电剌激中缝背核对家兔脑皮质微血流的影响

目的探讨电刺激家兔中缝背核(DRN)对家兔脑皮质微血流的影响及其机理. 方法应用氢清除法测定局部脑组织血流(rCBF)及观测软脑膜微循环.结果电刺激DRN后脑皮质rCBF减少44.2%(P<0.01),软脑膜微动脉管径缩小,血流速度减慢, 血流量减少,作用持续15min.切断颈交感神经或破坏蓝斑核(LC)后再刺激DRN,rCBF分别减少15.8%和16.6%(P<0.05).rCBF降低幅度均小于正常动物.电刺激DRN对半球脑血流动力学无显著影响.结论电刺激中缝背核可致家兔脑皮质微动脉收缩,局部组织血流减少.切断颈交感神经、破坏蓝斑核rCBF降低,但幅度小于正常动物.     

电剌激中缝背核对家兔脑皮质微血的影响

目的 探讨电剌激家兔中缝背核（DRN）对家兔脑皮质微血流的影响及其机理。方法 应用氢清除法测定局部脑组织血流(rCBF)及观测软脑膜微循环。结果 电剌激DRN后脑皮质rCBF减少44．2％（P＜0．01），软脑膜微动脉径缩小，血流速度减慢，血流量减少，作用持续15min。切断颈交感神经或破坏蓝斑核（LC）后再剌激DRN，rCBF分别减少15．8％和16．6％（P＜0．05）。rCBF降低幅度均小于正常动物。电剌激DRN对半球脑血流动力学无显著影响。结论 电剌激中缝背核可致家兔脑皮质微动脉收缩，局部组织血流减少。切断颈交感神经、破坏蓝斑核rCBF降低，但幅度小于正常动物。     

电刺激中缝背核对家兔脑皮质微血流的影响

目的应用氢清除法测定局部脑组织血流（ｒＣＢＦ）及观测软脑膜血管微循环,探讨电刺激兔中缝背核（ＤＲＮ）对脑皮质微血流的影响及其机理。方法选用健康家兔３３只、随机分为四组。单纯刺激组（ｎ＝１５）．单纯刺激ＤＲＮ后,连续观察３０ｍｉｎ内局部脑组织血流（ｒＣＢＦ,ｎ＝１０）或软脑膜血管微循环的变化（ｎ＝５）。尼莫地平组（ｎ＝６）,在电刺激ＤＲＮ之前先静注尼莫地平（５μｇ／ｋｇ）。切断颈交感神经组（ｎ＝６）。切断两侧预交感神经后、再刺激 ＤＲＮ,破坏兰斑核组（ＬＣ, ｎ＝６）,破坏同侧兰斑核后再刺激ＤＲＮ,分别观察ｒＣＢＦ的变化。结果电刺激ＤＲＮ后脑皮质ｒＣＢＦ减少４４．２％（Ｐ＜０．０１）,软脑膜微动脉管径缩小,血流速度减慢,血流量减少,作用持续 １５ｍｉｎ。而尼莫地平可取消其作用。切断颈交感神经或破坏ＬＣ后再刺激ＤＲＮ,ｒＣＢＦ分别减少１５．８％和１６．６％（Ｐ＜０．０５）。ｒＣＢＦ降低幅度均小于正常动物。电刺激ＤＲＮ对半球脑血流动力学无显著影响。结论电刺激中缝背核可致兔脑皮质微动脉收缩,局部组织血流减少、其途径有二;一是中枢性５－ＨＴ能神经元兴奋引起的直接缩血管作用;二是通过激活中枢和外周去甲肾上腺素能神经系统引起     

机体不同状态下高压氧暴露后对脑微血流动力作用的差异性

目的 :探讨正常及急性脑缺血损伤动物高压氧暴露后大脑微循环血流动力作用的变化。方法 :成年沙土鼠 61只 ,随机分为 0 .1MPa、0 .2MPa、0 .2 5MPa高压氧暴露组 ,脑缺血损伤组和对照组。实验时动物用urethane麻醉 ,在颅骨顶开窗 ,暴露软脑膜。用阻断双侧颈总动脉造成脑缺血损伤。用LMB 1检测软脑膜细动静脉管径和流速 ,用LDF 3检测脑皮质局部血流量。动物在小型氧舱进行了实验暴露。结果 :动物在 0 .2MPa氧暴露后软脑膜细动脉比暴露前收缩 10 .1% ,细动脉血流速度比高压氧暴露前减慢 0 .58mm/s ,细静脉流速比高压氧暴露前减慢 0 .2 9mm/s ,大脑皮质血流量减少 3 4 % ,有非常显著差异 (P <0 .0 1)。而脑缺血损伤动物暴露于 0 .2 5MPa高压氧 60min ,细动脉可在颈动脉再灌流后血流速度得到一定改善的基础上净增 0 .85mm/s ,细静脉血流速度增加 0 .3 1mm /s ,脑皮质血流量在高压氧暴露后可恢复到或接近脑损伤前水平。单纯脑缺血组在实验观测期间软脑膜细动静脉血液速度和脑皮质血流量均明显减少 (P <0 .0 1)。结论 :机体不同状态 (脑缺血性损伤与正常机体 )高压氧暴露后脑血流动力作用出现的差异 ,可能与机体在不同状态下对氧的反应与需求有关。     

