Carteolol
Bupranolol
Instillation, Drug
Adrenergic beta-Antagonists
Propanolamines
Cellular and molecular remodeling in a heart failure model treated with the beta-blocker carteolol. (1/36)
Broad-breasted white turkey poults fed furazolidone developed dilated cardiomyopathy (DCM) characterized by ventricular dilatation, decreased ejection fraction, beta1-receptor density, sarcoplasmic reticulum (SR) Ca2+-ATPase, myofibrillar ATPase activity, and reduced metabolism markers. We investigated the effects of carteolol, a beta-adrenergic blocking agent, by administrating two different dosages (0.01 and 10.0 mg/kg) twice a day for 4 wk to control and DCM turkey poults. At completion of the study there was 59% mortality in the nontreated DCM group, 55% mortality in the group treated with the low dose of carteolol, and 22% mortality in the group treated with the high dose of carteolol. Both treated groups showed a significant decrease in left ventricle size and significant restoration of ejection fraction and left ventricular peak systolic pressure. Carteolol treatment increased beta-adrenergic receptor density, and the high carteolol dose restored SR Ca2+-ATPase and myofibrillar ATPase activities, along with creatine kinase, lactate dehydrogenase, aspartate transaminase, and ATP synthase activities, to normal. These results show that beta-blockade with carteolol improves survival, reverses contractile abnormalities, and induces cellular remodeling in this model of heart failure. (+info)Betaxolol, a beta(1)-adrenoceptor antagonist, reduces Na(+) influx into cortical synaptosomes by direct interaction with Na(+) channels: comparison with other beta-adrenoceptor antagonists. (2/36)
Betaxolol, a beta(1)-adrenoceptor antagonist used for the treatment of glaucoma, is known to be neuroprotective in paradigms of ischaemia/excitotoxicity. In this study, we examined whether betaxolol and other beta-adrenoceptor antagonists interact directly with neurotoxin binding to sites 1 and 2 of the voltage-sensitive sodium channel (Na(+) channel) in rat cerebrocortical synaptosomes. Betaxolol inhibited specific [(3)H]-batrachotoxinin-A 20-alpha-benzoate ([(3)H]-BTX-B) binding to neurotoxin site 2 in a concentration-dependent manner with an IC(50) value of 9.8 microM. Comparison of all the beta-adrenoceptor antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>levobunolol approximately carteolol>/=timolol>atenolol. None of the drugs caused a significant inhibition of [(3)H]-saxitoxin binding to neurotoxin receptor site 1, even at concentrations as high as 250 microM. Saturation experiments showed that betaxolol increased the K(D) of [(3)H]-BTX-B binding but had no effect on the B(max). The association kinetics of [(3)H]-BTX-B were unaffected by betaxolol, but the drug significantly accelerated the dissociation rate of the radioligand. These findings argue for a competitive, indirect, allosteric mode of inhibition of [(3)H]-BTX-B binding by betaxolol. Betaxolol inhibited veratridine-stimulated Na(+) influx in rat cortical synaptosomes with an IC(50) value of 28. 3 microM. Carteolol, levobunolol, timolol and atenolol were significantly less effective than betaxolol at reducing veratridine-evoked Na(+) influx. The ability of betaxolol to interact with neurotoxin site 2 of the Na(+) channel and inhibit Na(+) influx may have a role in its neuroprotective action in paradigms of excitotoxicity/ischaemia and in its therapeutic effect in glaucoma. (+info)Topical ophthalmic beta blockers may cause release of histamine through cytotoxic effects on inflammatory cells. (3/36)
AIM: To evaluate the effects of beta blockers used in ophthalmology on the release of histamine from mixed cell preparations containing human leucocytes and basophils. METHODS: A mixed leucocyte and basophil preparation was obtained from venous blood of healthy non-atopic volunteers. Cell preparations were then incubated with betaxolol, metipranolol, timolol, or carteolol. After incubation for 1 hour the histamine content of the supernatant was analysed by automated fluorometric analysis. Cell viability was tested by measuring lactate dehydrogenase (LDH) concentrations. RESULTS: Betaxolol and metipranolol in concentrations between 10(-2) M and 10(-3) M liberated histamine from human blood cells in a dose dependent manner. Carteolol and timolol had no effect on histamine at these concentrations. At the same concentrations LDH was also detected in the supernatants of cell suspensions incubated with metipranolol or betaxolol. CONCLUSIONS: Betaxolol and metipranolol induce substantial histamine release from human leucocytes, probably as a result of their cytotoxic effect. (+info)Partial agonistic effects of carteolol on atypical beta-adrenoceptors in the guinea pig gastric fundus. (4/36)
