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: 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.

AimTo investigate the influence of tetramethylpyrazine(ligustrazine, Lig) on oxygen consumption and superoxide during the respiratory burst of human neutrophils. MethodsIt was observed by using ESR spin trapping, spin probe oxymetry and luminol-dependent chemiluminesence(CL) . Results Lig had no influence on oxygen consumption during the respiratory burst of neutrophils(P＞0.05), but had remarkable inhibition on CL response generated by neutrophils(P＜0.01), and had scavenging effect on O2 and OH ·generated by neutrophils, which were demonstrated in xanthine/ xanthine oxidase system and Fentons reaction(P＜0.01) . ConclusionLig has no inhibiting effect on oxygen metabolic function of neutrophils,but protects tissue from injury caused by activated neutrophils through scavenging oxygen radicals.

AIM To discuss the effects of losartan on AT 1R mRNA expression and renin angio tensin system (RAS) level in brain of spontaneously hypertensive rat (SHR). METHODS Sixteen 6 week old male SHR and 16 sex and age matched WKY were divided into losartan ( n =8) and control groups ( n =8) respectively. Losartan (30 mg?kg -1 ?d -1 ) or equal volume of 0.9% saline solution was administered for 18 weeks by gavage. AT 1R mRNA expression was examined by reverse transcription polymerase chain reaction (RT PCR). Renin activity (RA) and angiotensinⅡ(AngⅡ) levels were measured by radio immunoassay. Angiotensin converting enzyme activity (ACEA) was measured by ultraviolet spectrophotometar. RESULTS Enhanced brain AT 1R mRNA expression was found in SHR compared with WKY ( P 0.05, respectively). CONCLUSION The increase of AT 1R mRNA expression and RAS levels in brain may be involved in the pathogenesis of hypertension in SHR. Losartan protects brain by decreasing expression of brain AT 1R mRNA.

Objective To investigate the preventive effects of AT1 receptor antagonist Lorsartan on blood pressure and stroke in spentaneously hypertensive stroske prone rat (SHRsp). Methods Twenty six 6 week aged SHRsp were divided into Losartan 30 mg/kg/d group (n=8), Losartan 10 mg/kg/d group (n=9) and normal saline group (n=9), and 8 sex and age matched Wistar Kyoto(WKY ) as control group (n=8). SHRsp were subjected to 1 5% saline solution as intake and administered 30 mg/kg/d Losartan or 10 mg/kg/d Losartan or equal volume of 0 9% saline solution for 18 weeks by gavage, respectively. The systolic blood pressure was measured by tail cuff sphygmomanometry and clinical score of stroke and survival time of SHRsp were recorded. The coronal brain sections was examined by microscope and electron microscope after decapitation. Apoptosis was analyzed by TdT mediated dUTP biotin nick end labeling and image analysis system. Results Losartan 10mg/kg/d showed no affect on systolic blood pressure but it prevented the occurrence of stroke. The clinical scores of stroke in Losartan 30 mg/kg/d group (0 4?0 7) and Losartan 10 mg/kg/d group (0 7?1 1) were both more decreased than in normal saline group(3 5?0 6) ( P

Objective To evaluate the relationship between the concentration of nitric oxide (NO) and cytological change in cerebrospinal fluid ( CSF ) and the onset of neurocysticercosis in patients. . Methods. NO Level in CSF was detected in 30 cases of neurocysticercosis, 20 cases of tuberculous meningitis (TBM) and 20 healthy people as control by using Griess method. The cytological components in CSF were also examined.. Results and Conclusion . Griess method was proved to be a rapid and accurate technique for the detection of NO content in CSF. The NO concentration in cases of neurocysticercosis and TBM was significantly higher than that of control(P

Objective To evaluate the effect of calcitonic gene related peptide(CGRP) and endothelin(ET) on acute and delayed cerebral vasospasm(CVS) after subarachnoid hemorrhage(SAH).Methods The SAH model in rabbit were established by single injection of autologous arterial blood(0.5 ml/kg) to cisterna magna on percutaneous suboccpital route. Transcranial Dopper(TCD) was performed to detect the spastic of rabbit basilar artery(BA). The CGRP and ET concentrations in cerebrospinal fluid were examinated quntitatively by radioimmunologlc techniques at 30 minutes, 3 days, and 5 days after SAH.Results The results of TCD showed that rabbit basilar artery was spastic at 30 minutes, 3 days and 5 days after SAH. At 30 minutes after SAH, CGRP concentration significantly increased upto about 18 fold( P

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