2 research outputs found
ΠΡΡΠΈΠ½ΠΎΠ²ΡΠΉ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌ ΠΏΡΠΈ ΠΎΡΡΡΠΎΠΉ ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΈΡΠ΅ΠΌΠΈΠΈ
Objective: to study the specific features of purine metabolism in clinically significant acute cerebral ischemia. Subjects and materials. Three hundred and fifty patients with the acutest cerebral ischemic stroke were examined. The parameters of gas and electrolyte composition, acid-base balance, the levels of malonic dialdehyde, adenine, guanine, hypox-anthine, xanthine, and uric acid, and the activity of xanthine oxidase were determined in arterial and venous bloods and spinal fluid. Results. In ischemic stroke, hyperuricemia reflects the severity of cerebral metabolic disturbances, hemodynamic instability, hypercoagulation susceptiility, and the extent of neurological deficit. In ischemic stroke, hyperuri-corachia is accompanied by the higher spinal fluid levels of adenine, guanine, hypoxanthine, and xanthine and it is an indirect indicator of respiratory disorders of central genesis, systemic acidosis, hypercoagulation susceptibility, free radical oxidation activation, the intensity of a stressor response to cerebral ischemia, cerebral metabolic disturbances, the depth of reduced consciousness, and the severity of neurological deficit. Conclusion. The high venous blood activity of xanthine oxidase in ischemic stroke is associated with the better neurological parameters in all follow-up periods, the better early functional outcome, and lower mortality rates. Key words: hyperuricemia, stroke, xanthine oxidase, uric acid, cerebral ischemia.Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ . ΠΠ·ΡΡΠΈΡΡ ΠΎΡΠΎΠ±Π΅Π½Π½ΠΎΡΡΠΈ ΠΏΡΡΠΈΠ½ΠΎΠ²ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ° ΠΏΡΠΈ ΠΊΠ»ΠΈΠ½ΠΈΡΠ΅ΡΠΊΠΈ Π²ΡΡΠ°ΠΆΠ΅Π½Π½ΠΎΠΉ ΠΎΡΡΡΠΎΠΉ ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½ΠΎΠΉ ΠΈΡΠ΅ΠΌΠΈΠΈ. ΠΠ°ΡΠ΅ΡΠΈΠ°Π» ΠΈ ΠΌΠ΅ΡΠΎΠ΄Ρ. ΠΠ±ΡΠ»Π΅Π΄ΠΎΠ²Π°Π½Ρ 350 ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Π² ΠΎΡΡΡΠ΅ΠΉΡΠ΅ΠΌ ΠΏΠ΅ΡΠΈΠΎΠ΄Π΅ ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΠ½ΡΡΠ»ΡΡΠ°. Π Π°ΡΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ, Π²Π΅Π½ΠΎΠ·Π½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΈ Π»ΠΈΠΊΠ²ΠΎΡΠ΅ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΠΈ ΠΏΠΎΠΊΠ°Π·Π°ΡΠ΅Π»ΠΈ Π³Π°Π·ΠΎΠ²ΠΎΠ³ΠΎ, ΡΠ»Π΅ΠΊΡΡΠΎΠ»ΠΈΡΠ½ΠΎΠ³ΠΎ ΡΠΎΡΡΠ°Π²Π° ΠΈ ΠΊΠΈΡΠ»ΠΎΡΠ½ΠΎ-ΠΎΡΠ½ΠΎΠ²Π½ΠΎΠ³ΠΎ ΡΠ°Π²Π½ΠΎΠ²Π΅ΡΠΈΡ, ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΠ΅ ΠΌΠ°Π»ΠΎΠ½ΠΎΠ²ΠΎΠ³ΠΎ Π΄ΠΈΠ°Π»ΡΠ΄Π΅Π³ΠΈΠ΄Π°, Π°Π΄Π΅Π½ΠΈΠ½Π°, Π³ΡΠ°Π½ΠΈΠ½Π°, Π³ΠΈΠΏΠΎΠΊΡΠ°Π½ΡΠΈΠ½Π°, ΠΊΡΠ°Π½ΡΠΈΠ½Π° ΠΈ ΠΌΠΎΡΠ΅Π²ΠΎΠΉ ΠΊΠΈΡΠ»ΠΎΡΡ, Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΠΊΡΠ°Π½ΡΠΈΠ½ΠΎΠΊΡΠΈΠ΄Π°Π·Ρ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ. ΠΠΈΠΏΠ΅ΡΡΡΠΈΠΊΠ΅ΠΌΠΈΡ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΌ ΠΈΠ½ΡΡΠ»ΡΡΠ΅ ΠΎΡΡΠ°ΠΆΠ°Π΅Ρ ΡΡΠΆΠ΅ΡΡΡ ΡΠ°ΡΡΡΡΠΎΠΉΡΡΠ² ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ°, Π½Π΅ΡΡΠ°Π±ΠΈΠ»ΡΠ½ΠΎΡΡΠΈ Π³Π΅ΠΌΠΎΠ΄ΠΈΠ½Π°ΠΌΠΈΠΊΠΈ, ΡΠΊΠ»ΠΎΠ½Π½ΠΎΡΡΠΈ ΠΊ Π³ΠΈΠΏΠ΅ΡΠΊΠΎΠ°Π³ΡΠ»ΡΡΠΈΠΈ, Π³Π»ΡΠ±ΠΈΠ½Ρ Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΈΡΠΈΡΠ°. ΠΠΈΠΏΠ΅ΡΡΡΠΈΠΊΠΎΡΠ°Ρ
ΠΈΡ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΌ ΠΈΠ½ΡΡΠ»ΡΡΠ΅ ΡΠΎΠΏΡΠΎΠ²ΠΎΠΆΠ΄Π°Π΅ΡΡΡ ΠΏΠΎΠ²ΡΡΠ΅Π½ΠΈΠ΅ΠΌ ΡΠΎΠ΄Π΅ΡΠΆΠ°Π½ΠΈΡ Π² Π»ΠΈΠΊΠ²ΠΎΡΠ΅ Π°Π΄Π΅Π½ΠΈΠ½Π°, Π³ΡΠ°Π½ΠΈΠ½Π°, Π³ΠΈΠΏΠΎΠΊΡΠ°Π½ΡΠΈΠ½Π°, ΠΊΡΠ°Π½ΡΠΈΠ½Π°, ΡΠ²Π»ΡΠ΅ΡΡΡ ΠΊΠΎΡΠ²Π΅Π½Π½ΡΠΌ ΠΏΡΠΈΠ·Π½Π°ΠΊΠΎΠΌ Π΄ΡΡ
Π°ΡΠ΅Π»ΡΠ½ΡΡ
ΡΠ°ΡΡΡΡΠΎΠΉΡΡΠ² ΡΠ΅Π½ΡΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ Π³Π΅Π½Π΅Π·Π°, ΡΠΈΡΡΠ΅ΠΌΠ½ΠΎΠ³ΠΎ Π°ΡΠΈΠ΄ΠΎΠ·Π°, ΡΠΊΠ»ΠΎΠ½Π½ΠΎΡΡΠΈ ΠΊ Π³ΠΈΠΏΠ΅ΡΠΊΠΎΠ°Π³ΡΠ»ΡΡΠΈΠΈ, Π°ΠΊΡΠΈΠ²Π°ΡΠΈΠΈ ΡΠ²ΠΎΠ±ΠΎΠ΄Π½ΠΎΡΠ°Π΄ΠΈΠΊΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΡ, Π²ΡΡΠ°ΠΆΠ΅Π½Π½ΠΎΡΡΠΈ ΡΡΡΠ΅ΡΡΠΎΡΠ½ΠΎΠ³ΠΎ ΠΎΡΠ²Π΅ΡΠ° Π½Π° ΠΈΡΠ΅ΠΌΠΈΡ ΠΌΠΎΠ·Π³Π°, ΡΠ°ΡΡΡΡΠΎΠΉΡΡΠ² ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½ΠΎΠ³ΠΎ ΠΌΠ΅ΡΠ°Π±ΠΎΠ»ΠΈΠ·ΠΌΠ°, Π³Π»ΡΠ±ΠΈΠ½Ρ ΡΠ³Π½Π΅ΡΠ΅Π½ΠΈΡ ΡΠΎΠ·Π½Π°Π½ΠΈΡ ΠΈ ΡΡΠΆΠ΅ΡΡΠΈ Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ Π΄Π΅ΡΠΈΡΠΈΡΠ°. