. Seventeen drugs were identified and included in the review. Of the drugs with available data, topiramate, valproic acid, flunarizine, amitriptyline, and cyproheptadine have shown efficacy in decreasing migraine frequency and duration in children. However, larger clinical trials are necessary to validate the utility of these agents. Conflicting data exist for propranolol and pizotifen, and additional data are needed for gabapentin, leve-tiracetam, zonisamide, naproxen, and trazodone. In clinical trials, nimodipine, clonidine, and natural supplements have shown a lack of efficacy versus placebo for prophylaxis of migraines in children. Conclusions: Topiramate, valproic acid, and amitriptyline have the most data on their use for prophylaxis of migraines in children. Numerous agents have limited data in this population and several agents lack efficacy. Prospective, well designed, controlled clinical trials that include quality-of-life and functional outcomes are needed for guiding therapy of migraine prophylaxis for children.
28
Markowitz, John S., Barbara G. Wells, and William H. Carson. "Interactions Between Antipsychotic and Antihypertensive Drugs." Annals of Pharmacotherapy 29, no. 6 (June 1995): 603–9. http://dx.doi.org/10.1177/106002809502900610.
Full textAbstract:
Objective: To provide a comprehensive review of the pharmacokinetic and pharmacodynamic interactions between antipsychotics and antihypertensives and to provide recommendations for the selection of antihypertensives in patients receiving antipsychotic therapy. Data Sources: A MEDLINE search of the English-language literature was used to identify pertinent human and animal studies, reviews, and case reports. Study Selection: All available sources were reviewed. Data Extraction: Background information was obtained from comprehensive reviews. Individual case reports were assimilated, and pertinent data were extracted. Data Synthesis: Because hypertension is common in patients with psychiatric illness and antihypertensive agents are used for a multiplicity of indications, significant numbers of patients receive concurrent therapy with antihypertensives and antipsychotics. Many antipsychotics may block the antihypertensive efficacy of guanethidine and related drugs. The interaction between Clonidine and antipsychotics is defined less clearly. Limited data suggest possible additive hypotensive effects when chlorpromazine and methyldopa are given in combination. Increased plasma concentrations of thioridazine with a resultant increase in adverse effects have been reported when propranolol or pindolol are added to the regimen. A similar increase in chlorpromazine concentrations has been reported when propranolol was added. Although there are no reports documenting an interaction between a calcium-channel antagonist and an antipsychotic, the possible inhibition of oxidative metabolism of antipsychotics, additive calcium-blocking activity, and additive pharmacodynamic effects are theorized. Hypotension and postural syncope were reported in a patient given therapeutic dosages of chlorpromazine and Captopril, and in 2 patients when clozapine was added to enalapril therapy. Conclusions: No antipsychotic-antihypertensive combination is absolutely contraindicated, but no combination should be considered to be completely without risk. Antihypertensives with no centrally acting activity, such as diuretics, may be the least likely to result in adverse reactions. The combination of the beta-antagonists propranolol or pindolol with thioridazine or chlorpromazine should be avoided if possible. Scrupulous patient monitoring for attenuated or enhanced activity of either agent is essential whenever antipsychotics and antihypertensives are given concurrently.
29
Chiaramonte, Niccolò, Soumia Maach, Caterina Biliotti, Andrea Angeli, Gianluca Bartolucci, Laura Braconi, Silvia Dei, Elisabetta Teodori, Claudiu T. Supuran, and Maria Novella Romanelli. "Synthesis and carbonic anhydrase activating properties of a series of 2-amino-imidazolines structurally related to clonidine1." Journal of Enzyme Inhibition and Medicinal Chemistry 35, no. 1 (January 1, 2020): 1003–10. http://dx.doi.org/10.1080/14756366.2020.1749602.
Full text
30
Moayeri, Ardeshir, Reza Mehdizadeh, Elahe Karimi, Ali Aidy, Hori Ghaneialvar, and Naser Abbasi. "Thymol Nanopolymer Synthesis and Its Effects on Morphine Withdrawal Syndrome in Comparison With Clonidine in Rats." Frontiers in Behavioral Neuroscience 16 (June 29, 2022). http://dx.doi.org/10.3389/fnbeh.2022.843951.
