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1.
Bull Exp Biol Med ; 157(6): 728-31, 2014 Oct.
Article in English | MEDLINE | ID: mdl-25339588

ABSTRACT

Experiments on rats with acute myocardial ischemia accompanied by early postocclusive arrhythmias have shown normalizing, energy-stabilizing, and antiarrhythmic effects of uridine and uridine-5'-monophosphate. The drugs decreased lactate and restored reserves of glycogen and creatine phosphate depleted by ischemia. Uridine and uridine-5'-monophosphate significantly decreased the severity of ventricular arrhythmias. Both drugs reduced the incidence and duration of fibrillation. Uridine -5'-monophosphate demonstrated most pronounced antifibrillatory effectiveness. We hypothesize that the antiarrhythmic effect of the drugs is determined by their capacity to activate energy metabolism.


Subject(s)
Arrhythmias, Cardiac/drug therapy , Myocardial Ischemia/complications , Uridine Monophosphate/pharmacology , Uridine/pharmacology , Animals , Arrhythmias, Cardiac/etiology , Coronary Vessels/surgery , Energy Metabolism/drug effects , Energy Metabolism/physiology , Glycogen/blood , Lactic Acid/blood , Ligation , Male , Myocardial Ischemia/metabolism , Phosphocreatine/blood , Rats , Rats, Wistar
2.
Eksp Klin Farmakol ; 77(3): 33-6, 2014.
Article in Russian | MEDLINE | ID: mdl-24800524

ABSTRACT

The study was carried out on male Wistar rats with surgically ablated gonads. The rats with gonadectomy and intact rats received galantamine and/or testosterone over 10 days, after which the model arthritis was induced by injection of 200 ml of complete Freund's adjuvant. It was established that gonadectomy reduced arthritic reactions producing ulcer formation at a later time (21 days) as compared to control (rats with arthritis), where they are formed on the local stage of development (day 7). Testosterone replacement therapy completely blocks the development of ulcers on the paws. Galantamine suppresses the arthritic reaction more significantly, reducing paws and ankle-joint edema 1.5 and 1.3 times respectively (n = 12, p <0.05). The appearance of dopamine in the spleen during galantamine treatment may serve as a marker of protective action of the drug under hypoandrogenic conditions. Introduction of galantamine at high level of testosterone does not significantly influence on development of arthritic reaction, which is indicative of a marked imbalance between the hormonal and cholinergic systems and a possibility to modulate arthritic reaction with cholinergic drugs.


Subject(s)
Androgens/pharmacology , Arthritis, Experimental/drug therapy , Arthritis, Rheumatoid/drug therapy , Dopamine/metabolism , Galantamine/pharmacology , Parasympathomimetics/pharmacology , Testosterone/pharmacology , Animals , Arthritis, Experimental/metabolism , Arthritis, Experimental/pathology , Arthritis, Rheumatoid/metabolism , Arthritis, Rheumatoid/pathology , Edema/prevention & control , Hormone Replacement Therapy , Male , Prostatectomy , Rats , Rats, Wistar , Spleen/drug effects , Spleen/metabolism
3.
Vestn Ross Akad Med Nauk ; (2): 44-50, 2007.
Article in Russian | MEDLINE | ID: mdl-17396562

ABSTRACT

The cardioprotective properties of pharmacological and metabolic activators of mitoKATP are reviewed. Metabolic activators of the channels and data on their cardioprotective properties are discussed in the review. The authors adduce their own data concerning cardioprotective properties of mitoKATP channel metabolic activator (UDP). In experimental animals, UDP precursors, uridine and UMP, decrease myocardial ischemic alteration index and T-wave amplitude within 60 min after occlusion of the left coronary artery. Both effects are prevented by mitoKATP channel inhibitors, glibenclamide and 5-HD. UMP and uridine possess antiarrhythmic properties as well. These preparations decrease the number of premature ventricular beats, the duration of ventricular tachycardia and fibrillation, and these effects are eliminated mainly by glibenclamide. Thus, mitoKATP plays a significant role in prevention of both ischemic lesions and rhythm disorders. The prospects of application of metabolic activators to prevent and treat myocardial infarction are discussed.


