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.

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

BACKGROUND: After local injection of Botulinum toxin type-A (BoTX-A), not only the function of the neuromuscular conjunction was affected, but also the changes occurred remote from the injected site. F-waves result from the back fire of the motoneuron activation, which may indirectly reflect the functional state of the motoneurons.OBJECTIVE: To evaluate the remote effect of local BoTX-A injection by F-wave test.DESIGN: Self-control study based on patients with movement disorders.SETTING: Neruologic clinic in a university hospital.PARTICIPANTS: Twenty-six patients with movement disorders not received previous local BoTX-A were selected from Neurological Clinic in Renmin Hospital of Wuhan University between September 2002 and July 2003, including 19 cases with hemificiospasm, 5 Meige syndrome and 2 torticollis spasmodicus.INTERVENTIONS: F- and M-waves of ulnar and tibial nerves were recorded before 1, 12 - 24 weeks after local injection of BoTX-A in 26 patients.MAIN OUTCOME MEASURES: The following parameters were analyzed:latency(ML) and amplitude (Mamp) of M-wave, minimal (Fmin) and average latency (Fave), amplitude of negative peak(Famp), duration (Fdur), persistence (Fpcr) and chronodispersion (Fchr) of F-wave.RESULTS: No definite F-response of ulnar nerve stimulation was obtained 1 week after injection in 3 HFS patients (5 nerves) . Fave prolonged significantly on ulnar and tibal nerve and Fdur increased significantly on ulnar nerve 1 week after injection, but there was no significant difference 12 - 24 weeks later, compared with before injection. No significant correlation of the altered F-wave parameters was found with the dosage of BoTX-A.CONCLUSION: Fdur and Fave could sensitively assess the remote effect,which correlates with distance away from the injected muscle, rather than the dosage of BoTX-A.

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.

