ABSTRACT
We studied the effect of the α2-adrenergic receptor agonist clonidine hydrochloride (10-9-10-6 M) on the isolated heart of adult rats after 30-day restriction of motor activity. In hypokinetic rats, in comparison with control animals, clonidine caused a positive inotropic effect; the dynamics of coronary flow was changed after stimulation of α2-adrenergic receptors by clonidine in the minimum and maximum concentrations. Moreover, clonidine in concentrations of 10-8 and 10-7 M reduced coronary flow both in the control group and against the background of hypokinesia. Clonidine (10-8-10-6 M) had a negative chronotropic effect in control and hypokinetic animals, while the dynamics of HR was multidirectional, i.e. either an increase or decrease in the effects was observed depending of the agonist concentration. Overall, the data obtained indicate the participation of α2-adrenergic receptors in adaptive processes after motor activity limitation.
Subject(s)
Adrenergic Agents , Clonidine , Rats , Animals , Clonidine/pharmacology , Hypokinesia , Adrenergic alpha-2 Receptor Agonists/pharmacology , Receptors, Adrenergic , Receptors, Adrenergic, alpha-2ABSTRACT
Stimulation of ß-adrenoreceptors with low (10(-8) and 10(-7) M) or high (10(-6) M) doses of isoproterenol in hypokinetic rats treated with L-NAME (a non-selective blocker of NO synthases) decreased or increased myocardial contractility, respectively. In control rats, all examined doses of isoproterenol used under blockade of NO synthases inhibited myocardial contractility.
Subject(s)
Adrenergic beta-Agonists/pharmacology , Isoproterenol/pharmacology , Myocardial Contraction/drug effects , NG-Nitroarginine Methyl Ester/pharmacology , Nitric Oxide Synthase/antagonists & inhibitors , Animals , Depression, Chemical , Heart Ventricles/drug effects , Immobilization , Motor Activity , Nitric Oxide/physiology , Rats , Receptors, Adrenergic, beta/metabolism , Stimulation, Chemical , Ventricular FunctionABSTRACT
UNLABELLED: In children during the first months of life delayed sternum closure is one of the few techniques increasing cardiac output after simultaneous correction of complex congenital heart defects (CHD). The aim of study was evaluating mortality, predictors of adverse outcome and frequency noncardial complications at of delayed sternum closure after correction of CHD. METHODS: Study design: a prospective, uncontrolled, cohort. 22 children were studied 6 children died. Anesthesia was carried out on the basis ofpropofol (3 mg/kg/h) and fentanyl (5 pg/kg/h) infusion with sevoflurane inhalation in a dose of 1-1.5 WT, including during perfusion. Cardiopulmonary bypass (IR) was carried out by the "Stockert S50" using oxygenators ("Medtronic"). After IR in all cases the use of arterio--venous modified ultrafiltration. Sternum closure was performed on average 2.7 ± 1.4 days after surgery. RESULTS: The odds ratio (OR) of death development at the mean arterial pressure (MAP) < 35 Hg was 3.7, the OR for the risk of death development if SVO2 < 40% was 0.94. OR for risk of death when blood lactate level > 10 mmol/l during the first three days ofpostoperative intensive care was 2.1. CONCLUSIONS: The technique of delayed sternum closure is an acceptable method of maintaining cardiac output in children during the first months of life with CHD in the postoperative period. High blood lactate level (> 10 mmol/l) and especially its further growth and the MAP < 35 mm Hg can be predictors of adverse outcomes of surgical interventions with an open sternotomy.
Subject(s)
Cardiac Surgical Procedures/methods , Heart Defects, Congenital/surgery , Postoperative Care/methods , Sternum/surgery , Cardiac Output, Low/mortality , Cardiac Output, Low/prevention & control , Cardiac Surgical Procedures/mortality , Cohort Studies , Hemofiltration , Humans , Infant , Infant, Newborn , Postoperative Complications/mortality , Postoperative Complications/prevention & control , Prospective Studies , Respiration, Artificial , Time Factors , Treatment OutcomeABSTRACT
Electron paramagnetic (EPR) spectroscopy study showed that 90-day hypokinesia in rats is accompanied by an increase in NO production in the heart. A nonselective NO synthase inhibitor L-NAME decreased the content of NO in the heart atria and ventricles of hypokinetic rats by 67-70%. A selective inhibitor of inducible NO synthase, aminoguanidine, also decreased the level of NO in the heart atria and ventricles of hypokinetic rats by 60-65%. Our results indicate that the increase in NO production during hypokinesia is associated with activation of NO synthases.
Subject(s)
Immobilization , Myocardium/metabolism , Nitric Oxide Synthase/antagonists & inhibitors , Nitric Oxide/biosynthesis , Animals , Electron Spin Resonance Spectroscopy , Myocardium/enzymology , RatsABSTRACT
By electron paramagnetic resonance method analyzed the production of nitric oxide (NO) in atrias and ventricles of the rat's heart, spinal cord and liver of rats after the contained in conditions of hypokinesia during 30, 60 and 90 days. It was discovered that the regime of hypokinesia leads to increase NO production in all the investigated tissues, and the largest increases were observed in 30-day hypokinesia.
