Medication Systems, Hospital
Protection by imidazol(ine) drugs and agmatine of glutamate-induced neurotoxicity in cultured cerebellar granule cells through blockade of NMDA receptor. (1/11)This study was designed to assess the potential neuroprotective effect of several imidazol(ine) drugs and agmatine on glutamate-induced necrosis and on apoptosis induced by low extracellular K+ in cultured cerebellar granule cells. Exposure (30 min) of energy deprived cells to L-glutamate (1-100 microM) caused a concentration-dependent neurotoxicity, as determined 24 h later by a decrease in the ability of the cells to metabolize 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) into a reduced formazan product. L-glutamate-induced neurotoxicity (EC50=5 microM) was blocked by the specific NMDA receptor antagonist MK-801 (dizocilpine). Imidazol(ine) drugs and agmatine fully prevented neurotoxicity induced by 20 microM (EC100) L-glutamate with the rank order (EC50 in microM): antazoline (13)>cirazoline (44)>LSL 61122 [2-styryl-2-imidazoline] (54)>LSL 60101 [2-(2-benzofuranyl) imidazole] (75)>idazoxan (90)>LSL 60129 [2-(1,4-benzodioxan-6-yl)-4,5-dihydroimidazole](101)>RX82 1002 (2-methoxy idazoxan) (106)>agmatine (196). No neuroprotective effect of these drugs was observed in a model of apoptotic neuronal cell death (reduction of extracellular K+) which does not involve stimulation of NMDA receptors. Imidazol(ine) drugs and agmatine fully inhibited [3H]-(+)-MK-801 binding to the phencyclidine site of NMDA receptors in rat brain. The profile of drug potency protecting against L-glutamate neurotoxicity correlated well (r=0.90) with the potency of the same compounds competing against [3H]-(+)-MK-801 binding. In HEK-293 cells transfected to express the NR1-1a and NR2C subunits of the NMDA receptor, antazoline and agmatine produced a voltage- and concentration-dependent block of glutamate-induced currents. Analysis of the voltage dependence of the block was consistent with the presence of a binding site for antazoline located within the NMDA channel pore with an IC50 of 10-12 microM at 0 mV. It is concluded that imidazol(ine) drugs and agmatine are neuroprotective against glutamate-induced necrotic neuronal cell death in vitro and that this effect is mediated through NMDA receptor blockade by interacting with a site located within the NMDA channel pore. (+info)
Antazoline therapy of recurrent refractory supraventricular arrhythmias--a preliminary report. (2/11)Seven patients with chronic or recurrent supraventricular tachyarrhythmias were selected for a trial of antazoline therapy because sinus rhythm or a controlled ventricular response could not be achieved with quinidine, procainamide, digitalis or propranolol. Sinus rhythm was established by either intravenous administration of antazoline or direct-current countershock, and has been maintained in all for 4 to 16 months by oral administration of antazoline. Side effects were minor. Antazoline is a sufficiently promising antiarrhythmic agent to warrant large-scale controlled studies. (+info)
Imidazoline antagonists of alpha 2-adrenoceptors increase insulin release in vitro by inhibiting ATP-sensitive K+ channels in pancreatic beta-cells. (3/11)1. Islets from normal mice were used to study the mechanisms by which imidazoline antagonists of alpha 2-adrenoceptors increase insulin release in vitro. 2. Alinidine, antazoline, phentolamine and tolazoline inhibited 86Rb efflux from islets perifused with a medium containing 3 mM glucose, i.e. under conditions where many adenosine 5'-triphosphate (ATP)-sensitive K+ channels are open in the beta-cell membrane. They also reduced the acceleration of 86Rb efflux caused by diazoxide, an opener of ATP-sensitive K+ channels. 3. ATP-sensitive and voltage-sensitive K+ currents were measured in single beta-cells by the whole-cell mode of the patch-clamp technique. Antazoline more markedly inhibited the ATP-sensitive than the voltage-sensitive current, an effect previously observed with phentolamine. Alinidine and tolazoline partially decreased the ATP-sensitive K+ current. 4. The four imidazolines reversed the inhibition of insulin release caused by diazoxide (through opening of ATP-sensitive K+ channels) or by clonidine (through activation of alpha 2-adrenoceptors) in a concentration-dependent manner. Only the former effect correlated with the ability of each drug to increase control insulin release stimulated by 15 mM glucose alone. 5. It is concluded that the ability of imidazoline antagonists of alpha 2-adrenoceptors to increase insulin release in vitro can be ascribed to their blockade of ATP-sensitive K+ channels in beta-cells rather than to their interaction with the adrenoceptor. (+info)
