Objective To study the safety and efficacy of intensive reduction of blood pressure for the treatment of acute cerebral haemorrhage. Method A randomized control trial in 41 consecutive patients with intracerebral haemorrhage admitted from October 2006 to January 2007 were randomly assigned to intensive blood pressure reduction group ( n = 24) or guidelines blood pressure reduction group ( n = 17) (tho guidelines set by American Association of cardiologists). In the intensive reduction group, the systolic pressure was reduced immediately to lower than 140 mmHg, while the blood pressure was reduced to that just below 180 mmHg in guideline reduction group. The size of the haematoma was measured 24 h after treatment by CT scans and the patients were followed up for 90 days. Death and/or disability in 90 days, and the short-term and long-term neurological function and the size of haematoma in 24 hours of two groups were compared. The outcomes were statistically analyzed with SPSS version 10.0 software. Measurement data were analyzed with t -test while numeration data were analyzed with chisquare test. Results There were no significant differences either in death and/or disability or in short-term and long-term neurological function in 90 days after treatment ( P ＞ 0.05). The mean values of proportional enlargement of haematoma were 16.8% in the intensive group and 36. 1% in the guidelines group 24 hours after treatment ( P = 0.012). The mean values of absolute enlargement of haematoma of two groups were 2.7 mL and 5. 1 mL,respectively (P = 0.058). There was significant difference in rate of enlargement of haematoma in the early stage of acute cerebral haemorrhage (4.2% vs. 47. 1%, P = 0.012). Conclusions Although intensive reduction of blood pressure in patients with acute cerebral haemorrhage did not alter the clinical prognosis of patients, it could apparently attenuate the enlargement of haematoma in the early stage of acute cerebral haemorrhage.

Objective To observe the dynamic changes of the numbers of CD34 positive microvessel and RCA-1 positive cell and neutrophil in perihematoma tissue after intracerebral hemorrhage (ICH) in rats at different time points and the impact of thrombin-specific inhibitor hirudin on the above different indicators and to investigate the protective mechanisms of hirudin for brain injury following ICH. Methods An experimental model was made with autologous whole blood injecting into the rat brain basal ganglia by using the stereotactic method. The rats were randomly assigned to sham operation, ICH, hirudin intervention, and normal saline groups.CD34 and RCA-1 immunobistochemistry stainings and conventional HE staining were used to observe CD34-positive microvessel, RCA-1 positive cell and neutrophil.Results The numbers of CD34-positive microvessel began to decrease at 12 hours after ICH, it decreased to the lowest at 72 hours, and it gradually returned to normal levels at day 7. The RCA-1 positive cells could be observed at 6 hours after ICH. It reached the peak at 48 hours. A small amount could persist for two weeks. Neutrophil could be observed at 12 hours after ICH. It reached the peak at 48 hours and disappeared at week 2. The administration of hirudin significantly reduced the numbers of RCA-1 positive cell and neutrophil in the early stage of ICH (5 min). At the same time, it significantly inhibited the decreased numbers of CD34-positive microvessel (all P ＜0. 01). The administration of hirudin during the edema formation also significantly reduced the numbers of RCA-1 positive cell and neutrophil (all P＜ 0.05), however, it could not significantly increase the numbers of CD34-positive microvessel. Conclusions Thrombinmediated inflammatory response has involved in the process of brain injury after ICH, and early administration of hirudin may significantly relieve perihematoma tissue injury.

Objective To evaluate the efficacy and safety of intra-arterial thrombolysis with urokinase and intravenous thrombolysis with recombinant tissue plasminogen activator (rtPA) for acute ischemic stroke. Methods A total of 43 patients with acute ischemic stroke within 6 hours of onset were included, 31 of them underwent superselective intra-arterial thrombolysis in the intra-arterial thrombolysis group and 12 of them underwent intravenous thrombolysis with rtPA in the intravenous thrombolysis group. Vascular recanalization was observed in the intra-arterial thrombolysis group, and the modified Rankin scale (mRS) scores at day 90 were used to evaluate the outcomes in both groups. Results Eighteen patients (58.1%) had complete recanalization and 7 (22.6%) had partial recanalization in the intra-arterial thrombolysis group. The recanalization rate was 80.6%, 3 complicated symptomatic intracranial hemorrhage, and 1 died. There vere no significant differences between the good outcome rate (74.2% vs. 66.7%, x2 =0.24, P=0.622) and the incidence of symptomatic intracranial hemorrhage at 90 d (9. 68% vs. 8. 33%, x2 =0. 19, P =0. 892). Conclusions Urokinase intra arterial thrombolysis within the time window can significantly improve the recanalization rate of the occluded vessels and improve the clinical symptoms of the patents in acute phase and long term outcomes. Their short-term efficacy and long-term outcomes are almost the same with intrave nous thrombolysis with rtPA.

