BACKGROUND: Sub-hypothermia has been widely used to treat cerebral infarction. Whether sub-hypothermia treated on body surface affects blood pressure or not, or the effect is advantageous or disadvantageous should be researched further.OBJECTIVE: To observe the effect of sub-hypothermia on blood pressure of rats with experimental cerebral infarction so as to investigate its influence on cerebral protective function.DESIGN: Randomized controlled study.SETTING: Neurological Department of Renmin Hospital of Wuhan University.MATERIALS: The experiment was completed in the Neurological Laboratory of Renmin Hospital of Wuhan University. Totally 120 SD rats were selected and divided randomly into control group and experimental group with 60 in each group.METHODS: Rats in experimental group were maintained at 4 ℃ 3 hours after MCA obstruction, and rectal temperature was maintained at (34±1.0) ℃;rats in control group were maintained at room temperature (20 ℃). All animals were reperfused 2 hours after MCA obstruction. Heart rate,breath, blood oxygen saturation, anus temperature and blood pressure were assayed with monitor. Rats were sacrificed under anesthesia after 24 hours, and cerebral tissue was taken out to measure the total volume of infarct focus.MAIN OUTCOME MEASURES: ① Changes of heart rate, breath,blood oxygen saturation, · mean arterial blood and blood pressure of rats in the two groups before and after treatment; ② volume of infarct focus of rats in the two groups.RESULTS: ① Values of blood pressure in both groups were increased after obstruction as compared with those before obstruction [(150±7.2),(129±5.7) mm Hg; (149±7.5), (130±2.2) mm Hg, P ＜ 0. 01], and there was not significant difference (P ＞ 0.05). Blood pressure was decreased obviously in sub-hypothermia group at the beginning of sub-hypothermia (P＜ 0.01). ② Volume of cerebral infarction was obviously smaller in subhypothermia group than that in control group [(153.17±26.83) mm3,(251.45±36.70) mm3, P ＜ 0.01].CONCLUSION: Sub-hypothermia can both reduce the volume of cerebral infarction and decrease the blood pressure obviously.

BACKGROUND: Mild hypothermia might in some degree affect the functions and metabolism of the vital organs, and its effects can be harmful sometimes but may also be favorable on some other occasions, which remained to be further studied.OBJECTIVE: To examine the effect of mild hypotherrnia on cardiac function of rats with experimental cerebral infarction by observing the changes in the cardiac energy reserve and electrocardiogram (ECG) manifestations,as well as the ultrastructural changes of the myocardium.DESIGN: Randomized controlled experiment.SETTING: Department of Neurology, Renmin Hospital of Wuhan University.MATERIALS: This experiment was carried out in the Laboratory of Department of Neurology, Renmin Hospital of Wuhan University. Totally 58SD rats were randomized into sham operation group (n=10), cerebral infarction with normal temperature group (normal temperature group, n=24),cerebral infarction with mild hypothermia treatment group (mild hypothermia group, n=24).METHODS: Middle cerebral artery occlusion (MCAO) was induced in normal temperature group and mild hypothermia group with a suture intro duced into the middle cerebral artery of the rats. The rats in- sham opera tion group were only subjected to skin incision and vessel ligation without suture insertion into the middle cerebral artery. The rats in mild hypother mia group were kept at 4 ℃ with their anal temperature maintained at (34±1.0) ℃, while the rats in sham operation group and normal tempera ture group w ere kept at room temperature (20 ℃). Twelve hours later, the levels of myocardial ATP, DTP, adenosine phosphate and energy reserve were determined, and the changes in myocardial ultrastructure were ob served under electron microscope. MAIN OUTCOME MEASURES: ① Changes of myocardial energy metabolism; ② Changes of cardiac electrophysiology; ③ Ultrastructural changes of the myocardium. RESULTS: All the 58 rats survived the operation and all enter the re sult analysis. The levels of myocardial ATP, DTP and energy reserve were significantly lowered in normal temperature group and mild hypothermia 12 hours after the ischemia in comparison with the sham operation group (P ＜ 0.01), but the level of ATP and energy reserve in mild hypothermia group was higher than those of normal temperature group (P ＜ 0.01). No significant difference was noted in ECG abnormality rate between normal temperature group and mild hypothermia group (P ＞ 0.05), but the heart rate was found obviously lower in mild hypothermia group [(290.92±44.18) vs (472.20±12.79) bpm, P ＜ 0.01], with 3 rats showing heart rate less than 150 bpm. Ultrastructural observation revealed the presence of my ocardial ischemic impairment in normal temperature group and mild hy pothermia group, but the impairment in mild hypothermia group was less severe. CONCLUSION: Heart rate can be markedly reduced during general mild hypothermia treatment for cerebral infarction to improve myocardial energy reserve and alleviate myocardial ischemia due to cerebral infarction without increasing the abnormality rate of ECG.