The properties of the beta1-/beta2-adrenoceptor partial agonist carteolol were investigated in atypical beta-adrenoceptors on the guinea pig gastric fundus. Carteolol induced concentration-dependent relaxation in this tissue (pD2 = 5.55, intrinsic activity = 0.94). However, a combination of the selective beta1-adrenoceptor antagonist atenolol (100 microM) and the selective beta2-adrenoceptor antagonist butoxamine (100 microM) produced only small rightward shifts in the concentration-response curves of carteolol in the gastric fundus (pD2 = 4.91, intrinsic activity = 0.94). In the presence of both atenolol (100 microM) and butoxamine (100 microM), the non-selective beta1-, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol (10-100 microM) caused a concentration-dependent right-ward shift of the concentration-response curves for carteolol in the guinea pig gastric fundus. Schild plot analyses of the effects of (+/-)-bupranolol against carteolol gave the pA2 value of 5.29 and the Schild slope was not significantly different from unity. Furthermore, carteolol (10 microM) weakly but significantly antagonized the relaxant responses to catecholamines ((-)-isoprenaline, (-)-noradrenaline and (-)-adrenaline), a selective beta3-adrenoceptor agonist BRL37344 ((R*,R*)-(+/-)-4-[2-[(2-(3-chlorophenyl)-2-hydroxyethyl)amino]propyl]phenoxy-acet ic acid sodium salt) and a non-conventional partial beta3-adrenoceptor agonist (+/-)-CGP12177A ([4-[3-[(1,1dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimidazol-2- one] hydrochloride) in the guinea pig gastric fundus. These results suggest that the partial agonistic effects of carteolol are mediated by atypical beta-adrenoceptors in the guinea pig gastric fundus. (+info)Further evidence that (+/-)-carteolol-induced relaxation is mediated by beta2-adrenoceptors but not by beta3-adrenoceptors in the guinea pig taenia caecum. (5/36)
The properties of the beta1- and beta2-adrenoceptor partial agonist (+/-)-carteolol were investigated against the beta2- and beta3-adrenoceptors of the taenia caecum of the guinea pig. (--)-Isoprenaline and (+/-)-carteolol induced concentration-dependent relaxation in this tissue. The non-selective beta1- and beta2-adrenoceptor antagonist (+/-)-propranolol (10-100 nM), the selective beta2-adrenoceptor antagonist ICI 118,551 (10-100 nM) and the non-selective beta1-, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol (10-100nM), caused a concentration-dependent rightward shift of the concentration-response curves for (--)-isoprenaline and (+/-)-carteolol. Schild regression plot analyses carried out for (+/-)-propranolol against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.35 and 8.24, respectively. Schild plot analyses of ICI 118,551 against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.47 and 8.41, respectively. Schild plot analyses of (+/-)-bupranolol against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.47 and 8.53, respectively. Slopes of the Schild plots were not significantly different from unity. These results suggest that the relaxant effects of (+/-)-carteolol in the guinea pig taenia caecum are mediated by beta2-adrenoceptors but not by beta3-adrenoceptors. (+info)Ocular hypotensive efficacy and safety of once daily carteolol alginate. (6/36)