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅. ΠΡΡΠΎΠΊΠ°Ρ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡ ΠΊΡΠ°Π½ΡΠΈΠ½ΠΎΠΊΡΠΈΠ΄Π°Π·Ρ Π² Π²Π΅Π½ΠΎΠ·Π½ΠΎΠΉ ΠΊΡΠΎΠ²ΠΈ ΠΏΡΠΈ ΠΈΡΠ΅ΠΌΠΈΡΠ΅ΡΠΊΠΎΠΌ ΠΈΠ½ΡΡΠ»ΡΡΠ΅ Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π° Ρ Π»ΡΡΡΠΈΠΌΠΈ Π½Π΅Π²ΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΏΠ°ΡΠ°ΠΌΠ΅ΡΡΠ°ΠΌΠΈ Π²ΠΎ Π²ΡΠ΅ ΡΡΠΎΠΊΠΈ Π½Π°Π±Π»ΡΠ΄Π΅Π½ΠΈΡ, Π»ΡΡΡΠΈΠΌ ΡΠ°Π½Π½ΠΈΠΌ ΡΡΠ½ΠΊΡΠΈΠΎΠ½Π°Π»ΡΠ½ΡΠΌ ΠΈΡΡ
ΠΎΠ΄ΠΎΠΌ, ΠΌΠ΅Π½ΡΡΠ΅ΠΉ Π»Π΅ΡΠ°Π»ΡΠ½ΠΎΡΡΡΡ. ΠΠ»ΡΡΠ΅Π²ΡΠ΅ ΡΠ»ΠΎΠ²Π°: Π³ΠΈΠΏΠ΅ΡΡΡΠΈΠΊΠ΅ΠΌΠΈΡ, ΠΈΠ½ΡΡΠ»ΡΡ, ΠΊΡΠ°Π½ΡΠΈΠ½ΠΎΠΊΡΠΈΠ΄Π°Π·Π°, ΠΌΠΎΡΠ΅Π²Π°Ρ ΠΊΠΈΡΠ»ΠΎΡΠ°, ΡΠ΅ΡΠ΅Π±ΡΠ°Π»ΡΠ½Π°Ρ ΠΈΡΠ΅ΠΌΠΈΡ
Purine Metabolism in Acute Cerebral Ischemia
Objective: to study the specific features of purine metabolism in clinically significant acute cerebral ischemia. Subjects and materials. Three hundred and fifty patients with the acutest cerebral ischemic stroke were examined. The parameters of gas and electrolyte composition, acid-base balance, the levels of malonic dialdehyde, adenine, guanine, hypox-anthine, xanthine, and uric acid, and the activity of xanthine oxidase were determined in arterial and venous bloods and spinal fluid. Results. In ischemic stroke, hyperuricemia reflects the severity of cerebral metabolic disturbances, hemodynamic instability, hypercoagulation susceptiility, and the extent of neurological deficit. In ischemic stroke, hyperuri-corachia is accompanied by the higher spinal fluid levels of adenine, guanine, hypoxanthine, and xanthine and it is an indirect indicator of respiratory disorders of central genesis, systemic acidosis, hypercoagulation susceptibility, free radical oxidation activation, the intensity of a stressor response to cerebral ischemia, cerebral metabolic disturbances, the depth of reduced consciousness, and the severity of neurological deficit. Conclusion. The high venous blood activity of xanthine oxidase in ischemic stroke is associated with the better neurological parameters in all follow-up periods, the better early functional outcome, and lower mortality rates. Key words: hyperuricemia, stroke, xanthine oxidase, uric acid, cerebral ischemia