Effect of histamine receptor antagonists on aminophylline-induced seizures and lethality in mice. (4/11)The aim of this study was to evaluate the effects of H(1) (antazoline and astemizole) or H(2) (cimetidine and famotidine) histamine receptor antagonists on the clonic phase, tonic seizures and morality of mice challenged with aminophylline to induce convulsions in mice. Moreover, the total plasma and brain concentrations of theophylline were evaluated. Astemizole (1 mg/kg) did not affect the threshold for aminophylline-induced seizures, but when administered at a dose of 2 mg/kg, it significantly reduced the CD(50) value of aminophylline from 249 mg/kg to 211 mg/kg (p < 0.01). The remaining histamine receptor antagonists studied i.e., antazoline (up to 1 mg/kg), cimetidine (up to 40 mg/kg) and famotidine (up to 10 mg/kg) had no impact on seizure susceptibility in aminophylline-induced convulsions. Furthermore, astemizole (2 mg/kg) decreased latency to the clonic phase of aminophylline-induced convulsions from 51.1 +/- 4.5 to 32.1 +/- 4.3 min (p < 0.01). It is noteworthy that astemizole, a novel H(1) receptor antagonist, did not alter the brain and plasma levels of theophylline, so the existence of pharmacokinetic interactions was excluded. Our results indicate that some interactions between methylxanthines and histamine receptor antagonists may be clinically important since these drugs are usually combined during the treatment of status asthmaticus. (+info)
A rapid derivative spectrophotometric method for simultaneous determination of naphazoline and antazoline in eye drops. (5/11)A zero-crossing first-derivative spectrophotometric method is applied for the simultaneous determination of naphazoline hydrochloride and antazoline phosphate in eye drops. The measurements were carried out at wavelengths of 225 and 252 nm for naphazoline hydrochloride and antazoline phosphate, respectively. The method was found to be linear (r2>0.999) in the range of 0.2-1 microg/ml for naphazoline hydrochloride in the presence of 5 microg/ml antazoline phosphate at 225 nm. The same linear correlation (r2>0.999) was obtained in the range of 1-10 microg/ml of antazoline phosphate in the presence of 0.5 microg/ml of naphazoline hydrochloride at 252 nm. The limit of determination was 0.2 microg/ml and 1 microg/ml for naphazoline hydrochloride and antazoline phosphate, respectively. The method was successfully used for simultaneous analysis of naphazoline hydrochloride and antazoline phosphate in eye drops without any interference from excipients and prior separation before analysis. (+info)
Antazoline in the treatment of cardiac arrhythmias. (6/11)Antazoline was administered in sixty-five episodes of various types of cardiac arrhythmia. A complete suppression of the ectopic beats was achieved in five out of six episodes of premature atrial systoles and in twenty-one of the twenty-four episodes of ventricular premature systoles. Conversion to sinus rhythm was observed in seven out of ten and four out of five episodes of paroxysmal atrial and nodal tachycardia respectively. Six out of ten episodes of ventricular tachycardia were controlled by intravenous therapy. However, the drug proved to be ineffective in cases of atrial fibrillation. The side-effects were few and transitory, consisting of nausea, vomiting and drowsiness. (+info)
Clinical efficacy of antazoline in rapid cardioversion of paroxysmal atrial fibrillation--a protocol of a single center, randomized, double-blind, placebo-controlled study (the AnPAF Study). (7/11)(+info)
An analysis of the purinergic component of active muscle vasodilatation obtained by electrical stimulation of the hypothalamus in rabbits. (8/11)In anaesthetized rabbits, electrical stimulation of the hypothalamus in areas analogous to the defence area in cats produces the 'defence reaction.' This response includes signs of arousal and a large increase in blood flow to skeletal muscle in the hind limb caused by a vasodilatation in the skeletal muscle vasculature. The vasodilatation is a sympathetic response, and it is not dependent upon muscle activity in the hind limb. The muscle vasodilatation is insensitive to alpha-adrenoceptor, beta-adrenoceptor, cholinoceptor and histamine receptor antagonists. Intra-arterial injections of the purinoceptor agonists, adenosine triphosphate (ATP) and adenosine, mimic the vasodilatation produced by electrical stimulation. The P1-purinoceptor blocker, aminophylline, attenuates adenosine-induced vasodilatation, but it does not affect the vasodilatation produced by ATP or hypothalamic stimulation. The P2-purinoceptor blocker, antazoline, attenuates the vasodilatation produced by both ATP and hypothalamic stimulation. Our results suggest that the muscle vasodilatation produced by hypothalamic stimulation is mediated by purinergic nerves which release ATP and act on P2-purinoceptors. (+info)
The term cough is used to describe a wide range of symptoms that can be caused by various conditions affecting the respiratory system. Coughs can be classified as either dry or productive, depending on whether they produce mucus or not. Dry coughs are often described as hacking, barking, or non-productive, while productive coughs are those that bring up mucus or other substances from the lungs or airways.