BACKGROUND/AIM: Carteolol is a beta adrenoceptor antagonist used topically to reduce intraocular pressure, typically twice daily. In an effort to provide a once daily dosing regimen, carteolol was formulated with 1% alginic acid. The objective of this study was to evaluate the efficacy and safety of carteolol alginate solution in comparison with standard carteolol solution. METHODS: This was a double masked, parallel group, multicentre study. Patients with ocular hypertension or open angle glaucoma (n=235) were randomly assigned to receive either carteolol alginate once daily [corrected] or standard carteolol solution, twice daily. The masking was maintained through the use of a vehicle in the evening for the alginate group. Patients were evaluated at baseline, 15, 60, and 120 days. RESULTS: At 0900 (presumed trough) on day 60, mean reductions in intraocular pressure (IOP) from baseline were 6.09 (SD 2.97) and 6.09 (3.18) mm Hg for the standard carteolol and alginate, respectively. At 1100 (presumed peak), mean reductions were 6.51 (2.53) and 6.47 (2.76) mm Hg, respectively. Results were similar at other times (day 15 and day 120). The most common side effect was transient stinging on instillation of drops, which did not differ significantly between groups. There were no differences of note in other ocular or systemic signs or symptoms. CONCLUSION: The new alginate formulation of carteolol 2% given once daily was as effective as standard carteolol 2% given twice daily with no meaningful differences regarding safety. (+info)A 7 year prospective comparative study of three topical beta blockers in the management of primary open angle glaucoma. (7/36)
AIM: To determine the long term efficacy of monotherapy with topically applied beta blocking agents and to determine whether selective beta blockers were able to preserve the visual field more effectively than non-selective agents. METHOD: A prospective randomised, open, comparative study of three topically applied beta blockers-timolol, betaxolol, and carteolol-was carried out on 153 patients (280 eyes) with newly diagnosed open angle glaucoma. Those patients who were not withdrawn were followed by the same observers for a minimum of 2 years and a maximum of 7 years, with clinical observations, Goldmann tonometry and 24.2 Humphrey visual field analysis. RESULTS: All three drugs lowered the IOP significantly from untreated levels but betaxolol took up to 12 months in some instances to reach the maximum pressure reduction. After 7 years only 43% of the eyes begun on timolol, 34% of those started on carteolol, and 29% of those on betaxolol were still being treated with these medications alone. Visual fields were analysed throughout the trial by CPSD and MD and at the end by linear regression analysis (PROGRESSOR). The visual fields remained the same without apparent improvement or deterioration throughout the period of follow up. Eight patients (11 eyes) were withdrawn because of continuing field loss in spite of reduction in IOP (six using carteolol and five using betaxolol). CONCLUSIONS: Analysis shows that less than half the eyes initially treated with topical beta blockers might be expected to still be being treated with their original medication after 5 years. The rest required either additional medication or trabeculectomy. There was no statistically significant improvement or deterioration in the visual fields over a 7 year period. On the evidence of this trial there are no particular advantages in using selective beta blockers. (+info)Mitochondrial activity and glutathione injury in apoptosis induced by unpreserved and preserved beta-blockers on Chang conjunctival cells. (8/36)
PURPOSE: Quaternary ammonium ions have been demonstrated to induce apoptosis correlated with superoxide anion production in vitro. The purpose of this study was to further investigate the mechanisms of benzalkonium chloride (BAC), unpreserved and preserved beta-blocker eye-drops-induced programmed cell death, with special attention to the roles of mitochondrial transmembrane potential and intracellular reduced glutathione. METHODS: Chang conjunctival cells were incubated with different concentrations of unpreserved or preserved timolol (0.1%, 0.25%, and 0.4%), or carteolol (1% and 2%), or BAC (0.0001% to 0.01%) for 15 minutes, or for 15 minutes with a 24-hour recovery period in normal medium. Cellular viability (neutral red test), mitochondrial activity (rhodamine 123 test), intracellular reduced glutathione (monochlorobimane test), DNA condensation (Hoechst 33342 test), and reactive oxygen species (ROS) production (dichlorofluorescein diacetate and hydroethidine tests) were evaluated using microplate cold-light cytofluorometry. RESULTS: A significant, concentration-dependent decrease in cellular viability was found with preserved beta-blockers and with BAC alone, whereas unpreserved