[Hemodynamic effects of intravenous omeprazole in critically ill children.]
ABSTRACT INTRODUCTION: Critical patients usually have hemodynamic disturbances which may become worse by the administration of some drugs. Omeprazole is a drug used in the prophylaxis of the gastrointestinal bleeding in these patients, but its cardiovascular effects are unknown. The objective was to study the hemodynamic changes produced by intravenous omeprazole in critically ill children and to find out if there are differences between two different doses of omeprazole. MATERIAL AND METHODS: A randomized prospective observational study was performed on 37 critically ill children aged from 1 month to 14 years of age who required prophylaxis for gastrointestinal bleeding. Of these, 19 received intravenous omeprazole 0.5mg/kg every 12hours, and 18 received intravenous omeprazole 1mg/kg every 12hours. Intravenous omeprazole was administered in 20minutes by continuous infusion pump. Heart rate, systolic, diastolic and mean arterial blood pressure, central venous pressure and ECG were recorded at baseline, and at 15, 30, 60 and 120minutes of the infusion. RESULTS: There were no significant changes in the electrocardiogram, heart rate, blood pressure and central venous pressure. No patients required inotropic therapy modification. There were no differences between the two doses of omeprazole. CONCLUSIONS: Intravenous omeprazole administration of 0.5mg/kg and 1mg/kg is a hemodynamically safe drug in critically ill children.
New England Journal of Medicine 09/1979; 301(7):364-9. DOI:10.1056/NEJM197908163010707 · 54.42 Impact Factor
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ABSTRACT: Enzyme activity that represents ouabain-insensitive, potassium-dependent p-nitrophenylphosphatase (p-NPPase) was assessed in rat atrial myocytes by biochemical and cytochemical procedures. No activity was detected in parallel experiments with ventricular myocytes. Fixed tissues were incubated in a reaction medium containing Tricine buffer, p-nitrophenylphosphate (p-NPP), KCl, MgCl2, CaCl2, CeCl3. Triton X-100, levamisole, and ouabain. Final pH was adjusted to 7.5. Biochemical studies showed that accumulation of p-nitrophenol in the medium was increased proportionally in accordance with the amount of incubated tissue. This activity was optimal with incubation at pH 7.5 and in the presence of KCl. Approximately 70% of the enzyme was inhibited by 2 mM CeCl3. Electron microscopic observations revealed reaction product (RP) at sites of ouabain-insensitive, potassium-dependent p-NPPase activity as electron-dense precipitate localized at the inner surface of the plasma membrane and at the T-tubules of atrial myocytes. Control experiments indicated that the activity was strongly inhibited by sodium orthovanadate and was repressed by omeprazole and 1,3-dicyclohexylcarbodiimide. X-ray microanalysis confirmed the presence of cerium within the cytochemical RP. The ouabain-insensitive, K-dependent p-NPPase activity detected in the present study is considered to be an isoform of a P-type, H-transporting, K-dependent adenosine triphosphatase (H,K-ATPase).Journal of Histochemistry and Cytochemistry 03/1997; 45(2):177-87. DOI:10.1177/002215549704500204 · 2.40 Impact Factor
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ABSTRACT: The effect of H+-K+ ATPase inhibitors on airway smooth muscle tone was investigated in vitro. Four H+-K+ ATPase inhibitors, SCH 28080 (2-methyl-8-(phenylmethoxy)-imidazo[1,2-a] pyridine-3-acetonitrile), SK&F 96067 (3-butyryl-4-(2-methylphenylamino)-8-methoxy-quinoline), omaprezole (5-methoxy-2-(((4-methoxy-3,5-dimethyl-2-pyridinyl)-methyl)-sulfinyl)-1H -benzimidazole) and NC-1300-B (2-(2-dimethylaminobenzylsulfiny)-5-methoxybenzimidazole), induced concentration-dependent relaxation of guinea pig trachea with spontaneous tone, with IC50 values of 5.9, 7.1, 155 and 79 microM, respectively, SCH 28080 and omeprazole also relaxed airways precontracted with carbachol or histamine in the presence of indomethacin. Relaxation was similar in intact and epithelium-denuded tracheal preparations, suggesting that the airway epithelium neither mediates or modulates relaxation induced by H+-K+ ATPase inhibitors. SCH 28080-induced relaxation was not influenced by tetrodotoxin, suggesting that it is not neurogenically mediated. Bafilomycin A1 and concanamycin A had no effect on guinea pig tracheal spontaneous tone, suggesting that relaxation induced by H+-K+ ATPase inhibitors is not due to an interaction with a vacuolar H+ ATPase. SCH 28080 also induced concentration-dependent relaxation of human bronchi precontracted with histamine. These results demonstrate that several structurally and/or mechanistically distinct H+-K+ ATPase inhibitors cause relaxation of airway smooth muscle in vitro, and suggest that a H+-K+ ATPase or similar pathway may play a role in the maintenance of airway smooth muscle tone.Journal of Pharmacology and Experimental Therapeutics 04/1996; 276(3):897-903. · 3.86 Impact Factor