Orciprenaline 20mg tablets

This study aimed to elucidate the vasodilatory effects and cytotoxicity of various vasodilators used as antispasmodic agents during microsurgical anastomosis. Rat smooth muscle cells (RSMCs) and human coronary artery endothelial cells (HCAECs) were used to investigate the physiological concentrations and cytotoxicity of various vasodilators (lidocaine, papaverine, nitroglycerin, phentolamine, and orciprenaline). Using a wire myograph system, we determined the vasodilatory effects of each drug in rat abdominal aortic sections at the concentration resulting in maximal vasodilation as well as at the surrounding concentrations 10 min after administration. Maximal vasodilation effect 10 min after administration was achieved at the following concentrations: lidocaine, 35 mM; papaverine, 0.18 mM; nitroglycerin, 0.022 mM; phentolamine, 0.11 mM; olprinone, 0.004 mM. The IC50 for lidocaine, papaverine, and nitroglycerin was measured in rat abdominal aortic sections, as well as in RSMCs after 30 min and in HCAECs after 10 min. Phentolamine and olprinone showed no cytotoxicity towards RSMCs or HCAECs. The concentrations of the various drugs required to achieve vasodilation were lower than the reported clinical concentrations. Lidocaine, papaverine, and nitroglycerin showed cytotoxicity, even at lower concentrations than those reported clinically. Phentolamine and olprinone show antispasmodic effects without cytotoxicity, making them useful candidates for local administration as antispasmodics.

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Lung cancer is a type of cancer that is mostly diagnosed at an advanced stage and has a short survival time despite standard chemotherapy and targeted therapies. Terbutaline and Orci-prenaline are bronchodilator agents that are potent and selective β2 receptor agonists. The purpose of this study was to investigate to evaluate the effects of Terbutaline and Orci-prenaline on A549 human lung carcinoma cell line and Beas-2b human bronchial epithelial cell line. Cells were treated with 1, 10, 100, 200, 400 µM concentrations of Terbutaline and Orciprenaline. 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and xCELLigence real-time cell analyzer were used to determine their effects on cell viability. The cell index was monitored continuously by visualizing the impedance of the E-plate wells. Because of the roles of Glycogen Synthase Kinase 3β (GSK3β) in a diverse range of cellular processes like metabolism, cell proliferation, differentiation and survival and its key position at several signaling pathways, GSK3β inhibition by Terbutaline and Orciprenaline was also investigated. The results showed that Terbutaline and Orciprenaline inhibits GSK-3β. The overall results led to the conclusion that Terbutaline and especially Orciprenaline may have potential therapeutic effects in lung carcinoma.

Abstract licence: CC BY

Anaphylaxis is a rapid, potentially fatal systemic hypersensitivity reaction, with adrenaline recommended as first-line treatment, followed by beta-2-agonists, glucocorticoids, and antihistamines. H1-antihistamines play a limited role but help relieve skin symptoms; undue side effects, such as sedation decrease with newer generations. Fexofenadine, a third-generation antihistamine, is preferred for its non-sedative profile and lack of anticholinergic or adrenergic effects. It reaches peak plasma levels in 2-4 hours, lasts 12-24 hours, and is 60-70% protein-bound with a half-life of 11-15 hours. As a terfenadine metabolite, it avoids QT prolongation and is considered safe. This is a rare case of sinus bradycardia following fexofenadine use in a 35-year-old female with no known comorbidities, who presented with angioedema and anaphylactic shock after taking cefixime and aceclofenac. She was stabilised with intravenous hydrocortisone and intramuscular adrenaline, then admitted to the Intensive Care Unit (ICU). Fexofenadine 180 mg twice daily and hydrocortisone 100 mg thrice daily were initiated. After three doses of fexofenadine, the patient developed worsening bradycardia, with a lowest recorded heart rate of 30 bpm. No other triggers were identified. Fexofenadine was discontinued, and symptomatic treatment included atropine and oral orciprenaline. Her heart rate stabilised without requiring pacing. Bradycardia resolved within three days of stopping fexofenadine, and orciprenaline was discontinued. The patient was discharged after a week. This case highlights a rare but significant adverse effect of fexofenadine, a commonly prescribed antihistamine. Clinicians should be aware of its potential to cause bradyarrhythmia and exercise caution when prescribing, especially in acute care settings.