preparations did not show any toxicity. Only preserved beta-blockers induced chromatin condensation associated with an alteration of mitochondrial activity and a decrease of glutathione, suggesting an apoptotic phenomenon. BAC increased glutathione after 15 minutes, whereas a decrease was observed after a recovery period. ROS production was found with preserved formulations at significantly higher levels than those observed with unpreserved drugs. CONCLUSIONS: This in vitro study demonstrates that oxidative stress, evidenced by enhanced ROS production and mitochondrial injury rather than by cellular glutathione depletion, is a mechanism involved in apoptosis induced by preservative-containing eye-drops. (+info)Carteolol is a beta-blocker medication that is primarily used to treat hypertension (high blood pressure) and glaucoma. It works by blocking the action of certain natural substances in the body, such as adrenaline, on the heart and blood vessels. This helps to reduce heart rate, lower blood pressure, and increase the amount of fluid that drains from the eye, which can help to lower intraocular pressure in people with glaucoma.
Like other beta-blockers, carteolol may cause side effects such as dizziness, fatigue, and cold hands or feet. It may also interact with other medications, so it's important to tell your doctor about all the drugs you are taking before starting carteolol. Your doctor will also need to monitor your heart function regularly while you are taking this medication, especially if you have a history of heart disease or other medical conditions.
Bupranolol is a beta-blocker medication that is primarily used to treat high blood pressure, angina (chest pain), and certain types of irregular heartbeats. It works by blocking the action of certain natural substances in your body, such as epinephrine, that affect the heart and blood vessels. This helps to reduce heart rate, lower blood pressure, and improve blood flow, which can help prevent heart attacks and strokes.
Bupranolol may also be used for other purposes, such as preventing migraines or treating anxiety disorders. It is available in immediate-release and extended-release tablets, and the dosage may vary depending on the specific condition being treated. As with any medication, bupranolol can have side effects, including dizziness, fatigue, and gastrointestinal symptoms. It is important to follow your doctor's instructions carefully when taking this medication and to report any unusual or bothersome side effects promptly.
Instillation, in the context of drug administration, refers to the process of introducing a medication or therapeutic agent into a body cavity or onto a mucous membrane surface using gentle, steady pressure. This is typically done with the help of a device such as an eyedropper, pipette, or catheter. The goal is to ensure that the drug is distributed evenly over the surface or absorbed through the mucous membrane for localized or systemic effects. Instillation can be used for various routes of administration including ocular (eye), nasal, auricular (ear), vaginal, and intra-articular (joint space) among others. The choice of instillation as a route of administration depends on the drug's properties, the desired therapeutic effect, and the patient's overall health status.
Betaxolol is a selective beta-1 adrenergic receptor blocker, which is primarily used in the treatment of glaucoma. It works by reducing the production of aqueous humor inside the eye, thereby decreasing the intraocular pressure (IOP). This can help prevent optic nerve damage and vision loss associated with glaucoma.
Betaxolol ophthalmic solution is usually administered as eyedrops, one or two times per day. Common side effects of betaxolol may include stinging or burning in the eyes, blurred vision, headache, and a bitter taste in the mouth. Serious side effects are rare but can include allergic reactions, slow heart rate, and difficulty breathing.
It is important to note that betaxolol should not be used by people with certain medical conditions, such as severe heart block, uncontrolled heart failure, or asthma. Additionally, it may interact with other medications, so it is essential to inform your healthcare provider about all the drugs you are taking before starting treatment with betaxolol.