Causes of Cough:
There are many potential causes of cough, including:
* Upper respiratory tract infections such as the common cold and influenza
* Lower respiratory tract infections such as bronchitis and pneumonia
* Allergies, including hay fever and allergic rhinitis
* Asthma and other chronic lung conditions
* Gastroesophageal reflux disease (GERD), which can cause coughing due to stomach acid flowing back up into the throat
* Environmental factors such as smoke, dust, and pollution
* Medications such as ACE inhibitors and beta blockers.
Symptoms of Cough:
In addition to the characteristic forceful expulsion of air from the lungs, coughs can be accompanied by a range of other symptoms that may include:
* Chest tightness or discomfort
* Shortness of breath or wheezing
* Fatigue and exhaustion
* Sore throat or hoarseness
* Coughing up mucus or other substances.
Diagnosis and Treatment of Cough:
The diagnosis and treatment of cough will depend on the underlying cause. In some cases, a cough may be a symptom of a more serious condition that requires medical attention, such as pneumonia or asthma. In other cases, a cough may be caused by a minor infection or allergy that can be treated with over-the-counter medications and self-care measures.
Some common treatments for cough include:
* Cough suppressants such as dextromethorphan or pholcodine to relieve the urge to cough
* Expectorants such as guaifenesin to help loosen and clear mucus from the airways
* Antihistamines to reduce the severity of allergic reactions and help relieve a cough.
* Antibiotics if the cough is caused by a bacterial infection
* Inhalers and nebulizers to deliver medication directly to the lungs.
It is important to note that while cough can be a symptom of a serious condition, it is not always necessary to see a doctor for a cough. However, if you experience any of the following, you should seek medical attention:
* A persistent and severe cough that lasts for more than a few days or weeks
* A cough that worsens at night or with exertion
* Coughing up blood or mucus that is thick and yellow or greenish in color
* Shortness of breath or chest pain
* Fever, chills, or body aches that are severe or persistent.
It is also important to note that while over-the-counter medications can provide relief from symptoms, they may not address the underlying cause of the cough. If you have a persistent or severe cough, it is important to see a doctor to determine the cause and receive proper treatment.
There are several types of food hypersensitivity, including:
1. Food Allergy: An immune system reaction to a specific food that can cause symptoms ranging from mild hives to life-threatening anaphylaxis. Common food allergies include reactions to peanuts, tree nuts, fish, shellfish, milk, eggs, wheat, and soy.
2. Non-Allergic Food Hypersensitivity: Also known as non-IgE-mediated food hypersensitivity, this type of reaction does not involve the immune system. Symptoms can include bloating, abdominal pain, diarrhea, and headaches. Common culprits include gluten, dairy, and high-FODMAP foods.
3. Food Intolerance: A condition where the body cannot properly digest or process a specific food. Symptoms can include bloating, abdominal pain, diarrhea, and gas. Common food intolerances include lactose intolerance, fructose malabsorption, and celiac disease.
4. Food Aversion: An emotional response to a specific food that can cause avoidance or dislike of the food. This is not an allergic or physiological reaction but rather a psychological one.
The diagnosis of food hypersensitivity typically involves a thorough medical history, physical examination, and diagnostic tests such as skin prick testing or blood tests. Treatment options for food hypersensitivity depend on the type and severity of the reaction and may include avoidance of the offending food, medication, or immunotherapy.
There are several types of hypersensitivity reactions, including:
1. Type I hypersensitivity: This is also known as immediate hypersensitivity and occurs within minutes to hours after exposure to the allergen. It is characterized by the release of histamine and other chemical mediators from immune cells, leading to symptoms such as hives, itching, swelling, and difficulty breathing. Examples of Type I hypersensitivity reactions include allergies to pollen, dust mites, or certain foods.