Subject(s)
Mitochondrial Proton-Translocating ATPases/physiology , Myocardial Ischemia/physiopathology , Potassium Channels/physiology , Adaptation, Physiological/physiology , Humans
4.
Bull Exp Biol Med ; 144(3): 322-5, 2007 Sep.
Article in English | MEDLINE | ID: mdl-18457027

ABSTRACT

In experiments on rats, uridine-5'-monophosphate and uridine-5'-triphosphate reduced the intensity of anaerobic glycolysis and preserved glycogen stores and creatine phosphate balance during the first 60 min after occlusion of the left coronary artery. However, the energy-protective effect of uridine-5'-triphosphate developed 15 min later than the effect of uridine-5'-monophosphate. Uridine-5'-monophosphate, but not uridine-5'-triphosphate, reduced T wave amplitude on ECG and decreased the volume of ischemic injury to the myocardium.


Subject(s)
Cardiotonic Agents/metabolism , Myocardial Ischemia/metabolism , Uridine Monophosphate/metabolism , Uridine Triphosphate/metabolism , Animals , Energy Metabolism , Male , Myocardial Ischemia/pathology , Rats , Rats, Wistar
5.
Bull Exp Biol Med ; 141(1): 44-7, 2006 Jan.
Article in English | MEDLINE | ID: mdl-16929961

ABSTRACT

A new taurine derivative chlorohydrate-N-isopropylamide-2-(1-phenylethyl)aminoethanesulfonic acid normalized energy metabolism, inhibited lipid peroxidation, and reactivated antioxidant enzymes in the brain of rats exposed to ischemia. This taurine derivative decreased the mortality rate of animals with ischemic changes in cerebral circulation. The test compound was more potent than piracetam in producing the cerebroprotective effect.


Subject(s)
Brain Ischemia/drug therapy , Neuroprotective Agents/therapeutic use , Taurine/analogs & derivatives , Taurine/chemistry , Animals , Energy Metabolism/drug effects , Lipid Peroxidation/drug effects , Neuroprotective Agents/chemistry , Neuroprotective Agents/pharmacology , Rats , Taurine/pharmacology , Taurine/therapeutic use
6.
Bull Exp Biol Med ; 140(5): 529-31, 2005 Nov.
Article in English | MEDLINE | ID: mdl-16758616

ABSTRACT

Antiarrhythmic properties of taurhythman were demonstrated on experimental models of ventricular (early occlusion and calcium chloride-induced) and atrioventricular (aconitine-induced) arrhythmias. The preparation reduced or prevented episodes of paroxysmal tachycardia and ventricular fibrillation, decreased the incidence of arrhythmias, and increased the lethal dose (LD) of arrhythmogenic agents. By its efficiency, taurhythman was superior to procainamide and comparable to lidocaine.


Subject(s)
Alkanesulfonic Acids/pharmacology , Arrhythmias, Cardiac/drug therapy , Cardiotonic Agents/pharmacology , Lidocaine/pharmacology , Procainamide/pharmacology , Tachycardia, Paroxysmal/prevention & control , Ventricular Fibrillation/prevention & control , Aconitine/pharmacology , Animals , Anti-Arrhythmia Agents/pharmacology , Disease Models, Animal , Heart Arrest , Male , Rats , Tachycardia, Paroxysmal/drug therapy , Ventricular Fibrillation/drug therapy
7.
Bull Exp Biol Med ; 137(4): 411-4, 2004 Apr.
Article in English | MEDLINE | ID: mdl-15452617

ABSTRACT

Cytoflavin and neuronol produce vasoactive and neuroprotective effects in rats with cerebral ischemia. Vasoactive activity of neuronol was higher than that of cytoflavin. These differences were most pronounced at the level of microcirculation. Test preparations were equally potent in producing the neuroprotective effect. Cytoflavin and neuronol markedly decreased the mortality rate of animals. Over the first 6 h of ischemia the relative effectiveness of cytoflavin was higher than that of neuronol. However, neuronol exceeded cytoflavin in the relative effectiveness during the follow-up period (days 1-21).