Xamoterol is not generally considered to have a medical definition, as it is not an approved or commonly used medication in clinical practice. However, it is a chemical compound that has been studied in the past for its potential therapeutic effects.
Xamoterol is a beta-adrenergic receptor agonist, which means that it binds to and activates certain types of receptors found on cells throughout the body. Specifically, xamoterol is a partial agonist of both beta-1 and beta-2 adrenergic receptors, which are involved in various physiological processes such as heart rate, contractility, and bronchodilation.
In clinical trials, xamoterol was investigated for its potential to improve cardiac function and exercise capacity in patients with chronic heart failure. However, the drug was found to have only modest benefits and was associated with an increased risk of serious arrhythmias, which ultimately led to its discontinuation in further development and use.
Therefore, while xamoterol may have a chemical definition as a beta-adrenergic receptor agonist, it is not commonly used or recognized as a medical term in clinical practice.
Adrenergic beta-antagonists, also known as beta blockers, are a class of medications that block the effects of adrenaline and noradrenaline (also known as epinephrine and norepinephrine) on beta-adrenergic receptors. These receptors are found in various tissues throughout the body, including the heart, lungs, and blood vessels.
Beta blockers work by binding to these receptors and preventing the activation of certain signaling pathways that lead to increased heart rate, force of heart contractions, and relaxation of blood vessels. As a result, beta blockers can lower blood pressure, reduce heart rate, and decrease the workload on the heart.
Beta blockers are used to treat a variety of medical conditions, including hypertension (high blood pressure), angina (chest pain), heart failure, irregular heart rhythms, migraines, and certain anxiety disorders. Some common examples of beta blockers include metoprolol, atenolol, propranolol, and bisoprolol.
It is important to note that while beta blockers can have many benefits, they can also cause side effects such as fatigue, dizziness, and shortness of breath. Additionally, sudden discontinuation of beta blocker therapy can lead to rebound hypertension or worsening chest pain. Therefore, it is important to follow the dosing instructions provided by a healthcare provider carefully when taking these medications.
Propanolamines are a class of pharmaceutical compounds that contain a propan-2-olamine functional group, which is a secondary amine formed by the replacement of one hydrogen atom in an ammonia molecule with a propan-2-ol group. They are commonly used as decongestants and bronchodilators in medical treatments.
Examples of propanolamines include:
* Phenylephrine: a decongestant used to relieve nasal congestion.
* Pseudoephedrine: a decongestant and stimulant used to treat nasal congestion and sinus pressure.
* Ephedrine: a bronchodilator, decongestant, and stimulant used to treat asthma, nasal congestion, and low blood pressure.
It is important to note that propanolamines can have side effects such as increased heart rate, elevated blood pressure, and insomnia, so they should be used with caution and under the supervision of a healthcare professional.
Timolol is a non-selective beta blocker drug that is primarily used to treat hypertension, angina pectoris, and glaucoma. It works by blocking the action of certain hormones such as epinephrine (adrenaline) on the heart and blood vessels, which helps to lower heart rate, reduce the force of heart muscle contraction, and decrease blood vessel constriction. These effects can help to lower blood pressure, reduce the workload on the heart, and improve oxygen supply to the heart muscle. In glaucoma treatment, timolol reduces the production of aqueous humor in the eye, thereby decreasing intraocular pressure.
The medical definition of Timolol is:
Timolol (tim-oh-lol) is a beta-adrenergic receptor antagonist used to treat hypertension, angina pectoris, and glaucoma. It works by blocking the action of epinephrine on the heart and blood vessels, which results in decreased heart rate, reduced force of heart muscle contraction, and decreased blood vessel constriction. In glaucoma treatment, timolol reduces aqueous humor production, thereby decreasing intraocular pressure. Timolol is available as an oral tablet, solution for injection, and ophthalmic solution.