Abstract licence: CC BY-NC-ND

BACKGROUND: Oxaliplatin resistance significantly impairs therapeutic outcomes in colorectal cancer. However, reliable diagnostic markers for early detection of resistance remain limited. This study aimed to identify novel diagnostic signatures through integrative bioinformatics and machine learning approaches. METHODS: We performed comprehensive bioinformatics analyses combining transcriptomics data from multiple cohorts. The diagnostic signatures were identified and validated using machine learning algorithms. Weighted gene co-expression network analysis (WGCNA) was employed to explore resistance-associated gene modules. Multiple computational methods including functional enrichment, protein-protein interaction networks, and immune infiltration assessment were conducted to comprehensively characterize the molecular features of oxaliplatin resistance. RESULTS: Through integrative analysis and machine learning, we identified an 8-gene diagnostic signature (CHFR, TGFBRAP1, RPS4Y1, CYP26B1, NR4A2, FLJ20021, TNFSF9, CAV2) that demonstrated robust performance in distinguishing resistant cases (AUC = 0.868). Functional characterization revealed significant enrichment in metabolic reprogramming, DNA repair mechanisms, and immune modulation pathways. Systematic evaluation of tumor-immune interactions demonstrated distinct patterns of immune cell infiltration between resistant and sensitive groups, particularly in Natural killer cells and Activated CD8 T cells. Computational drug screening identified Glycidamide and orciprenaline as promising candidates, with favorable binding profiles against key resistance-associated targets. CONCLUSIONS: Our study establishes a novel multi-gene diagnostic signature for oxaliplatin resistance through integrative bioinformatics and machine learning approaches. The comprehensive molecular characterization and identification of potential therapeutic candidates provide new insights into resistance mechanisms and clinical management strategies for oxaliplatin-resistant colorectal cancer.

Abstract licence: CC BY-NC-ND

Dear Editor, A 21-year-old unmarried male, studying degree 3rd year, from an upper middle socioeconomic background, was brought by his parents with history of polysubstance use. Upon a brief history taking, it was revealed that he used to go out with his friends and started experimenting with various substances out of curiosity for 5 years such as alcohol, inhalants, nitrazepam tablets, meth crystals but stopped using them after 2 to 3 months due to fear of health risks. But he continued using cigarettes and cannabis (in the form of bong, chillum, and joints) for 5 years. He smokes about 7 to 8 cigarettes, as well as about 20 joints of cannabis per day, the last intake being the previous day of admission. He had only experienced short periods of abstinence in the past due to religious reasons, promptly returning to substance use thereafter. Notably, the patient had a medical history of syncopal episodes for 6 years, 5 episodes until now, the last episode being 8 months back, which was not investigated medically but did not exhibit a temporal correlation with cannabis intoxication. As per the patient, these episodes occurred when he was tired or dehydrated. There is no significant familial background of substance use, cardiac disease, or sudden cardiac deaths. His premorbid personality was indicative of impulsive traits. Following admission to the de-addiction ward, the patient’s vital signs were recorded and routine diagnostic tests were conducted. His BP was 118/80 mmHg, and he was afebrile. An irregular and low pulse rate was observed, while all his other vitals and blood test results such as complete blood picture, liver function tests, renal function tests, viral screening, and ultrasound abdomen, were within normal limits. His electrocardiogram (ECG) displayed ST segment and T wave alterations in leads V1 and V2 as shown in Figure 1b when compared to a normal ECG as shown in [Figure 1a].Figure 1: (a) shows V1,V2,V3 leads in a normal ECG for reference, (b) shows V1,V2,V3 leads with saddle-back pattern in the patient’s ECG (blue arrows), (c) shows Holter monitor strip of the patient confirming Brugada’s type 3 pattern (blue arrows)Cardiology referral was done and he was kept on Holter monitoring. His Holter report showed type 3 Brugada ECG pattern with saddle-back pattern of ST segment and T wave as shown in Figure 1c with sinus pauses occasionally. 2D echocardiogram showed a preserved left ventricular ejection fraction (LVEF) of 60% without structural and functional abnormality. He was managed conservatively by Tab. Orciprenaline 10 mg thrice daily, which is a β2 adrenergic agonist. The cardiologist planned on permanent pacemaker implantation if syncopal episodes continue. The patient was maintaining well on the conservative treatment and was discharged. DISCUSSION Brugada syndrome is an autosomal dominant disorder that affects the heart rhythm leading to sudden cardiac deaths. There is evidence to suggest a potential association between cannabis use and the manifestation of Brugada syndrome. Several case reports and studies have documented cannabis consumption has been linked to the unmasking or induction of Brugada pattern on ECGs.[1-3] For instance, a case reported by Seri et al.[1] revealed that vaping tetrahydrocannabinol unmasked Brugada pattern and induced ventricular fibrillation in a patient with Brugada syndrome. These findings are significant as they suggest a potential link between cannabis use and the development or unmasking of Brugada syndrome. There are some case reports, which link cannabis use to syncopal episodes.[4,5] Risk factors for serious arrhythmic event in Brugada’s syndrome include.[6] History of cardiogenic syncope, presence of a spontaneous type 1 ECG Drugs like antiarrhythmics (like flecainide, procainamide), psychotropics (like TCAs, Lithium, Fluoxetine), anaesthetic agents (like propofol) Febrile illness Non-prescription drugs like antihistamines Illicit substances like cocaine, cannabis, alcohol. It is important to consider these associations in clinical practice, especially when evaluating patients with a history of cannabis use and unexplained cardiac symptoms. Further research is warranted to elucidate the underlying mechanisms and the extent of the relationship between cannabis and Brugada syndrome. There is a scarcity of such reports in India despite frequent use of cannabis use. CONCLUSION Cannabis is linked to ECG abnormalities, especially Brugada Syndrome. As cannabis is frequently abused in India, unexplained cardiac events should be thoroughly investigated for underlying Brugada Syndrome. Cardiac evaluation should be a priority in cannabis users, as Brugada syndrome may cause sudden cardiac deaths in susceptible individuals. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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