葛根素、川芎嗪、丹参注射液对家兔软脑膜微循环的影响

目的 :探讨葛根素、川芎嗪、丹参注射液治疗脑血管疾病的疗效机制。方法 :采用闭合式颅骨开窗法 ,应用多部位微循环观察仪及微循环计算机图像处理系统 ,观察用药前后家兔软脑膜微血管管径及血流速度的变化。结果 :正常家兔静脉注射葛根素 ( 5 0 mg/kg) ,对微血管的管径及血流速度的影响较小 ;静脉注射丹参注射液 ( 1ml/ kg)、川芎嗪 ( 2 0 ml/ kg)、维脑路通 ( 1ml/ kg)均有扩张微动脉、增加微动脉血流速度的作用 ,对微静脉作用较小。其中丹参注射液作用最为明显。结论 :静脉注射丹参注射液、川芎嗪、维脑路通系通过扩张软脑膜微动脉、增加微动脉血流速度而达到治疗目的。     

刺激颈部交感神经节对椎动脉血流影响的实验研究

目的 :探讨颈部交感神经因素在造成椎 -基底动脉系统缺血过程中的作用。方法 :健康家兔3 0只 ,手术暴露颈部交感神经节及基底动脉 ,不同方式刺激颈部交感神经节 ,记录、分析基底动脉血流的变化。结果 :刺激前测得基底动脉基线血流为 (5 48± 2 7)PU :分别刺激颈上、中、下交感神经节后测得基底动脉血流为 (5 2 9± 16)PU、(4 74± 16)PU和 (3 70± 3 6)PU。与基线血流相比分别下降了 3 .4%、13 .5 %和 3 2 .5 %。颈部交感神经节阻滞并不能使正常状态下的基底动脉血流增加 ,但可以阻断交感神经缩血管作用。结论 :颈部交感神经受到刺激 ,可造成椎 -基底动脉系统供血不足。     

葛根素对自发性高血压大鼠脑微循环的影响

目的:研究葛根素对于自发性高血压大鼠(SHR)脑微循环的影响及其与脑组织损伤的关系。方法:SHR随机分为葛根素治疗、溶剂对照(20%丙二醇)、阳性药物(尼莫地平)对照和空白对照等4组,连续观察14天,记录颈总动脉血压、软脑膜微循环和脑组织血流量变化,HE染色观察脑组织改变,Ⅷ因子染色测定微血管密度。结果:葛根素治疗14天后SHR血压降至正常范围内,软脑膜细动脉血管内径明显大于对照组,病理切片显示治疗组脑细动脉壁重塑,局部缺血明显减轻。结论:葛根素治疗可以扩张SHR脑细动脉、减轻高血压引起的微血管与脑组织损伤。     

应用单宁酸-氯化铁法显示小脑不同部位的微血管构筑

目的　光镜下观察 6只大鼠小脑前叶、后叶及蚓部微血管构筑。方法　用单宁酸 -氯化铁法 (TAFM)媒染显示小脑内血管。结果　小脑各部位皮质、髓质动脉均来源于软脑膜动脉和小脑动脉中央支 ,软脑膜动脉分支多以直角进入小脑皮质 ,分别在分子层、蒲肯野细胞层、颗粒层形成毛细血管网 ;小脑后叶髓质中微动脉呈爪状分支 ,小叶两侧皮质深层微动脉或毛细血管可跨过髓质互相沟通。结论　 TAFM显示小脑微血管构筑清晰、立体感强 ,并发现小叶内皮质深层微血管之间有吻合支     

