硝普钠对大鼠局脑缺血/再灌注后神经型一氧化氮合酶的影响

Objective To investigate the effect of sodium nitroprusside (SNP) on hippocampal neuronal nitricoxide synthase (nNOS)expression after focal cerebral ischemia-reperfusion in rats and the mechanism of neuroprotective effect of SNP. Method 108 male SD rats weighting 250 g-300 g were randomly divided into 3 groups (n=36). Focal ischemia-reperfusion was established by occlusion of middle cerebral artery (MCA ).Control group (C): in which sham operation was performed; Ischemia-reperfusion group (I): after sodium chloride(5 μl) was injected into the lateral cerebral ventricle using microsyringe, MCA was occluded for 2 h; SNP group (S): SNP (0.055 mg/kg, 5μl ) was injected into the lateral cerebral ventricle using microsyringe, then MCA was occluded for 2 h. The experimental groups were further divided into 3 subgroups(n=12) according to the reperfusion time: 2 h, 6 h and 12 h. Neurological function score were tested before reperfusion; Pathological changes were observed by HE staining; The hippocampal tissue were obtained for detection of nNOS protein expression by immuno-histochemistry technique and nNOS mRNA expression by RT-PCR technique. Results Neuronal mortality in every subgroup of group I and S increased significantly compared with that in group C(P<0.05); Compared with that in 2 h(43.8 ± 2.1),6h (73.9±4.7) subgroup of group I, neuronal mortality in 2 h (36.5 ±1.2), 6h (42.6 ± 1.9) subgroup of group S decreased significantly (P<0.05); There were more nNOS mRNA expression in every subgroup of group I and S compared with that in group C (P<0.05),nNOS mRNA expression in 2 h (0.428 3 ± 0.000 4), 6 h (0.482 7 ± 0.005 2 )subgroup of group S decreased compared with that in 2 h (0.472 1 ±0.011 5), 6h(0.744 2±0.011 6)subgroup of group I(P<0.05); The expression of nNOS protein in other subgroup of group I and S increased except that in 6 h subgroup of group S(P<0.05); Compared with that in 2 h(0.265 8 ± 0.000 5), 6 h(0.284 0 ± 0.013 4) subgroup of group I, the expression of nNOS protein in 2 h (0.251 4 ±0.001 1), 6h (0.258 9 ±0.004 0) subgroup of group S decreased (P<0.05). Conclusion SNP coμld attenuate the focal cerebral ischemia/reperfusion injury and the possible mechanism may be related to the inhibition of nNOS expvession.     

克罗卡林预处理对脑缺血/再灌注大鼠水通道蛋白4表达及血脑屏障通透性的影响

Objective To investigate the effects of ATP-sensitive potassium channel openers (Cromakalim) on the expression of aquaporin-4 and permeability of blood-brain barrer (BBB) after cerebral ischemic/repeffusion. Methods Thirty healthy male Wistar rats were randomized into three groups for different conditioning, the sham-operated group(A,n=10), the cerebral I/R group(B,n=10),and the cerebral I/R+Cromakalim group (C,n=10). Intraluminal suture methods were applied to establish the middle cerebral artery occlusion(MCAO) model with occlusion 2 h and reperfusion 24 h. The neurobehavioral function was evaluated with Bederson's test, and the pathological changes were observed with hematoxylin-eosin(HE) staining. The water content of brain was evaluated by wet-dry weight method, and the expressions of IgG and AQP-4 in brain were observed by immunohistochemistry staining. Results In comparison with group A's water content(78.2±1.3 )% and expressions of IgG and AQP-4 (0.0±0.0,13.6±1.5) ,the expressions of IgG and AQP-4(2.4±0.4,19.8±1.9) and the water content (81.3±1.2)% in group B both were significantly higher (P<0.05). However,in group C,the water content (79.5±0.6)%was similar to group A( 78.2± 1.3 )%. Interestingly, the expressions of IgG and AQP-4( 1.1 ±0.2, 15.7± 1.2 ) of group C were higher than that of group A' s (P<0.05); compared with group B, The neurobehavioral deficit scores were obviously reduced, the expressions of IgG and AQP-4 (1.1 ±0.2,15.7±1.2) and the water content (79.5 ±0.6)% were significantly lower in group C (P<0.05).Conclusion Cromakalim maybe can alleviate cerebral edema via reducing permeability of blood-brain barrier and inhibit the expression of AQP-4 in cerebral ischemia/reperfusion mice.     