Objective:To explore the relationship between plasma endothelin and migraine attack. Methods:The plasma endthelin(ET-1) levels were measured by radioimmunoassay in 54 patients with migraine ( classic: 18, common:36 ) and 20 patientsvith tension headache. Results:The plasma ET-1 level in patients with migraine attack was higher than that of normal con-trols or patients with tension headache (P ＜0.01). During intermission, the ET-1 level of patients with classic migraine washigher than that of patients with common migraine (P ＜0.01),and the ET-1 level in male patients was higher than in fe-male ones. Conclusion: The data suggest that there are abnormalities of vascular endothelial cell system in patients with mi-graine. ET-1 may be one of factors causing migraine attack.

Elevated blood pressure in acute cerebral hemorrhage is very common and is associated with the poor clinical outcomes.Due to the acute elevated blood pressure has impact on hematoma volume,cerebral perfusion pressure and perihematomal edema,etc.,whether aggressively control blood pressure in acute phase still remains controversial.This article reviews the theoretical basis of acute blood pressure management,the relevant clinical trials,and the current problems in spontaneous intracerebral hemorrhage.

The relationship between carotid artery stenosis and cognitive function are receiving increasing attention.Most studies have shown that carotid artery stenosis has a direct impact on cognitive impairment.Carotid endarterectomy or stenting can improve the cognitive function to varying degrees in patients with carotid artery stenosis.The mechanism of cognitive impairment in patients with carotid artery disease may be associated with hypoperfusion,white matter lesions,multiple lacunar infarction and spontaneous emboli.

Objective To ecaluatc the diagnostic value of digital subtraction angiography (DSA) and carotid artery ultrasound for transient ischemia attack (TIA). Methods Among the 74 patients with TIA, 45 had internal carotid artery (ICA)-TIA and 29 had vertebrobasilar artery (VBA)-TIA. DSA examination was performed in order to detect intracranial and extracranial arterial stenosis in the above two systems. Cervical artery ultrasound examination was used to understand the distribution of arterial plaques. Results DSA shoved that the detection rate of vascular stenosis in patients with ICA-TIA was 84. 4% (n = 38),and the patients with serious, moderate and slight stenoses were 31.1% (n = 14), 26. 7% (n = 12) and 11.1% (n =5), respectively. Of those, intracranial arterial stenosis was 44.4% (n =20), and it was significantly higher than 22.2%(n = 10) in extracranial arterial stenosis (P ＜0. 001 ); the detection rate of vascular stenosis in patients with VBA-TIA was 65.5% (n = 19), and the patients with serious, moderate and slight stcnoscs were 17. 2% (n = 5), 27. 5% (n = 8), and 20. 7% (n = 6), respcctivegly. Of those, cxtracranial arterial stenosis was 44.8% (n = 13), and it was significantly higher than 13.8% (n = 4) in intracranial stenosis (P ＜ 0. 001 ). Carotid artery ultrasound shoved that the detection rate of ICA plaque was 44.4% (n = 20), and it was higher than 24, 1% (n =7) in patients with VBA-TIA; the detection rate of the plaques in the initial segment of subclavian artery in patients with VBA-TIA was 44. 8% (n = 13), and it was significantly higher than 13.3% (n = 6) in patients with ICA-TIA (P ＜ 0.001 ). Conclusions There were differences between the intracranial and extracranial vascular lesions and the distribution of atherosclerotic plaques in patients with ICA-TIA and VBA-TIA. 1he former was more common in intracranial lesions, and the latter was more common in extracranial lesions.

Method for measuring interleukin 1 ( IL -1 ) and effects of total glucosides of paeony(TGP) on IL -1 production were studied. The results showed that the best concentration for LPS -induced IL-1 production of M s in rats was 8mg/L, the best dilution for IL-1 of LPS-induced M s production was 1 : 90. TGP ( 0 .5 - 12 .5mg/L ) enhanced LPS-induced IL -1 production in a concentration dependent manner, but diminished in the higher concentration of TGP ( 62 .5~l25mg/L ) , the concentration-effect curve seems to be bell-shaped. The data suggested that TGP had two-sided regulatory effects on LPS -induced IL production of M s in rats.

Objective To investigate the chemical constituents in the vines of Piper hancei for obtaining a more comprehensive understanding on its effective components. Methods Compounds were separated by column chromatography with silica gel and polyamide, and their structures were elucidated by spectral analysis and chemical evidence (IR, UV, MS, (~1H-NMR), (~(13)C-NMR)). Results Nine compounds were isolated from the chloroform extract fraction. Their structures were identified as: futoamide (Ⅰ), trichostachine (Ⅱ), retrofractamide A (Ⅲ), pipercide (Ⅳ), guineensine (Ⅴ), piperine (Ⅵ), piperettine (Ⅶ), piperovatine (Ⅷ), and (2E, 4E)-N-isobutyl-7-(3, 4-methylenedioxyphenyl)-hepta-2, 4-dienamide (Ⅸ). (Conclusion )Compounds Ⅱ-Ⅳ and Ⅶ-Ⅸ are isolated from the plant for the first time.