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1.
Paediatr Anaesth ; 17(6): 540-6, 2007 Jun.
Article in English | MEDLINE | ID: mdl-17498015

ABSTRACT

BACKGROUND: The implementation of sevoflurane in pediatric anesthesia practice led to a decrease in the incidence of cardiac arrest previously reported with halothane. Nevertheless, the effects of sevoflurane on cardiac rhythm and function have not been systematically investigated in infants. Thus, we compared cardiac rhythm and left ventricular function at 1 MAC sevoflurane and halothane anesthesia and investigated the potential benefit effect of atropine. METHODS: Twenty infants ASA physical status I or II were randomly assigned to have anesthesia induced with either sevoflurane (up to 5%) or halothane (up to 1.5%). After insertion of an i.v. line, anesthesia was maintained at 1 MAC sevoflurane (group S) or 1 MAC halothane (group H) with infants breathing spontaneously in 100% oxygen. Cardiac output and contractility were measured by transthoracic echocardiography. Three sets of hemodynamic parameters were averaged prior to and after administration of 20 microg x kg(-1) of i.v. atropine. RESULTS: Infants breathing spontaneously 1 MAC halothane or 1 MAC sevoflurane were found to have comparable hemodynamic parameters. After atropine administration, heart rate and cardiac index (CI) increased significantly in both groups (19.6 +/- 7.6% in group H and 21.3 +/- 13.1% in group S, 18.6 +/- 8.8% in group H and 17.7 +/- 12% in group S respectively). Moreover, atropine induced an increase in left ventricular shortening fraction with no difference between groups. In contrast, only infants in group S presented a significant increase in ejection fraction. CONCLUSIONS: Indices of left ventricular function were comparable between groups with no clinically significant change following atropine administration. The present study confirms the favorable hemodynamic profile of sevoflurane in infants breathing spontaneously at 1 MAC concentration.


Subject(s)
Anesthetics, Inhalation/pharmacology , Halothane/pharmacology , Heart Rate/drug effects , Methyl Ethers/pharmacology , Ventricular Function, Left/drug effects , Anti-Arrhythmia Agents/administration & dosage , Atropine/administration & dosage , Blood Pressure/drug effects , Cardiac Output/drug effects , Elective Surgical Procedures/methods , Electrocardiography/methods , Female , Humans , Infant , Male , Monitoring, Intraoperative/methods , Myocardial Contraction/drug effects , Sevoflurane
2.
Med Sci Monit ; 9(6): BR193-8, 2003 Jun.
Article in English | MEDLINE | ID: mdl-12824941

ABSTRACT

BACKGROUND: In order to compare the effects of inhaled nitric oxide (NO) and magnesium (Mg) and their potential synergism on hemodynamics in pulmonary hypertension, we compared the effect of NO and Mg alone and in combination. The fact that simultaneous administration selectively increases pulmonary vascular relaxation would suggest that their association would allow for a decrease in the NO concentration required for optimal pulmonary vasodilation, thus lowering the risk of side effects. MATERIAL/METHODS: We compared the effects of 20 ppm inhaled NO, 25 mg/kg Mg, and combined therapy in a pig model of hypoxic pulmonary hypertension. Twelve animals were randomly assigned to one of 3 treatment groups: control (group 1); Mg+NO group, receiving Mg followed by NO 15 min later (group 2); NO+Mg group, receiving NO followed by Mg 15 min later (group 3). The cardiac index, pulmonary and systemic pressures, pulmonary and systemic resistance, and the pulmonary to systemic resistance ratio (PVR/SVR) were recorded at baseline, on hypoxia and 15 minutes after each drug alone and in combination. RESULTS: PVR/SVR decreased with NO alone (0.32+/-0.07 to 0.18+/-0.04; p<0.05) but not with Mg alone. When NO was added to Mg, PVR/SVR decreased significantly (0.31+/-0.06 to 0.16+/-0.02; p<0.05) but not when Mg was added to NO. CONCLUSIONS: Inhaled NO is a selective pulmonary vasodilator in a pig model of hypoxic pulmonary hypertension. The simultaneous administration of intravenous Mg does not enhance the selective pulmonary vasodilation induced by NO inhalation.


Subject(s)
Hypertension, Pulmonary/drug therapy , Magnesium Sulfate/therapeutic use , Nitric Oxide/therapeutic use , Administration, Inhalation , Animals , Cyclic GMP/blood , Disease Models, Animal , Drug Therapy, Combination , Female , Heart Rate/drug effects , Hypertension, Pulmonary/physiopathology , Hypoxia , Injections, Intravenous , Magnesium/blood , Magnesium Sulfate/administration & dosage , Nitric Oxide/administration & dosage , Oxygen/blood , Partial Pressure , Swine , Vascular Resistance/drug effects
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