实验性蛛网膜下腔出血后软脑膜微循环的动态变化

目的探讨SAH后软脑膜微循环的动态变化。方法采用Wistar大鼠雌雄各半 ,将动物随机分入非SAH组和SAH组 ;非SAH组于股动脉抽血0.4ml后 ,枕大池注入0.3ml生理盐水 ;SAH组于股动脉抽血0.4ml后 ,枕大池注入经冻 -溶方法制备的自体动脉血溶解物0.3ml。以矢状缝外3mm、前囟后3mm为中心制备一直径约0.6cm区域的观察骨窗 ,去除颅骨内板、硬脑膜和蛛网膜。用微循环显微镜观察并通过摄像系统从微机屏幕上观察软脑膜微循环并录制图像 ,MCIP微循环图像处理系统分析。实验过程中保持环境温度于(26±2)℃。结果在非SAH组大鼠 ,脑池注入生理盐水前后软脑膜微血管管径、血流流速和流态均无明显改变 ,软脑膜微血管表面光洁 ,血供较丰富 ,微动脉、微静脉不完全伴行 ,常因出入脑实质而形成血管盲端 ,除少数A4级微动脉呈线粒流外 ,其它各级微血管均呈线流 ,血流快速而无凝集现象。SAH组和溶媒组大鼠在脑池注入动脉血裂解物后软脑膜微循环变化相似 ,微动脉、微静脉逐渐出现收缩变细 ,流速减慢 ,出现红细胞中至重度凝集 ,有的微血管出现血流停滞、摆动甚至微静脉向微动脉的逆流动。SAH后5min ,SAH组软脑膜微动脉管径和微静脉管径分别减低至术前的60.8 %和70.0 % ,在脑池注入自体动脉血溶解物结束后2h内 ,持续维持于低水平状态 ,     

实验高压电烧伤软脑膜微循环动态变化和意义

目的通过研究高压电烧伤后动物软脑膜微循环的变化 ,探讨高压电对机体脑微循环的影响 ,为临床防治高压电脑损伤提供实验依据。方法复制家兔高压电烧伤模型 ,用WX -9B型微循环显微镜及视频图像分析系统 ,观察软脑膜微血管形态、微血管流态及微血管周围状态的变化 ,应用SAS软件进行统计学处理。结果与对照组比较,电烧伤(A、B)组软脑膜微血管形态、微血管流态及微血管周围状态各时相均发生变化 ,观察各时相高压电对微动脉和微静脉、毛细血管管径均有影响 (P<0.01),对微静脉血流速度亦有影响(P<0.01)。脑血流灌流值与对照组比较差别显著(P<0.01)。结论高压电烧伤能引起家兔软脑膜微循环发生病理性改变。     

Regional cerebral blood flow in the frontal, parietal and occipital cortices increases independently of systemic arterial pressure during slow walking in conscious rats

Regional cerebral blood flow (rCBF) in the frontal, parietal and occipital cortices was measured using laser Doppler flowmetry during walking in conscious rats at moderate speed on a treadmill (4 cm/s) for a 30 s period. During walking rCBF increased in all these three cortices. The rCBF in the parietal cortex started to increase within a few seconds after the start of walking, and continued to increase 42 ± 16% (mean ± S.D.) until the end of walking. Within 90 s after walking had ceased, the increased rCBF returned to pre-walking basal levels. The rCBF responses in the frontal and occipital cortices were identical to that in the parietal cortex. Mean arterial pressure (MAP) in a caudal artery of the tail during walking was increased by about 10%. Injection of atropine (5 mg/kg, i.p.), a muscarinic cholinergic receptor antagonist that permeates the blood brain barrier (BBB), reduced the walking-induced increase in cortical rCBF, as determined by measurement of parietal rCBF, from 42 ± 12% to 28 ± 15%. However, injection of methylatropine (5 mg/kg, i.p.), a muscarinic cholinergic receptor antagonist that does not permeate the BBB, did not affect the response of rCBF. Neither drug affected the walking-induced response of MAP. Injection of mecamylamine (20 mg/kg, s.c.), a nicotinic cholinergic receptor antagonist that permeates the BBB, reduced the walking-induced increase in cortical rCBF from 47 ± 12% to 30 ± 12%. Injection of hexamethonium (20 mg/kg, s.c.), a nicotinic cholinergic receptor antagonist that does not permeate the BBB, did not affect the responses of rCBF. Both mecamylamine and hexamethonium decreased the resting basal MAP by about 50%, and abolished the walking-induced increase in MAP. It is suggested that the increase in cortical rCBF during walking, which is independent of MAP, is attributable to the walking-associated activation of cortical cholinergic nerves. Possible contribution of cholinergic neurons in the nucleus basalis of Meynert (NBM) to the walking-induced increase in cortical rCBF is discussed.     

Reduced temporal lobe blood flow in Alzheimer's disease.

