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1.
Acta cir. bras ; 32(6): 459-466, June 2017. tab, graf
Article in English | LILACS | ID: biblio-886207

ABSTRACT

Abstract Purpose: To investigate the effects of dexmedetomidine (DEX) on amino acid contents and the cerebral ultrastructure of rats with cerebral ischemia-reperfusion injury (I/R). Methods: Thirty-six, male, Wistar rats were randomly divided into three groups: the sham operation group (group C), the ischemia-reperfusion group (group I/R), and the DEX group (group D). The middle cerebral artery occlusion model was prepared by the modified Longa method. The time of ischemia was 180 min, and 120 min after reperfusion, the amount of glutamate (Glu), and γ-aminobutyric acid (GABA) in the brain were measured, and the ultrastructure-level changes in the cerebral cortex were examined using electron microscopy. Results: Compared to group C, Glu contents in group D, and I/R significantly increased. Compared to group I/R, Glu contents in group D significantly decreased. Compared to group C, GABA contents in group D, and I/R significantly increased, and those in group D significantly increased, as compared to group I/R. The cerebral ultrastructure was normal in group C. Vacuolar degeneration in the plastiosome and nervous processes, was more critical than in group D. Vascular endothelial cells (VEC) were damaged. On the contrary, these changes in group D significantly improved. Conclusion: Dexmedetomidine is capable of decreasing glutamergic content, and increasing GABAergic content, in order to decrease the injury of the cerebral ultrastructure, following cerebral ischemia-reperfusion injury.


Subject(s)
Animals , Male , Rats , Reperfusion Injury/metabolism , Cerebral Cortex/chemistry , Brain Ischemia/drug therapy , Neuroprotective Agents/pharmacology , Dexmedetomidine/pharmacology , Glutamine/metabolism , Cerebral Cortex/ultrastructure , Brain Ischemia/metabolism , Rats, Wistar , gamma-Aminobutyric Acid/drug effects , gamma-Aminobutyric Acid/metabolism , Amino Acids/drug effects , Amino Acids/metabolism
2.
Gut and Liver ; : 607-614, 2015.
Article in English | WPRIM | ID: wpr-216110

ABSTRACT

BACKGROUND/AIMS: Proton pump inhibitors (PPIs) act by irreversibly binding to the H+-K+-ATPase of the proton pump in parietal cells and may possibly affect the vacuolar H+-ATPase in osteoclasts. METHODS: We investigated the effect of 8 weeks of PPI treatment on the parameters of bone turnover and compared PPI with revaprazan, which acts by reversibly binding to H+-K+-ATPase in proton pumps. This study was a parallel randomized controlled trial. For 8 weeks, either a PPI or revaprazan was randomly assigned to patients with gastric ulcers. The parameters of bone turnover were measured at the beginning of and after the 8-week treatment period. RESULTS: Twenty-six patients (PPI, n=13; revaprazan, n=13) completed the intention-to-treat analysis. After the 8-week treatment period, serum calcium and urine deoxypyridinoline (DPD) were increased in the PPI group (serum calcium, p=0.046; urine DPD, p=0.046) but not in the revaprazan group. According to multivariate linear regression analysis, age > or =60 years was an independent predictor for the changes in serum calcium and urine DPD. CONCLUSIONS: In elderly patients, administering a PPI for 8 weeks altered bone parameters. Our study suggested that PPIs might directly alter bone metabolism via the vacuolar H+-ATPase in osteoclasts.


Subject(s)
Aged , Female , Humans , Male , Middle Aged , Amino Acids/drug effects , Bone Remodeling/drug effects , Bone and Bones/metabolism , Calcium/blood , Intention to Treat Analysis , Linear Models , Multivariate Analysis , Osteoclasts/metabolism , Prospective Studies , Proton Pump Inhibitors/pharmacology , Pyrimidinones/pharmacology , Tetrahydroisoquinolines/pharmacology
3.
Arab Journal of Pharmaceutical Sciences. 2005; 2 (10): 41-56
in Arabic | IMEMR | ID: emr-69876

ABSTRACT

The effects of long-term administration of cholesterol on free amino acids in the heart of rats were investigated, using an automatic LKB Amino Acid Analyzer [Biochrom Ltd., Cambridge, England]. Feeding cholesterol intake 100 mglkg/day for 20 weeks significantly elevates the contents of aspartate from 135 +/- 014 to 187 +/- 008 [micro] mol/100 g wet tissues [P< 0.005], glutamine from 204 +/- 017 to 293 +/- 025 [micro] mol/100 g wet tissues [P< 0.01], ornithine from 7 +/- 001 to 114 +/- 008 [micro] mol /100 g wet tissues [P< 0.001], histidine from 44 +/- 005 to 79 +/- 008 [micro] mol/100 g wet tissues [P< 0.005] and arginine from 74 +/- 009 to 390 +/- 010 [micro] mol/100 g wet tissues [P< 0.001] in the heart. These increases are concomitant with slight increase in cardiac taurine from 1891 +/- 156 to 2064 +/- 136. However, this increase was insignificant [P > 0.05]. These alterations in the contents of the amino acids present in the heart were associated with a significant elevation in the plasma Gamma Glutamyl transferase [[gamma] GT] activity. It is suggested that mobilization of the protective amino acids in the cardiac tissue indicates that there are interaction mechanisms between cholesterol intake and these certain amino acids that are considered as factors for generating metabolic events, which may play a physiological function in the protection of myocardium muscle from the action of cholesterol. Thus, under pathological conditions, there is an imbalance between these interaction mechanisms which enhance risk for atherosclerosis and coronary heart disease


Subject(s)
Animals, Laboratory , Amino Acids/drug effects , Rats , Heart , Arginase , Histidine , Ornithine , Glutamine
4.
Alexandria Journal of Pharmaceutical Sciences. 1992; 6 (2): 189-192
in English | IMEMR | ID: emr-22861

ABSTRACT

The effect of lormetazepam and midazolam on norepinephrine, dopamine, gamma-amino-butyric acid [GABA], L-glutamic acid and their enzymes were investigated in both acute and chronic experiments. A significant decrease in the levels of norepinephrine and dopamine was observed in midazolam group in acute and chronic studies, while an insignificant change was observed with lormetazepam. Both drugs caused a significant increase in GABA and glutamic acid decarboxylase in L-glutamic acid and gamma-aminobutyric alpha ketoglutaric transaminase activity [GABA-T]


Subject(s)
Pharmacology , Amino Acids/drug effects
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