Full textAbstract:
The drug delivery system is valuable in the treatment of the disease. A nanopolymer as a thymol and Thymbra spicata release system was synthesized and its effects on morphine withdrawal syndrome in comparison with clonidine in rats were studied. The nanopolymer was characterized by different methods, namely, IR, HNMR, CNMR, GPC, DLS, and AFM. Thymol in T. spicata extract was assessed. The loading and release rate of thymol and T. spicata extract on the nanopolymer were evaluated by HPLC. The median lethal dose (LD50) of the T. spicata extract, thymol, extract nanopolymer, and thymol nanopolymer was studied. The frequency of jumping, rearing, and teeth chattering in naloxone-induced morphine withdrawal syndrome was studied. Synthesized nanopolymer was desirable as a carrier for the drug. The loaded amount of extract and thymol on nanopolymer was estimated 55 ± 3.2% and 48 ± 2.6% and the drug released was 71 and 68%, respectively. LD50 of the T. spicata extract, thymol, extract nanopolymer, and thymol nanopolymer was 975, 580, 1,250, and 650 mg/kg, respectively. This study showed that thymol nanopolymer was more effective than clonidine to reduce the frequency of morphine withdrawal symptoms. Our results suggest that T. spicata extract, thymol, extract nanopolymer, and thymol nanopolymer are mighty in reducing the narcotic withdrawal signs. The mechanism of action and therapeutic potential is maybe similar to clonidine.
31
Flanders, Charles A., Alistair S. Rocke, Stuart A. Edwardson, J. Kenneth Baillie, and Timothy S. Walsh. "The effect of dexmedetomidine and clonidine on the inflammatory response in critical illness: a systematic review of animal and human studies." Critical Care 23, no. 1 (December 2019). http://dx.doi.org/10.1186/s13054-019-2690-4.
Full textAbstract:
Abstract Background The α2 agonists, dexmedetomidine and clonidine, are used as sedative drugs during critical illness. These drugs may have anti-inflammatory effects, which might be relevant to critical illness, but a systematic review of published literature has not been published. We reviewed animal and human studies relevant to critical illness to summarise the evidence for an anti-inflammatory effect from α2 agonists. Methods We searched PubMed, the Cochrane library, and Medline. Animal and human studies published in English were included. Broad search terms were used: dexmedetomidine or clonidine, sepsis, and inflammation. Reference lists were screened for additional publications. Titles and abstracts were screened independently by two reviewers and full-text articles obtained for potentially eligible studies. Data extraction used a bespoke template given study diversity, and quality assessment was qualitative. Results Study diversity meant meta-analysis was not feasible so descriptive synthesis was undertaken. We identified 30 animal studies (caecal ligation/puncture (9), lipopolysaccharide (14), acute lung injury (5), and ischaemia-reperfusion syndrome (5)), and 9 human studies. Most animal (26 dexmedetomidine, 4 clonidine) and all human studies used dexmedetomidine. In animal studies, α2 agonists reduced serum and/or tissue TNFα (20 studies), IL-6 (17 studies), IL-1β (7 studies), NFκB (6 studies), TLR4 (6 studies), and a range of other mediators. Timing and doses varied widely, but in many cases were not directly relevant to human sedation use. In human studies, dexmedetomidine reduced CRP (4 studies), TNFα (5 studies), IL-6 (6 studies), IL-1β (3 studies), and altered several other mediators. Most studies were small and low quality. No studies related effects to clinical outcomes. Conclusion Evidence supports potential anti-inflammatory effects from α2 agonists, but the relevance to clinically important outcomes is uncertain. Further work should explore whether dose relationships with inflammation and clinical outcomes are present which might be separate from sedation-mediated effects.
32
AYYANGAR, N. R., K. C. BRAHME, and K. V. SRINIVASAN. "ChemInform Abstract: A Novel Synthesis of Clonidine, an Anti-Hypertensive Drug from o-Chloronitrobenzene." ChemInform 18, no. 22 (June 2, 1987). http://dx.doi.org/10.1002/chin.198722183.
Full text
33
Ghosh, Abhishek, Tathagata Mahintamani, Shinjini Choudhury, Nidhi Sharma, and Sauvik Das. "The Effectiveness of Non-Benzodiazepine, Non-Barbiturate Medications for Alcohol Withdrawal Syndrome: A Rapid Systematic Review." Alcohol and Alcoholism, December 3, 2020. http://dx.doi.org/10.1093/alcalc/agaa125.