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1

To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (H0-1), a cytoprotective defense against oxidative injury. Methods: After being anesthetized with chloralhy-drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO- 1 was injected intraperitoneally at 40 μmol.kg-1·day-1 for two con-secutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin Ⅸ, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO2) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-his-tochemical technique and for light microscopic examination. Results: The PaO2 was significantly lower in all the experimental groups compared with sham group (90 mm Hg ±11 mm Hg). However, the values ofPaO2 in IPO (81 mm Hg ±7 mm Hg) and HM+I/R (80 mm Hg±9 mm Hg) were higher than that in I/R (63 mm Hg±9 mm Hg) and ZnPPIX+IPO (65 mm Hg±8 mm Hg) groups (P<0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P<0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P<0.05, P<0.01). The lung wet/ dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P<0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P<0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX. Condusion: Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.     

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1

To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (H0-1), a cytoprotective defense against oxidative injury. Methods: After being anesthetized with chloralhy-drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO- 1 was injected intraperitoneally at 40 μmol.kg-1·day-1 for two con-secutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin Ⅸ, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO2) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-his-tochemical technique and for light microscopic examination. Results: The PaO2 was significantly lower in all the experimental groups compared with sham group (90 mm Hg ±11 mm Hg). However, the values ofPaO2 in IPO (81 mm Hg ±7 mm Hg) and HM+I/R (80 mm Hg±9 mm Hg) were higher than that in I/R (63 mm Hg±9 mm Hg) and ZnPPIX+IPO (65 mm Hg±8 mm Hg) groups (P<0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P<0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P<0.05, P<0.01). The lung wet/ dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P<0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P<0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX. Condusion: Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.     

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1

To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (H0-1), a cytoprotective defense against oxidative injury. Methods: After being anesthetized with chloralhy-drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO- 1 was injected intraperitoneally at 40 μmol.kg-1·day-1 for two con-secutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin Ⅸ, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO2) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-his-tochemical technique and for light microscopic examination. Results: The PaO2 was significantly lower in all the experimental groups compared with sham group (90 mm Hg ±11 mm Hg). However, the values ofPaO2 in IPO (81 mm Hg ±7 mm Hg) and HM+I/R (80 mm Hg±9 mm Hg) were higher than that in I/R (63 mm Hg±9 mm Hg) and ZnPPIX+IPO (65 mm Hg±8 mm Hg) groups (P<0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P<0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P<0.05, P<0.01). The lung wet/ dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P<0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P<0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX. Condusion: Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.     

艾芬地尔预先给药对脑缺血再灌注损伤大鼠缺血半暗带区iNOS和细胞凋亡的影响

Objective To explore the possible mechanism for the neuroprotective effect of ifenprodil by investigating its effects on inducible nitric oxide synthase (iNOS) expression and activity and apoptosis in the ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male SD rats weighing 280-320 g were randomly divided into 3 groups ( n = 18 each) : I sham operation group (group S) ; II focal cerebral I/R group (group I/R) and Ⅲ ifenpradil preconditioning group (group IF) received intraperitoneal ifenprodil 10 mg/kg before focal cerebral I/R. Focal cerebral I/R was induced by middle cerebral artery occlusion (MCAO) . A 3-0 nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. MCAO was maintained for 2 h. At 48 h after reperfusion, the animals were assessed for neurological function which was scored (0 = no functional deficit, 4 = unable to crawl, unconscious) and then decapitated. The brains were immediately removed for microscopic examination and determination of iNOS protein expression and activity, NO content and apoptosis in the ischemic core (IC) and penumbra (IP). Results Ifenprodil pretreatment significantly decreased the cerebral infarct size and neurological scores in group IF as compared with group I/R. In group I/R the iNOS activity was increased compared with group S.The iNOS activity and NO content were significantly lower in IP than in IC in group IR and IF. The TUNEL-positive cells were also mainly confined to IP. Compared with group I/R, in group IF the iNOS protein expression was significantly down-regulated in IC and IP and the iNOS activity and NO content in IC and IP were suppressed and TUNEL-positive cells were significantly reduced in IP. Conclusion Ifenprodil pretreatment has protective effect against cerebral I/R injury by inhibiting iNOS protein expression in IP, suppressing iNOS activity and NO content and reducing apoptosis.     