Subject(s)
Brain Ischemia/metabolism , Brain/drug effects , Cerebrovascular Circulation , Flavin Mononucleotide/pharmacology , Inosine Diphosphate/pharmacology , Neuroprotective Agents/pharmacology , Niacinamide/pharmacology , Succinates/pharmacology , Succinic Acid/pharmacology , Animals , Brain/pathology , Brain Ischemia/pathology , Brain Ischemia/physiopathology , Drug Combinations , Male , Rats , Regional Blood Flow , Reperfusion Injury/pathology , Reperfusion Injury/physiopathology , Reperfusion Injury/prevention & control , Survival Rate
8.
Patol Fiziol Eksp Ter ; (1): 14-6, 2002.
Article in Russian | MEDLINE | ID: mdl-11998397

ABSTRACT

Occlusion of the left coronary artery in rats provoked ventricular tachycardia (VT) and ventricular fibrillation (VF) within the first 30 min of ischemia leading to death in 20% animals. Methacin (i.v., 100 micrograms/kg) significantly prolonged VT and VF without effects on the survival. Acetylcholine (i.v., 10 micrograms/kg/min) had no influence on VT frequency and severity but prevented VF. Rats from this group survived. The same effect was observed for neostigmine (i.v., 25 micrograms/kg). Nicotine (i.v., 2.5 micrograms/kg/min) prolonged VT episode duration but did not change frequency and severity of VF and survival. Ganglioblockers hexametony and azametony (i.v., both in a dose 500 micrograms/kg) significantly attenuated VT, prevented VF and death of the animals. Thus, cholinotropic drugs may have both antiarrhythmic and proarrhythmogenic effects in early arrhythmias induced by ischemia.


Subject(s)
Arrhythmias, Cardiac/chemically induced , Arrhythmias, Cardiac/prevention & control , Cholinergic Agents/pharmacology , Myocardial Ischemia/complications , Acetylcholine/pharmacology , Animals , Cholinesterase Inhibitors/pharmacology , Ganglionic Blockers/pharmacology , Hexamethonium/pharmacology , Male , Muscarinic Antagonists/pharmacology , Myocardial Ischemia/drug therapy , Myocardial Ischemia/physiopathology , Neostigmine/pharmacology , Nicotine/pharmacology , Oxyphenonium/pharmacology , Quaternary Ammonium Compounds/pharmacology , Rats , Tachycardia/chemically induced , Ventricular Fibrillation/chemically induced
10.
Eksp Klin Farmakol ; 62(3): 25-7, 1999.
Article in Russian | MEDLINE | ID: mdl-10439943

ABSTRACT

The authors studied the effect of m-cholino-, adreno-, and purinotropic agents on the development of postischemic reperfusion fibrillation of isolated rat hearts. Pilocarpine, norepinephrine, phenylephrine, and adenosine caused a proarrhythmogenic effect. Atropine, trimedoxim, prazosin, and chloroquine made fibrillation less expressed. A direct correlation was found between the arrhythmogenic effect of reperfusion and the size of the no-reflow zone, with the use of the drugs too. It is concluded that the phospholipid mechanism contributes to realization of the arrhythmogenic effect of reperfusion and vascular disorders, leading to the occurrence of the no-reflow phenomenon.


Subject(s)
Heart/physiopathology , Myocardial Ischemia/complications , Myocardial Reperfusion Injury/complications , Receptors, Adrenergic/physiology , Receptors, Muscarinic/physiology , Receptors, Purinergic P1/physiology , Ventricular Fibrillation/etiology , Adrenergic Agonists/pharmacology , Adrenergic Antagonists/pharmacology , Animals , Heart/drug effects , In Vitro Techniques , Male , Muscarinic Agonists/pharmacology , Muscarinic Antagonists/pharmacology , Myocardial Ischemia/physiopathology , Myocardial Reperfusion Injury/physiopathology , Purinergic P1 Receptor Agonists , Purinergic P1 Receptor Antagonists , Rats , Receptors, Adrenergic/drug effects , Receptors, Muscarinic/drug effects , Receptors, Purinergic P1/drug effects , Time Factors , Ventricular Fibrillation/physiopathology
11.
Ross Fiziol Zh Im I M Sechenova ; 84(5-6): 507-12, 1998.
Article in Russian | MEDLINE | ID: mdl-9785417

ABSTRACT

Administration of adenosine increased the RR interval in greater degree at hyper- than in hypodynamic blood circulation type. The AV-blockade and atrial flutter were maximal in rats with hyperdynamic type of blood circulation. Propranolol weakened the adenosine cardiotropic effect whereas cholinoblockators enhanced it. Neurohumoral regulation exerted no effect on the adenosine hypotensive action.


