Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test. | Szatmári et al. Critical Care 2010 14 R50 http content 14 2 R50 c CRITICAL CARE RESEARCH Open Access Impaired cerebrovascular reactivity in sepsis-associated encephalopathy studied by acetazolamide test Szilard Szatmári1 Tamás Végh 1 Ákos Csomós2 Judit Hallay1 István Takács3 Csilla Molnár1 and Béla Fulesdi 1 Abstract Introduction The pathophysiology of sepsis-associated encephalopathy SAE is not entirely clear. One of the possible underlying mechanisms is the alteration of the cerebral microvascular function induced by the systemic inflammation. The aim of the present work was to test whether cerebral vasomotor-reactivity is impaired in patients with SAE. Methods Patients fulfilling the criteria of clinical sepsis and showing disturbance of consciousness of any severity were included n 14 . Non-septic persons whithout previous diseases affecting cerebral vasoreactivity served as controls n 20 . Transcranial Doppler blood flow velocities were measured at rest and at 5 10 15 and 20 minutes after intravenous administration of 15 mg kgBW acetazolamide. The time course of the acetazolamide effect on cerebral blood flow velocity cerebrovascular reactivity CVR and the maximal vasodilatory effect of acetazolemide cerebrovascular reserve capacity CRC were compared among the groups. Results Absolute blood flow velocities after adminsitration of the vasodilator drug were higher among control subjects than in SAE. Assessment of the time-course of the vasomotor reaction showed that patients with SAE reacted slower to the vasodilatory stimulus than control persons. When assessing the maximal vasodilatory ability of the cerebral arterioles to acetazolamide during vasomotor testing we found that patients with SAE reacted to a lesser extent to the drug than did control subjects CRC controls CRC SAE 31 5 P . Conclusions We conclude that cerebrovascular reactivity is impaired in patients with SAE. The clinical significance of this pathophysiological .