Objective To investigate the protective effect of mild hypothermia during cerebral ischemia and reperfusion. Methods After 3 hours of middle cerebral artery occlusion (MCAO) in rats, the myeloperoxi-dase (MPO) activity, the positive expression of intercellular adhesion molecule-1 (ICAM-1) , and the leukocyte integrin Mac-1 (CD11b/CD18) level in the ischemic regions were determined at different times (6 h,12 h,24 h, 48 h and 72 h) during and after 24 h of reperfusion. Cerebral infarction volume and neurological function were also evaluated in a control group, in addition to the above variables, at 24 hours of reperfusion. Results The MPO activity and the expression of ICAM-1 and Mac-1 were significantly elevated at 6 h after cerebral ischemia during reperfusion. These variables peaked at 48 h. There was a remarkable difference between the various groups and a sham-operated group ( P

Objective To evaluate the protective effect of mild hypothermia against inflammatory cascade reaction in rats during cerebral ischemia and reperfusion.Methods After middle cerebral artery occlusion(MCAO)for 3 h in rats,the expression levels of ICAM-1,TNF-? and IL-1 ? in the ischemic regions were determined at different reperfusion time (6 h,12 h,24 h,48 h and 72 h).At 24 h,the cerebral infarction volume and neurologic function were evaluated.In the control,these were assessed at 24 hours reperfusion.Results (1)Mild hypothermia could ameliorate neurological deficit score and decrease infarct volume induced by cerebral ischemia and reperfusion.(2)The expression of ICAM-1,TNF-? and IL-1? rose obviously at 6 h after cerebral ischemia-reperfusion,and peaked each at 48 h,24 h and 6 h.There was significant difference between the various groups and the sham-operative group(P

Objective To explore the effects of clinical psychological intervention on anxiety and depression in hemodialysis patients .Methods Hemodialysis patients were randomly divided into two groups:psychological inter-vention group and control group ,25 patients in each group .In intervention group ,besides routine clinical treatment and nursing measures ,we analyzed the clinical information of the patients ,consulted the relevant documents ,combined the evidence and clinical experience ,and finally conducted the psychological intervention .Self-Rating Anxiety Scale and Self-Rating Depression Scale of these patients were analyzed .Results Before the intervention , the SAS and SDS scores of intervention group and control group were (57.3 ±1.5) versus (56.9 ±1.6) and (55.3 ±2.3) versus (56.1 ±3.5),respectively.The t values were 0.912(P>0.05) and 0.955(P>0.05),respectively.After interven-tion,the score before and after the trial between these two groups were significantly different (P<0.05).The SAS and SDS scores of intervention group and control group were (16.4 ±0.9) versus (10.1 ±1.3) and (14.3 ±2.1) ver-sus (9.7 ±1.5),respectively.Conclusion Clinical psychological intervention can effectively relieve anxiety and depression in hemodialysis patients .

Objective To compare the internal fixation methods for treatment of intertrochanteric fractures in elderly patients.Methods One hundred and sixty four elderly patients with intertrochanteric fractures were treated from June 2006 to September 2011.The fractures were fixed with dynamic hip screws (DHS,n =42),locking proximal femur plate (LPFP,n =40),Gamma nails (n =36) or proximal femoral nail anti-rotation (PFNA,n =46),respectively.The clinical data were collected and the operative time,blood loss,time of clinical healing,postoperative complications and Harris hip scores of 6 months after surgery were compared among groups.Results All patients were followed-up for 6 to 36 months.The operative times of DHS,LPFP,Gamma nails and PFNA groups were (103 ± 15),(90 ± 13),(79 ± 11)and (65 ±9)min,respectively(F =2.87,P ＜0.05).The blood loss of 4 groups was (202 ±23),(181 ±23),(98 ± 13) and (87 ± 11) ml,respectively (F =3.21,P ＜ 0.05).The times of clinical fracture healing were (16.1±1.9),(14.6±1.8),(12.9±1.7) and (11.5±1.4) weeks,respectively(F=2.66,P＜0.05).The postoperative complications of 4 groups were 4/42,3/40,2/36 and 1/46,respectively (x2 =5.67,P ＜0.05).The Harris hip scores of 6 months after surgery of 4 groups were 81％ (34/42),85％ (34/40),89％ (32/36)and 93％ (43/46),respectively(H =20.03,P ＜0.05).Conclusions In treatment for intertrochanteric fractures in elderly patients,the efficacy of intramedullary fixation (Gamma nails and PFNA) is better than extramedullary fixation DHS and LPFP).PFNA is more effective than other 3 methods and should be preferentially chosen.