2. Type II hypersensitivity: This is also known as cytotoxic hypersensitivity and occurs within days to weeks after exposure to the allergen. It is characterized by the immune system producing antibodies against specific proteins on the surface of cells, leading to their destruction. Examples of Type II hypersensitivity reactions include blood transfusion reactions and serum sickness.
3. Type III hypersensitivity: This is also known as immune complex hypersensitivity and occurs when antigens bind to immune complexes, leading to the formation of deposits in tissues. Examples of Type III hypersensitivity reactions include rheumatoid arthritis and systemic lupus erythematosus.
4. Type IV hypersensitivity: This is also known as delayed-type hypersensitivity and occurs within weeks to months after exposure to the allergen. It is characterized by the activation of T cells, leading to inflammation and tissue damage. Examples of Type IV hypersensitivity reactions include contact dermatitis and toxic epidermal necrolysis.
The diagnosis of hypersensitivity often involves a combination of medical history, physical examination, laboratory tests, and elimination diets or challenges. Treatment depends on the specific type of hypersensitivity reaction and may include avoidance of the allergen, medications such as antihistamines or corticosteroids, and immunomodulatory therapy.
Symptoms of whooping cough typically appear within 7-14 days after exposure and may include:
* Mild fever
* Runny nose
* Dry, irritating cough that progresses to spasmodic, convulsive coughing fits
* Vomiting after coughing
* Apnea (pause in breathing)
In infants, the symptoms may be milder and include:
* Mild fever
* Lack of appetite
* Cyanosis (blue discoloration of the skin)
If left untreated, whooping cough can lead to serious complications such as pneumonia, seizures, and brain damage. Diagnosis is based on a combination of clinical findings, laboratory tests, and medical imaging. Treatment typically involves antibiotics and supportive care to manage symptoms and prevent complications.
Prevention measures include immunization with the pertussis vaccine, which is routinely given to infants and children in early childhood, as well as booster shots during adolescence and adulthood. Good hygiene practices, such as frequent handwashing and avoiding close contact with people who are sick, can also help prevent the spread of the disease.
Ulnar neuropathy can be caused by a variety of factors, including:
1. Pressure on the nerve at the elbow (cubital tunnel syndrome)
2. Pressure on the nerve at the wrist (guardian syndrome)
3. Injury or trauma to the nerve
4. Compression from a benign tumor or cyst
5. Nerve compression due to repetitive motion or overuse
6. Nerve damage due to diabetes, alcoholism, or other systemic conditions.
Symptoms of ulnar neuropathy can include:
1. Numbness or tingling in the little finger and half of the ring finger
2. Pain or burning sensation in the elbow, forearm, or hand
3. Weakness in the hand, making it difficult to grip or perform manual tasks
4. Wasting away of the muscles in the hand (atrophy)
5. Difficulty coordinating movements or performing fine motor tasks
Diagnosis of ulnar neuropathy typically involves a physical examination, medical history, and electromyography (EMG) testing to evaluate the function of the nerve and muscles. Treatment options depend on the underlying cause of the condition and can include:
1. Physical therapy to improve strength and range of motion in the hand and wrist
2. Medications to relieve pain or inflammation
3. Surgery to release pressure on the nerve or remove a tumor/cyst
4. Lifestyle modifications, such as avoiding activities that exacerbate the condition.
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antazoline hydrochloride meaning in Marathi मराठी #KHANDBAHALE
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- Medicinal Ingredients: Antazoline Phosphate 0.51% Antihistamine Naphazoline hydrochloride 0.051% Decongestant Non-Medicinal Ingredients: Benzalkonium Chloride 0.004% (As Preservative), Edetate Disodium, Liquifilm (Polyvinyl Alcohol), Povidone, Sodium Acetate, Sodium Chloride. (well.ca)
- OBJECTIVES: The aim of the study was to evaluate the efficacy and safety of antazoline, a first-generation antihistamine, for cardioversion of recent-onset AF in the setting of an emergency department. (bvsalud.org)
- This real-world registry analysis revealed a different influence of CKD on the effectiveness of individual drugs, and while propafenone and amiodarone maintained their AF termination efficacy, antazoline became significantly less effective in restoring sinus rhythm. (bvsalud.org)
- 26. A comparison of aspiration, antazoline sclerotherapy and surgery in the treatment of hydrocele. (nih.gov)