艾芬地尔预先给药对脑缺血再灌注损伤大鼠缺血半暗带区iNOS和细胞凋亡的影响

Objective To explore the possible mechanism for the neuroprotective effect of ifenprodil by investigating its effects on inducible nitric oxide synthase (iNOS) expression and activity and apoptosis in the ischemic penumbra following focal cerebral ischemia-reperfusion (I/R) in rats.Methods Fifty-four adult male SD rats weighing 280-320 g were randomly divided into 3 groups ( n = 18 each) : I sham operation group (group S) ; II focal cerebral I/R group (group I/R) and Ⅲ ifenpradil preconditioning group (group IF) received intraperitoneal ifenprodil 10 mg/kg before focal cerebral I/R. Focal cerebral I/R was induced by middle cerebral artery occlusion (MCAO) . A 3-0 nylon thread with rounded tip was inserted into right internal jugular vein and threaded cranially until resistance was met. MCAO was maintained for 2 h. At 48 h after reperfusion, the animals were assessed for neurological function which was scored (0 = no functional deficit, 4 = unable to crawl, unconscious) and then decapitated. The brains were immediately removed for microscopic examination and determination of iNOS protein expression and activity, NO content and apoptosis in the ischemic core (IC) and penumbra (IP). Results Ifenprodil pretreatment significantly decreased the cerebral infarct size and neurological scores in group IF as compared with group I/R. In group I/R the iNOS activity was increased compared with group S.The iNOS activity and NO content were significantly lower in IP than in IC in group IR and IF. The TUNEL-positive cells were also mainly confined to IP. Compared with group I/R, in group IF the iNOS protein expression was significantly down-regulated in IC and IP and the iNOS activity and NO content in IC and IP were suppressed and TUNEL-positive cells were significantly reduced in IP. Conclusion Ifenprodil pretreatment has protective effect against cerebral I/R injury by inhibiting iNOS protein expression in IP, suppressing iNOS activity and NO content and reducing apoptosis.     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

阿片受体在异氟醚延迟预处理减轻兔心肌缺血再灌注损伤中的作用

Objective To investigate the role of opioid receptors in the protective effects of isoflurane-induced delayed preconditioning against myocardial ischemia-reperfusion (I/R) injury in rabbits. Methods Forty male New Zealand white rabbits weighing 2.0-2.5 kg were randomly assigned into 4 groups ( n = 10 each) : group I sham operation (S); group II I/R; group Ⅲ isoflurane + I/R (Iso) and group IV Iso + naloxone + I/R (Nal). Myocardial I/R was induced by 40 min occlusion of left anterior descending branch (LAD) of coronary artery followed by 120 min reperfusion. In group Ⅲ (Iso) 2% isoflurane in 100% O2 was inhaled for 2 h and I/R was produced 24 h later. In group IV (Nal) naloxone 6 mg/kg was given iv 10 min before 2 h of 2% isoflurane inhalation and I/R was produced 24 h later. At the end of 120 min reperfusion, infarct size (IS) and area at risk (AAR) were determined by Evan's blue and TTC staining. Myocardial ultrastructure was examined by electron microscopy. The phosphorylated p38MAPK protein expression in myocardium was determined by Western blot. Results The IS was significantly smaller in group Iso ( Ⅲ ) ( 19.7% ± 2.8%) than in I/R group ( II ) (37.8% ±1.7%) (P<0.05). The phosphorylated p38MAPK protein expression in myocardium was significantly lower in group Iso than in group I/R. Microscopic examination showed less myocardial damage in Iso group than in group I/R. The protective effects of delayed preconditioning by isoflurane was prevented by naloxone pretreatment. ConclusionOpioid receptors may be involved in the protective effects of delayed preconditioning by isoflurane against myocardial I/R injury.     

Effects of sevoflurane preconditioning on p-IκBα in a rat model of myocardial ischemia-reperfusion

Objective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection.     

Spontaneous dissecting aneurysms of anterior and middle cerebral artery associated with brain infarction: a case report and review of the literature

BACKGROUND

Intracranial dissecting aneurysms have been reported with increasing frequency and are recognized as a common cause of stroke. In some reviews and case reports, attempts have been made to compare the outcomes of surgical and medical treatments. However, the appropriate management of dissecting aneurysms in the anterior circulation remains controversial, especially in patients who also manifest cerebral infarction.