Carteolol
Beta blocker
Hydroxycarteolol
Penbutolol
ATC code S01
List of MeSH codes (D03)
List of adrenergic drugs
Sympatholytic
Sonophoresis
List of MeSH codes (D02)
ATC code C07
Peripherally selective drug
List of drugs: C-Ca
Antihypertensive drug
Carteolol - Wikipedia
Carteolol Hydrochloride Ophthalmic Solution USP, 1% (Bausch & Lomb), Drug Reference Encyclopedia
The 12-hour control of intraocular pressure on carteolol 2% twice daily. | British Journal of Ophthalmology
Carteolol Hydrochloride: Medgend
Carteolol (Cartrol) | Davis's Drug Guide
EP Carteolol Hydrochloride - reference spectrum
Randomized, Controlled, Phase 3 Trials of Carteolol/Latanoprost Fixe
Carteolol (ophthalmic) vs Nonsteroidal Anti-Inflammatory Agents drug - drug interaction
Metaproterenol: MedlinePlus Drug Information
NHANES 2001-2002: Cardiovascular Fitness Data Documentation, Codebook, and Frequencies
Tamsulosin (Oral Route) Before Using - Mayo Clinic
Acnex Topical Advanced Patient Information - Drugs.com
Sitagliptin And Simvastatin (Oral Route) Before Using - Mayo Clinic
Glaucoma | Specsavers UK
The Prohibited List | World Anti Doping Agency
Heads of Medicines Agencies: Outcome of informal PSUR worksharing procedures
Primary Open-Angle Glaucoma (POAG): Practice Essentials, Background, Pathophysiology
Drug Summary
Drug Summary
FAA Accepted Medications - Pilot Medical Solutions - LeftSeat.com
Metaproterenol - Mechanism, Indication, Contraindications, Dosing, Adverse Effect, Interaction, Hepatic Dose | Drug Index |...
KEGG DGROUP: CYP2D6 substrate
Acetohexamide - Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol | RxWiki
3-210601123129.pdf
Information for BronchospasmAPI-Audits und API-Auditberichte: Liste der Wirkstoffe | Diapharm
Complementary and Alternative Medicine - Myocardial infarction
Betaxolol Ophthalmic
Hydrochloride5
- Carteolol Hydrochloride Ophthalmic Solution, 1%, is a nonselective beta-adrenoceptor blocking agent for ophthalmic use. (theodora.com)
- ACTIVE: Carteolol Hydrochloride 10mg (1%), INACTIVES: Sodium Chloride, Monobasic and Dibasic Sodium Phosphate, Purified Water. (theodora.com)
- Carteolol hydrochloride reduces normal and elevated intraocular pressure (IOP) whether or not accompanied by glaucoma. (theodora.com)
- Carteolol hydrochloride ophthalmic solution, 1%, has been shown to be effective in lowering intraocular pressure and may be used in patients with chronic open-angle glaucoma and intraocular hypertension. (theodora.com)
- At the first sign or symptom of cardiac failure, carteolol hydrochloride should be discontinued. (theodora.com)
Timolol2
- In a 15-week double-blind, placebo-controlled, crossover study both carteolol 2% and timolol 0.5% produced a significant reduction in intraocular pressure. (bmj.com)
- Twelve hours after administration the reduction in pressure on carteolol was significantly less than that obtained on timolol. (bmj.com)
Intraocular pressure2
- The 12-hour control of intraocular pressure on carteolol 2% twice daily. (bmj.com)
- To assess the intraocular pressure (IOP)-lowering effects and safety of a carteolol/latanoprost fixed combination drug (OPC-1085EL) vs latanoprost (Study 1) and carteolol (Study 2) in patients with primary open-angle glaucoma (POAG) or ocular hypertension (OH). (researcher-app.com)
Intrinsic sympathomimetic activity1
- Carteolol is a nonselective beta-adrenergic blocking agent with associated intrinsic sympathomimetic activity and without significant membrane-stabilizing activity. (theodora.com)
Ophthalmic1
- However, as with other topically applied ophthalmic preparations, carteolol may be absorbed systemically. (theodora.com)
