CARDIO NEUROLOGICAL SYMPTOMS CAUSED BY AN ACUTE POISONING WITH SLOW CALCIUM CHANNEL BLOCKING AGENT (VERAPAMIL)

The research of an analysis of the cardiac hemodynamic effects of an acute chemical trauma with slow calcium channels blockers (verapamil) shows that the depth of disorder of cardiac hemodynamic parameters and the level and frequency of occurrence of consciousness disorder were determined in 46 patients within the period of 2007–2017 in this nosological form of acute poisoning.

Influence of l-type slow calcium channels blockers on cardiac, respiratory and motor activity at the intact and poisoned by physostigmine (eserine) of rats during the early ontogeny

The effects of calcium-channel blockers (CCBs) (verapamil, nifedipine) on heart rate, respiration rate and motor activity were studied in 3-30-day-old rats. The role of calcium channels in development of disturbances of a heart and respiratory rhythms after introduction to newborn rats of acetylcholinesterase (AChE) inhibitor of physostigmine was revealed. Parameters of functional activity of heart, respiratory and somatomotor systems in case of blockade of calcium channels were studied also under conditions of the activation of cholinoceptive structures caused by an injection to infant rats of AChE inhibitor after premedication by CCBs. It is shown that use of calcium channels blockers leads to development of bradycardia, and verapamil causes more expressed disturbance of a heart rhythm in rats of younger age, while blockade of dihydropyridinic receptors by nifedipine has no ontogenetic specifics. Similar ontogenetic dynamics concerns also reaction of respiratory system. Verapamil have a detrimental effect on respiration, up to a stop, in 3-7-day-old and to a lesser extent in 16-30-day-old infant rats. Nifedipine slightly reduces a respiration rate at younger infant rats, but raises it at the mature rats. The nifedipine injection more in comparison with verapamil changes the level and a pattern of motor activity. Preliminary blockade of calcium channels does not render significant change of reaction at the subsequent introduction of physostigmin.

Drug Repurposing for Retinoblastoma: Recent Advances

Retinoblastoma is the intraocular malignancy that occurs during early childhood. The current standard of care includes chemotherapy followed by focal consolidative therapies, and enucleation. Unfortunately, these are associated with many side and late effects. New drugs and/or drug combinations need to be developed for safe and effective treatment. This compelling need stimulated efforts to explore drug repurposing for retinoblastoma. While conventional drug development is a lengthy and expensive process, drug repurposing is a faster, alternate approach, where an existing drug, not meant for treating cancer, can be repurposed to treat retinoblastoma. The present article reviews various attempts to test drugs approved for different purposes such as calcium channels blockers, non-steroidal antiinflammatory drugs, cardenolides, antidiabetic, antibiotics and antimalarial for treating retinoblastoma. It also discusses other promising candidates that could be explored for repurposing for retinoblastoma.

PHOTODEGRADATION OF 1, 4-DIHYDROPYRIDINE ANTIHYPERTENSIVE DRUGS: AN UPDATED REVIEW

1, 4-dihydropyridine calcium channels blockers (DHPs) are the most commonly used antihypertensive drugs. Unfortunately, these compounds have a significant degradability to light. The oxidation to the pyridine derivative represents the first, and in many cases the only, step of the degradation mechanism. The photodegradation process causes the complete loss of pharmacological activity and may trigger the formation of single and superoxide oxygen species, potentially responsible for phototoxic reactions. Several analytical techniques have been proposed for DHP determination in the presence of their photoproducts. Nowadays, DHPs are all marketed in solid formulations, especially tablets, because photodegradation is particularly fast in solution. Various approaches aimed to protect molecular integrity and therapeutic activity of these drugs from the effects of light are currently studied. This review covers the studies over the last years about photodegradation of the DHPs and the approaches to obtain photostable formulations of these drugs.

Pheochromocytoma, diagnosis and treatment: Review of the literature

Objective.We conducted an extensive review of the literature and tried to cite the most recent recommendations concerning the pheochromocytoma (PHEO).Methods.Pub Med and Google Scholar databases were searched systematically for studies concerning pheochromocytomas (intra-adrenal paragangliomas) from 1980 until 2016. Bibliographies were searched to find additional articles.Results.More than four times elevation of plasma fractionated metanephrines or elevated 24-h urinary fractionated metanephrines are keys to diagnosing pheochromocytoma. If the results are equivocal then we perform the clonidine test. If we have not done it already, we preferably do a CT scan and/or an MRI scan. The patient needs pre-treatment with α1-blockers at least 10–14 days before operation. Alternatives or sometimes adjuncts are Calcium Channels Blockers and/or β-Blockers. Several familial syndromes are associated with PHEO and genetic testing should be considered.Conclusions.The biggest problem for pheochromocytoma is to suspect it in the first place. Elevated metanephrines establish the diagnosis. With the proper preoperative preparation the risks during operation and the postoperative period are minimal. If there is a risk of the hereditable mutation, it is strongly suggested that all the patients with pheochromocytoma need clinical genetic testing.