CASE DESCRIPTION

A 45-year-old male was diagnosed as having a dissecting aneurysm of the right middle cerebral artery (MCA) with cerebral infarction. In the course of conservative treatment, he developed a new cerebral infarction in the territory of the right anterior cerebral artery (ACA). Repeat cerebral angiograms revealed an increase in the aneurysmal dilatation of the right M2 and the appearance of a segmental dilatation of the right A2. He continued to be treated conservatively and his course was satisfactory. On subsequent angiograms, we observed resolution of the right A2 dissection and no further progression of the dilatation of the right M2.

CONCLUSION

This is the first reported case of simultaneous idiopathic dissecting aneurysms of different major arterial branches in the anterior circulation. Our review of the literature disclosed 36 and 23 cases, respectively, of dissecting aneurysms of the ACA and MCA. Many previously reported patients with these dissecting aneurysms involving subarachnoid hemorrhage (SAH) underwent surgery, which resulted in better outcome. More than half of the patients with ACA and MCA dissecting aneurysms had cerebral infarction. All ACA dissecting aneurysms involving ischemia occurred in the A2 region. The outcomes of both surgical and conservative management were equally satisfactory. On the other hand, in patients with MCA dissecting aneurysms, the area of ischemia frequently involved the M1 region; in these patients, conservative treatment resulted in poor outcomes. Therefore, revascularization distal to the compromised artery should be considered in patients with MCA-dissecting aneurysms who have ischemia. Careful interpretation of serial angiograms and/or magnetic resonance (MR) images is necessary because of the possibility of disease progression. If the aneurysmal size increases or there is progression of ischemic symptoms in the course of conservative treatment, surgery must be urgently evaluated.     

Intracranial aneurysms: Characteristics of aneurysms by site,with special reference to anterior communicating artery aneurysms

Data are presented from an unselected series of 212 aneurysm patients for aneurysms at three major sites: the internal carotid-posterior communicating artery junction, the anterior communicating artery, and the middle cerebral artery. More than 70% of the anterior communicating artery aneurysms occurred as single aneurysms; less than 30% of the middle cerebral artery aneurysms were single. Anterior communicating artery aneurysms showed a right-side predominance in males but not in females. Both males and females had significantly higher mean systolic and diastolic blood pressures for left-side anterior communicating artery aneurysms than for right-side aneurysms. A brief review of factors relevant to anterior communicating artery aneurysms is presented.     

Surgery of Proximal Anterior Cerebral Artery Aneurysms

Summary.  Background: Aneurysms of the proximal segment of anterior cerebral artery (A1) are uncommon, but present a unique challenge to surgeons because of the risk of injury to the nearby perforating arteries. Surgical issues and treatment options, however, have not been detailed in the previous literature.  Method: We report a consecutive series of 11 patients with A1 aneurysms focusing on the surgical considerations. The A1 aneurysms represented 3.4% of the 322 cerebral aneurysms treated in our hospital in the last 6 years. All patients presented with subarachnoid hemorrhage, and 8 patients (73%) had multiple aneurysms.  Findings: All aneurysms were secured by neck clipping via pterional craniotomy without any surgery-related morbidity. All of the aneurysms projected superiorly or posteriorly from the origin of the perforating artery of the A1 segment. The aneurysm dome was tightly adherent to the perforating arteries in 7 cases (64%) and the base extended broadly along the axis of the parent artery in 4 cases (36%).  Interpretation: Separating the perforating arteries from the neck or dome of the A1 aneurysm and preserving the vessel presents a substantial challenge to the surgeon, because the aneurysm is almost always behind the parent artery in the surgical field, making it difficult to achieve good access for this particular type of dissection. Consideration should be given to additional orbitotomy, wide opening of the Sylvian fissure, mobilization of the MCA and ICA, selection of aperture clip and intra-operative shortening of the clip blades. Published online December 5, 2002  Correspondence: Akihiko Hino, M.D., Department of Neurosurgery, Saiseikai Shigaken Hospital, Ohashi 2-4-1, Ritto, Shiga 520-30, Japan.     