BACKGROUND: Hypertension is one of the most important risk factors for stroke, and brain focal renin-angiotensin system has been proved to play a vital role in the development of hypertension and stroke.OBJECTIVE: To observe the influence of long-term administration of losartan, an angiotensin-1 receptor antagonist, on the incidence of strokeprone spontaneous hypertension in rats.DESIGN: Randomized controlled experiment.SETTING: Renmin Hospital Affiliated to Wuhan University.MATERIALS: This experiment was carried out in Wuhan University between July 1999 and March 2001. Totally 26 six-week-old male rats with stroke-prone spontaneous hypertension and 8 Kyoto male Wistar rats were recruited in this experiment with the body mass of 144.5-182.1 g.METHODS: Totally 26 six-week-old male rats with spontaneous hypertension were randomized into stroke-Rrone spontaneous hypertension group (n=9) which received gastric perfusion of physiological saline at a dosage of 5 mL/d; losartan 10 mg/(kg·d) group of 9 rats which received gastric perfusion of losartan at a dosage of 10 mg/(kg ·d) and losartan 30 mg/(kg ·d)group of 8 rats which received gastric perfusion of losartan at a dosage of 30 mg/(kg·d). Rats in the three groups were provided with high-protein feed when entering the group, and drank 15 g/L salty water (5 mL/d) from the onset of week 2. At the same time, 8 six-week-old male Wistar rats were taken as normal controls to receive gastric perfusion of physiological saline at a dosage of 5 mL/d once a day; they took ordinary feed and drank running water. All rats lived with 12 hours' day-night alternation at room temperature of 18-20 ℃ and with humidity of 40%-50%. Totally 18weeks later, the incidence of stroke and BP changes were observed. The clinical manifestation of stroke was scored 1 if rats appeared few activities,with movements slightly reduced or excited; 2 score referred to very few activities, with movements obviously reduced or violently stimulated; 3score referred to inability to walk, lying motionless with melancholy symptoms; score 4 referred to paralysis and inability to stand, lateral or bilateral limb paralysis. Transmission electron microscope was used for histological observation of cell apoptosis in the brain.MAIN OUTCOME MEASURES: ① Observation of brain structure at week 18 when rats were decapitated. ② Results of nerve cell apoptosis detected with TUNEL technique. ③ Rat body mass, BP, as well as the incidence and changes of stroke were recorded.RESULTS: Totally 34 rats entered the result analysis. ① The incidence of stroke in the three groups: It was 100%, 22%, and 13%, respectively, in stroke-prone spontaneous hypertension group, losartan 10 mg/(kg·d) group,and losartan 30 mg/(kg·d) group. ② Score for stroke: The score was remarkably higher in stroke-prone spontaneous hypertension group than in losartan 10 mg/(kg·d) group and losartan 30 mg/(kg·d) group [(3.50±0.55,0.67±1.12, 0.38±0.74) minutes]. ③ Electron-microscopic observation: In stroke-prone spontaneous hypertension group, electron density was found increased in necrotic neurons; moreover, some nuclear membrane lost double-layer structure with ridges broken, even reduced or disappeared, displaying vacuolated changes. In losartan 30 mg/(kg·d) group and losartan 10 mg/(kg·d) group, most of neurons displayed basically normal morphology, with neuron chromatin evenly distributed and nuclear envelops regular, but there were still some neurons that had dense chromatin, with ridges broken and reduced. ④ Nerve cell apoptosis in the three groups: It was found obviously lower in normal group than in losartan 30 mg/(kg ·d)group, losartan 10 mg/(kg·d) group, and stroke-prone spontaneous hypertension group [(2.5±0.8, 13.9±4.3, 14.0±4.4, 52.0±16.7)%, P ＜ 0.05]. ⑤ BP changes: At week 18, BP was obviously lower in normal group than in losartan 30 mg/(kg·d) group, losartan 10 mg/(kg·d) group and strokeprone spontaneous hypertension group [(120.1±7.9, 169.4±10.1,216.7±8.3,225.5±6.8) mmHg (1 mm Hg=0.133 kPa), P ＜ 0.05]. ⑥ Changes of body mass: At week 18, body mass was obviously higher in normal group than in losartan 30 mg/(kg·d) group, losartan 10 mg/(kg·d) group, and stroke-prone spontaneous hypertension group [(313.3 ±10.1, 270.8 ± 10.4,258.7±12.7, 231.0±6.5) g, P ＜ 0.05].CONCLUSION: Losartan can obviously reduce the incidence of stroke and nerve cell apoptosis in rats with spontaneous hypertension, suggesting that losartan as an angiotensin-1 receptor antagonist may prevent and delay the onset of stroke through antagonizing angiotensin I receptor, thus exerting brain-protecting function.

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 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 evaluate the remote effect of local injection of botulinum toxin by use of the F-wave measures. Methods The F-wave responses as well as M-waves were recorded before injection, and at 1 week,12 to 24 weeks after local injection of botulinum toxin type-A (BTX-A) in 26 patients, including 19 with hemi-facial spasm (HFS),5 Meige syndrome and 2 torticollis spasmodicus (TS).The following parameters were analyzed: M-wave latency (ML) and amplitude (Mamp), F-wave minimal latency(Fmin) and average latency(Fave),amplitude (Famp), duration (Fdur), persistence (Fper) and chronodispersion (Fchr). The above parameters were obtained through the electric stimulation of ulnar and tibial nerves, and recorded from the abductor digiti minimi and extensor digitorum brevis, respectively. Results No definite F-wave was obtained by electric stimulation of ulnar nerve at 1 week after injection in 3 HFS patients (5 nerves). The Fave recorded from electric stimulation of ulnar and tibial nerves prolonged significantlyand Fdur from ulnar nerve increased significantly at 1 week after injection, but were not significantly different from those of pre-injection when recorded at 12 to 24 weeks after injection. No significant correlation of the altered F-wave parameters was found with the dosage of BTX-A. Conclusion Fdur and Fave could sensitively assess the remote effect of the local injection of BTX-A, the remote effect might be correlated with the distance between injected muscle and tested muscle, rather than the dosage of BTX-A.

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 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