Search

Introduction: The study of innovative drugs at the molecular, tissue, organ, systemic and organismic levels with an assessment of their safety are part of preclinical studies. In this case, studies aimed at specific pharmacological targets are especially important. The search for a selective arginase 2 inhibitor is necessary in terms of the treatment of pulmonary hypertension. One of the most common models of LH is the monocrotalin model of pulmonary hypertension. Research tasks: To evaluate the protective effects of a selective arginase 2 inhibitor, including the right ventricular contractility parameters on a monocrotalin model of pulmonary hypertension in rats. Material and Methods: A study was conducted of 5 groups of animals of 10 rats. After using a selective arginase 2 inhibitor, blood pressure, heart rate, Fulton's index, BT index, and condition of the right ventricle were evaluated. Results and Discussion: It was found that L207-0525 at doses of 1 and 3 mg/kg and tadalafil 10 mg/kg prevents the development of pulmonary hypertension. This is expressed in preventing an increase in systolic pressure in the right ventricle, Fulton, RV/BW and WT indices. L207-0525 showed a dose of 3 mg/kg for the activity shown. Conclusion: The results indicate a dose-dependent protective activity of the selective arginase 2 inhibitor L207-0525 in relation to the development of monocrotaline pulmonary hypertension. [ABSTRACT FROM AUTHOR]

Introduction: Cardiovascular disease (CVD) is the leading cause of death worldwide: no other reason causes as many deaths a year as CVD. An estimated 17.9 million people died of CVD in 2016, accounting for 31% of all deaths in the world. People with CVD or at high risk for these diseases (due to one or more risk factors, such as high blood pressure, diabetes, hyperlipidemia, or an already developed disease) need early detection and assistance through counseling and, if necessary, taking medication. Ways to find new targets for the correction of endothelium-associated pathology: The basis of the modern therapy for arterial hypertension and other cardiovascular diseases is the postulate of the need to correct endothelial dysfunction as an indication of the adequacy of antihypertensive and other types of treatment. Lowering blood pressure (BP) without normalizing endothelial function cannot be considered a successfully resolved clinical task. Currently, there are no drugs for specific pharmacological correction of endothelial dysfunction in cardiovascular diseases, and the search for new targets for pharmacological correction of endothelial dysfunction is one of the main tasks of pharmacology. [ABSTRACT FROM AUTHOR]

A series of novel 2-(N-pyrrolidino, N-piperidino or N-morpholino)-7-phenyl-(α-furoyl or α-thienyl)-[1,3]thiazolo[4,5-d]pyridazinones 10a-c, 14-16a,b was synthesized in 78-87% yields via the reaction of methyl 5-benzoyl(α-furoyl or α-thienyl)-2-aminosubstituted-thiazol-4-carboxylates 9a-c, 13a-e with hydrazine. These new compounds have been tested for their in vivo analgesic and anti-inflammatory activities. All compounds have been characterized by ¹H-NMR, 13C-NMR spectroscopy, and liquid chromatography-mass spectrometry. [ABSTRACT FROM AUTHOR]