19721
- citation needed] Carteolol was patented in 1972 and approved for medical use in 1980. (wikipedia.org)
Bronchospasm1
- In patients with non-allergic bronchospasm or with a history of non-allergic bronchospasm (e.g., chronic bronchitis, emphysema), carteolol should be administered with caution since it may block bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta 2 receptors. (theodora.com)
Therapy1
- In Study 2, 193 patients applied OPC-1085EL (n = 78), carteolol (n = 78), or carteolol/latanoprost concomitant therapy (n = 37) for 8 weeks. (researcher-app.com)
Daily1
- Efficacy and safety of long-acting carteolol 1% once daily. (wikipedia.org)
Drug1
- Emergency Central , emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51133/all/carteolol. (unboundmedicine.com)
Found1
- Carteolol has also been found to act as a serotonin 5-HT1A and 5-HT1B receptor antagonist in addition to being a beta blocker. (wikipedia.org)
Study1
- 35 mm Hg in the study eye after 4 weeks' treatment with latanoprost (Study 1) or carteolol (Study 2) (defined as baseline). (researcher-app.com)
Hydrochloride protects1
- Carteolol hydrochloride protects LECs against UVB irradiation by inhibiting the intracellular production of ROS. (openophthalmologyjournal.com)
Ophthalmic Solution3
- Carteolol Hydrochloride Ophthalmic Solution USP, 1% is a nonselective beta-adrenoceptor blocking agent for ophthalmic use. (nih.gov)
- Carteolol Hydrochloride Ophthalmic Solution 1% has been shown to be effective in lowering intraocular pressure and may be used in patients with chronic open-angle glaucoma and intraocular hypertension. (nih.gov)
- In patients with non-allergic bronchospasm or with a history of non-allergic bronchospasm (e.g., chronic bronchitis, emphysema), Carteolol Hydrochloride Ophthalmic Solution should be administered with caution since it may block bronchodilation produced by endogenous and exogenous catecholamine stimulation of beta 2 receptors. (nih.gov)
Epithelial cells1
- The aim of the present study was to investigate the effect of carteolol hydrochloride, an adrenergic β-blocker, on the production of reactive oxygen species (ROS) and the viable cell number after ultraviolet irradiation of cultured lens epithelial cells (LECs). (openophthalmologyjournal.com)
Arteoptic1
- Arteoptic 點眼液,是大塚製藥開發的B阻斷劑Carteolol. (pharmacistplus.com)
19801
- citation needed] Carteolol was patented in 1972 and approved for medical use in 1980. (wikipedia.org)
Excretion2
- Because its excretion into breastmilk is probably extensive, other beta-adrenergic blocking drugs are preferred to oral carteolol while breastfeeding a neonate. (nih.gov)
- With 60% protein binding, 15% renal excretion and a moderately long half-life, carteolol presents a relatively high risk for accumulation in infants, especially neonates. (nih.gov)
Ocular1
- Carteolol has not been detected in plasma following ocular instillation. (nih.gov)
Medication1
- Pricing is displayed for CARTEOLOL , a generic medication. (americaspharmacy.com)
Https1
- 2023. https://emergency.unboundmedicine.com/emergency/view/Davis-Drug-Guide/51133/all/carteolol. (unboundmedicine.com)
Action1
- Carteolol: Antagonism of action and increased effect of theophylline . (pediatriconcall.com)
Normal2
Chemical1
- Pharmaceutical chemical and analytical data for the pharmaceutically-active substance carteolol hydrochloride]. (nih.gov)
Addition1
- In addition, 10 -3 M carteolol hydrochloride significantly increased the viable cell number after exposure to UVB at 400 mJ/cm 2 . (openophthalmologyjournal.com)