Full textAbstract:
Abstract Aim There are potential clinical, ethical and legal concerns with overdosing benzodiazepines (or barbiturates) for the treatment of moderate to severe alcohol withdrawal symptoms (AWS) through telemedicine or ambulatory outpatients. A rapid systematic review to (a) qualitatively summarize the non-benzodiazepine treatment alternatives, (b) evaluate the quality of evidence for the same to effectively manage moderate to severe AWS. Methods We conducted searches on PubMed (January 1990 to 31 March 2020), Cochrane Central Register of Controlled Trials, and Google Scholar. We selected the English language randomized controlled trials (RCTs) assessing the efficacy and adverse effects of non-benzodiazepine and non-barbiturate medications among adults with a diagnosis of AWS. Data extraction was done in a predefined format. Risk of bias (RoB) assessment and qualitative synthesis of evidence was done with the RoB2 tool and Grading of Recommendations Assessment, Development, and Evaluation (GRADE) proGDT. Results Thirty-four RCTs were included. Gabapentin (n = 6), carbamazepine (n = 5), baclofen (n = 5), valproate (n = 3), clonidine/lofexidine (n = 3) and acamprosate (n = 2) had more than one trial with a particular comparison group. Four studies were found to have a low ROB. The GRADE evidence summary showed gabapentin had a ‘moderate’ level of evidence against standard benzodiazepine treatments for reducing the severity of AWS. The level of certainty was ‘low’ for carbamazepine, baclofen and valproate and ‘very low’ for acamprosate and clonidine/lofexidine. Reported adverse events between these alternative medications and benzodiazepines or placebo were generally unremarkable. Conclusions Although benzodiazepines remain the treatment of choice for AWS, during particular circumstances, gabapentin could be an alternative although like benzodiazepines is not without risk when used in the community. Future RCTs must aim to improve upon the quality of evidence.
34
Dreucean, Diane, Jesse E. Harris, Prakruthi Voore, and Kevin R. Donahue. "Approach to Sedation and Analgesia in COVID-19 Patients on Venovenous Extracorporeal Membrane Oxygenation." Annals of Pharmacotherapy, April 22, 2021, 106002802110107. http://dx.doi.org/10.1177/10600280211010751.
Full textAbstract:
Objective: To describe clinically pertinent challenges of managing sedation in COVID-19 patients on venovenous extracorporeal membrane oxygenation (VV-ECMO) and describe considerations for enhanced safety and efficacy of pharmacological agents used. Data Sources: A PubMed search was performed using the following search terms: ECMO, ARDS, sedation, COVID-19, coronavirus, opioids, analgesia, fentanyl, hydromorphone, morphine, oxycodone, methadone, ketamine, propofol, dexmedetomidine, clonidine, benzodiazepines, midazolam, lorazepam, and diazepam. Study Selection and Data Extraction: Relevant clinical and pharmacokinetic studies were considered. All studies included were published between January 1988 and March 2021. Data Synthesis: Patients with acute respiratory distress syndrome secondary to COVID-19 may progress to requiring VV-ECMO support. Agents frequently used for sedation and analgesia in these patients have been shown to have significant adsorption to ECMO circuitry, leading to possible diminished clinical efficacy. Use of hydromorphone-based analgesia has been associated with improved clinical outcomes in patients on VV-ECMO. However, safety and efficacy regarding use of other agents in this patient population remains an area of further research. Relevance to Patient Care and Clinical Practice: This review addresses clinical challenges associated with sedation management in COVID-19 patients requiring VV-ECMO support and provides potential strategies to overcome these challenges. Conclusions: Historically, sedation and analgesia management in patients requiring ECMO support have posed a challenge for bedside clinicians given the unique physiological and pharmacokinetic changes in this patient population. A multimodal strategy to managing analgesia and sedation should be used, and the use of enteral agents may play a role in reducing parenteral agent requirements.
35
"Neuropsychiatric consequences of cardiovascular medications." Neuropsychiatry and Cardiovascular Disease 9, no. 1 (March 2007): 29–45. http://dx.doi.org/10.31887/dcns.2007.9.1/jchuffman.
Full textAbstract:
The use of cardiovascular medications can have a variety of neuropsychiatric consequences. Many cardiovascular agents cause higher rates of fatigue and sedation than placebo, and case reports of medication-induced mood syndromes, psychosis, and cognitive disturbances exist for many cardiovascular drugs. Depression has been associated with P3-blockers, methyldopa, and reserpine, but more recent syntheses of the data have suggested that these associations are much weaker than originally believed. Though low cholesterol levels have been associated with depression and suicide, lipid-lowering agents have not been associated with these adverse effects. Finally, cardiovascular medications may have beneficial neuropsychiatric consequences; for example, the use of clonidine in patients with attention deficit-hyperactivity disorder, the use of prazosin for patients with post-traumatic stress disorder; and the use of propranolol for performance anxiety and akathisia.