Objective To investigate the changes of blood pressure in rats with experimental brain infarction caused by use of mild hypothermia. Methods One hundred and twenty Sprague Dawley rats were used and divided randomly and equally into a control group and an experiment group. In all of the rats, the middle cerebral artery occlusion (MCAO) was made to cause the experimental brain infarction, and reperfused 2 hours later. Three hours after MCAO, the rats in the experiment group were placed in the 4℃ with the rectal temperature controlled at 34? 1.0℃ , while those in the control group in the room temperature. The heart rate, breath, blood pressure, oxygen saturation and rectal temperature were monitored. The rats were sacrificed 24 hours after MCAO and the infarction volume were observed. Results After MCAO, the blood pressure was significantly increased as compared with that prior to MCAO ( P 0.05) . Hypothermia significantly reduced the blood pressure after being used for more than 3 hours ( P

Objective To investigate the effects of systemic mild hypothermia on heart. Methods Fifty-eight Wistar rats were divided randomly into three groups: control group (n=10), normal thermic group (n=24) and mild hypothermic group (n=24). After the model of middle cerebral artery occlusion (MCAO) was made, electrocardiograph (ECG) was used to monitor the cardiac function of the animals. The changes of myocardial high-energy phosphates (ATP,ADP,AMP) and energy charge (EC) were evaluated after 12 hours of ischemia, and the myocardial ultrastructure observed. Results Compared with the control group, the ATP, ADP and EC in the normal thermic group and mild hypothermic group were lower after 12 hours of ischemia (P

Objective To investigate correlation between post-stroke depression (PSD) and multiple factors during onset of acute cerebral infarction. Methods Depression was measured with Hamilton Depression Rating Scales (HAMD) in 58 patients with acute cerebral infarction, and their neurological function were evaluated by neurological function defect (NFD) score. Their immunoglobulin G (IgG) index was calculated and level of nitric oxide (NO) in cerebrospinal fluid (CSF) was measured. Lesion and nature of cerebral infarction in 58 patients with acute stroke were located by CT. All the data were statistically analyzed with student-t test and ? 2 test, as well as linear regression model. Results Seventeen of 58 patients of stroke appeared PSD with an occurrence rate of 29.3%. Occurrence rate of PSD was significantly higher in patients with cerebral infarction than in those with cerebral hemorrhage  2=4.86, P

BACKGROUND: With the deep investigations of pathophysiological mechanism of acute cerebral infarction, it is discovered that inflammation occupies an important stance in the ischemic injuries of central nervous system ( CNS ), in which tumor necrosis factor-αt (TNF-α), interleukin- 1β(IL-1β), and soluble intercellular adhesion molecule(sICAM-1) become hotspots in the researches.OBJECTIVE: To investigate the relationship between the levels of serous inflammatory cell factors and the course of the disease, the severity of the situation in patients with ischemic stroke.DESIGN: A case-control study based on patients and healthy individuals.SETTING: Department of neurology in a university hospital.PARTICIPANTS: Fifty ischemic stroke patients including 23 males and 27 females with an average age of(60.26 ± 8.77) years old were selected from the outpatient and inpatient Departments of Neurology of the Renmin Hospital of Wuhan University between January 2001 and December 2003. Forty healthy controls including 18 males and 22 females with an average age of (61.05 ± 8.09) years old were selected from the subjects who had physical check up at outpatient department during corresponding period.INTERVENTIONS: Serous TNF-α, IL-1 β and sICAM-1 levels were detected by double-antibody-ELISA.MAIN OUTCOME MEASURES: Serous levels of TNF-α, IL-1β and sICAM-1 in patients with ischemic stroke of different stage, with different infarction volume and different neural functional defects.RESULTS: Serous TNF-α, IL-1β and sICAM-1 levels of patients with cerebral infarction during acute phase and convalescence were significant higher than that of control group( P ＜ 0.01 ), and the levels was significantly higher in acute phase than convalescence ( P ＜ 0.05 ) . The elevation was closely correlated with the degree of neural functional defect and the size of infarction volume, and furthermore, the serous content of TNF-α was also correlated with IL-1β and sICAM-1 levels.CONCLUSION: TNF-α, IL-1β and sICAM-1 interact and participate in the inflammation and reperfusion injury of acute cerebral infarction. Surveillance on them can provide experimental indicators for early clinical therapy and rehabilitative intervention, which is good for the control of the development and recurrence of stroke.