The three phases of vasospasm

We propose the theory that prolonged cerebral vasospasm involves three phases: (1) the initial muscular contraction of the arterial wall; (2) a secondary injury to the artery that consists of endothelial desquamation with adherence of platelets to the denuded internal elastic lamina and mural thrombus formation; and (3) the repair process, which is the proliferative endarteropathy that has been observed in autopsy specimens. Cerebral ischemia can be the end product of any of these three conditions. We have postulated a possible subcycle in the overall scheme by which adherence of platelets to the denuded internal elastic lamina of the artery provide a continuously replenishing supply of spasmogenic chemical factors to the mural receptors and stimulate prolonged contraction of the muscular layer. We propose that this cycle may be interrupted by the administration of heparin. To test this hypothesis, the records of 112 consecutive patients who received systemic heparin in conjunction with carotid ligation were compared with the results of carotid ligation reported in the Cooperative Study, in which heparin was not used. The incidence of ischemic complications in the group of patients receiving heparin was 6%, as compared to 23% in the control group, with a concomitant reduction in mortality from 16% to 10%. The incidence of recurrent sub-arachnoid hemorrhage was slightly less in the patients receiving heparin than in patients in the Cooperative Study. We conclude that the data provide support for our hypothesis of the mechanism of prolonged cerebral vasospasm and cerebral ischemia associated with subarachnoid hemorrhage, and that systemic heparin may be used with relative safety in patients in whom the aneurysm is protected by partial carotid ligation.     

Aneurysm of distal anterior cerebral artery associated with azygos anterior cerebral artery

Summary An aneurysm arising from the distal anterior cerebral artery distal to the bifurcation of the azygos anterior cerebral artery is reported. A review of the literature emphasizes the rarity of this lesion.     

兔出血性脑水肿与血浆肿瘤坏死因子关系的研究

目的研究肿瘤坏死因子在脑出血急性期的变化及与脑水肿的关系.方法采用随机方法分实验组、对照组.实验组制造兔脑出血模型检测脑组织水含量及不同时点血浆肿瘤坏死因子浓度,结果与对照组比较.结果实验组兔48小时后脑组织水含量79.57%±0.44%,6小时后血浆肿瘤坏死因子浓度(12.65±3.37)ng/dl;对照组分别是78.49%±0.48%、(7.51±2.55)ng/dl.结论脑出血后血浆肿瘤坏死因子浓度发生动态变化,在出血后6小时达到高峰,随后下降.脑出血后脑水肿可能与肿瘤坏死因子大量释放有关.     

脑出血合并脑梗死临床治疗分析

目的通过对脑出血合并脑梗死病例的临床分析，探讨迟发性损害的重要性，进一步加深对该病的认识，指导临床治疗。方法总结临床54例脑出血合并脑梗死病例，通过对临床症状、体征的分析，CT及MR的诊断，迟发性损害的研究，治疗效果的观察，总结经验。结果统计结果显示，通过手术和保守治疗，重视迟发病变的治疗，该组病例，有5例死亡，疗效理想。结论脑出血合并脑梗死是一种混合性中风，各种原因所致的疾病，治疗并不矛盾，最终治疗通路是统一的，预防迟发性损害，防止神经细胞受损，恢复缺血区血供，改善脑细胞神经功能。     

Pharmacological and pathological modulation of cerebral physiology

Homeostatic mechanisms exist to enable the supply of oxygen and glucose for cerebral metabolism and neuronal function. In health, cerebral autoregulation, neurogenic and metabolic processes ensure that the supply of these nutrients is adequate to meet the metabolic requirements, hence preventing neuronal cell damage. The goals of neuroanaesthesia are to provide optimal operating conditions and provide adequate cerebral blood flow, often in the context of a vulnerable brain which is exposed to the physiological stress of surgical trauma. This article outlines how delivery of anaesthesia and disease processes affecting the brain modulate the mechanisms that regulate cerebral blood flow and metabolism.     

Intracerebral mass lesions in patients affected by AIDS

Summary Toxoplasma gondii cerebral abscess is a common opportunistic infection in patients affected by AIDS. Making a reliable diagnosis of acute cerebral toxoplasmosis is difficult in AIDS patients because of the lack of specificity of serological data and neuroradiological findings. Brain biopsy is the only procedure which enables a reliable diagnosis to be made a trial of specific medical therapy for toxoplasmosis in patients affected by AIDS and intracranial mass lesion can be advisable before performing brain biopsy. The authors report the cases of three patients affected by AIDS and cerebral toxoplasmosis.Tissue diagnosis was made in the first patient from autopsy material while a presumptive diagnosis was made in the other two cases since specific medical therapy resulted in a dramatic improvement of the neurological status.Despite the good possibilities in the treatment of this complication AIDS, however, carries a poor prognosis.