Subject(s)
Adenosine/pharmacology , Antihypertensive Agents/pharmacology , Blood Circulation/physiology , Cardiovascular Agents/pharmacology , Adenosine/toxicity , Animals , Atrial Fibrillation/chemically induced , Atrial Fibrillation/physiopathology , Blood Pressure/drug effects , Blood Pressure/physiology , Cardiovascular Agents/toxicity , Electroencephalography , Heart Block/chemically induced , Heart Block/physiopathology , Heart Rate/drug effects , Heart Rate/physiology , Male , Rats
12.
Kardiologiia ; 28(12): 98-9, 1988 Dec.
Article in Russian | MEDLINE | ID: mdl-3244268

ABSTRACT

In rabbit experiments, adenosine was studied for its effects on the sizes of myocardial infarction and "no reflow" zones after coronary artery occlusion and reperfusion. Intravenous administration of adenosine resulted in a steady drop in blood pressure, decrease in heart rate and increase in the extent of infarction and "no reflow" zone.


Subject(s)
Adenosine/adverse effects , Coronary Circulation/drug effects , Coronary Vessels/drug effects , Myocardial Infarction/pathology , Myocardial Reperfusion Injury/chemically induced , Myocardium/pathology , Animals , Coronary Vessels/physiopathology , Ligation , Male , Myocardial Infarction/physiopathology , Myocardial Reperfusion , Myocardial Reperfusion Injury/pathology , Rabbits
13.
Kardiologiia ; 28(11): 103-6, 1988 Nov.
Article in Russian | MEDLINE | ID: mdl-3230762

ABSTRACT

Adenosine, administered intravenously (0.25 mg/kg-1/min-1) to rabbits with experimental myocardial infarction, produced a drop in arterial pressure and total peripheral resistance, normalized stroke volume, increased ATP content at the margin of the infarcted area, and reduced LDG activity and increased SDG activity in the ischemized region.


Subject(s)
Hemodynamics/drug effects , Myocardial Infarction/drug therapy , Myocardium/metabolism , Adenosine/therapeutic use , Adenosine Triphosphate/metabolism , Animals , Drug Evaluation, Preclinical , L-Lactate Dehydrogenase/metabolism , Male , Myocardial Infarction/physiopathology , Rabbits , Succinate Dehydrogenase/metabolism
15.
Biull Eksp Biol Med ; 104(7): 43-5, 1987 Jul.
Article in Russian | MEDLINE | ID: mdl-3040145

ABSTRACT

In anesthetized rats a 30-min intravenous infusion of adenosine (2.5 mg/kg/min) performed after the coronary artery ligation significantly decreased the incidence and severity of early ischemic arrhythmias. After the infusion of adenosine, there was an increase in cGMP level in the left ventricular myocardium, cAMP content remained unchanged.


Subject(s)
Adenosine/therapeutic use , Anti-Arrhythmia Agents , Coronary Disease/drug therapy , Cyclic AMP/metabolism , Cyclic GMP/metabolism , Heart/drug effects , Myocardium/metabolism , Animals , Arrhythmias, Cardiac/etiology , Arrhythmias, Cardiac/prevention & control , Coronary Disease/complications , Coronary Disease/metabolism , Drug Evaluation, Preclinical , Male , Rats , Time Factors
16.
Fiziol Zh SSSR Im I M Sechenova ; 72(6): 763-6, 1986 Jun.
Article in Russian | MEDLINE | ID: mdl-3015695

ABSTRACT

The chronotropic and inotropic effects of guanosine-5'-monophosphate (5'-GMP) and inosine were investigated in isolated frog hearts. 5'-GMP induced biphasic chronotropic and inotropic responses: positive those were inhibited with propranolol, the negative inotropic response could not be inhibited with atropine. Inosine was able to enhance the positive inotropic response to 5'-GMP.


Subject(s)
Guanine Nucleotides/pharmacology , Guanosine Monophosphate/pharmacology , Heart/drug effects , Inosine/pharmacology , Animals , Atropine/pharmacology , Drug Interactions , Heart Rate/drug effects , In Vitro Techniques , Myocardial Contraction/drug effects , Propranolol/pharmacology , Rana temporaria
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