We used single photon emission computed tomography with the blood flow tracer [123I]N-isopropyl-p-iodoamphetamine (IMP) to study regional cerebral blood flow (rCBF) in 50 mildly and moderately demented Alzheimer's disease (AD) patients to evaluate rCBF as a function of disease severity. Relative rCBF (normalized to occipital cortex) was significantly lower than controls in temporal cortex for both mildly and moderately demented patients. Similar numbers of patients in both groups demonstrated perfusion abnormalities in temporal neocortex. Parietal cortex was more variably involved with greater numbers of moderately than mildly demented patients showing perfusion abnormalities. Relative rCBF in dirsolateral frontal cortex was reduced only in the moderately demented patients. Disease severity, as measured by the Mini Mental Status Examination, was associated with relative rCBF only in dorsolateral frontal and parietal cortex. These results suggest that the temporal lobes are the first neocortical regions affected by AD and that other cortical areas become involved as the disease progresses.     

Combined rCBF and CSF biomarkers predict progression from mild cognitive impairment to Alzheimer's disease

This study aimed to identify preclinical Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI) using measurements of both regional cerebral blood flow (rCBF) and cerebrospinal fluid (CSF) biomarkers. Baseline rCBF assessments ((133)Xe method) were performed in 70 patients with MCI who were cognitively stable for 4-6 years, 69 patients with MCI who subsequently developed AD, and 33 healthy individuals. CSF was collected at baseline and analyzed for beta-amyloid(1-42), total tau and phophorylated tau. In contrast to patients with stable MCI, those who subsequently developed AD had decreased rCBF in the temporo-parietal cortex already at baseline. The relative risk of future progression to AD was particularly increased in MCI patients with decreased rCBF in parietal cortex (hazard ratio 3.1, P<0.0001). Subjects with pathological levels of both CSF tau and beta-amyloid(1-42) were also at high risk of developing AD (hazard ratio 13.4, P<0.0001). The MCI patients with a combination of decreased parietal rCBF and pathological CSF biomarkers at baseline had a substantially increased risk of future development of AD, with a hazard ratio of 24.3 (P<0.0001), when compared to those with normal CSF biomarkers. Moreover, decreased parietal rCBF (but not CSF biomarkers) was associated with a more rapid progression to AD. In conclusion, the combination of rCBF and CSF biomarkers improves the risk assessment of progression to AD in patients with MCI.     

Changes in cerebral blood flow under the prone condition with and without massage

To investigate changes in regional cerebral blood flow (rCBF) under the prone condition with and without light massage on the back, we measured rCBF quantitatively in healthy human subjects using positron emission tomography with H₂¹⁵O. Biochemical tests showed that the light massage (palm-pressure) reduced levels of stress-related serum cortisol and salivary stress protein chromogranin-A measured after the PET examination. Absolute rCBF significantly increased in the parietal cortex (precuneus) under the prone condition compared with the supine condition, and this rCBF increase was in parallel with comfortable sensation and slowing heart rate during the massage. Correlation analysis in statistical parametric mapping showed that the amygdalar and basal forebrain rCBF correlated with parasympathetic function (heart rate reduction), indicating involvement of the forebrain-amygdala system in mediating activities in the autonomic nervous system in the presence of comfortable sensation. To conclude, prone posture itself can stimulate the precuneus region to raise awareness, and the light massage on the back may help accommodate the brain to comfortable stimulation.     

Placebo analgesia: a PET study

Placebo analgesia involves complex mechanisms and sometimes has a marked effect on patients in pain. In this study we examined changes in regional cerebral blood flow (rCBF) under three different conditions (resting, hot, painful) before and after placebo administration using H₂¹⁵O and positron emission tomography in ten healthy subjects. In five subjects, placebo administration significantly decreased pain-intensity score (placebo responders), and rCBF in the medial prefrontal cortex (MPFC), posterior parietal cortex (PPC), and inferior parietal lobe (IPL) increased after placebo administration compared with before placebo administration under the painful condition. Furthermore, in the placebo responders, rCBF in the MPFC, PPC and IPL also increased under the resting condition (without sensory stimulation) after placebo administration compared with before placebo administration. However, there was no rCBF change under the rest condition in the placebo nonresponders after placebo administration. These results suggest that placebo analgesia has its effect under the resting condition and MPFC, IPL and PPC may have an important role in placebo analgesia.     

Control of cerebral cortical blood flow by stimulation of basal forebrain cholinergic areas in mice

We examined whether activity of the nucleus basalis of Meynert (NBM) regulates regional cerebral cortical blood flow (rCBF) in mice, using laser speckle and laser Doppler flowmetry. In anesthetized mice, unilateral focal stimulation, either electrical or chemical, of the NBM increased rCBF of the ipsilateral cerebral cortex in the frontal, parietal and occipital lobes, independent of changes in systemic blood pressure. Most of vasodilative responses to low intensity stimuli (2 times threshold intensity: 2T) were abolished by atropine (a muscarinic cholinergic blocker), whereas responses to higher intensity stimuli (3T) were abolished by atropine and mecamylamine (a nicotinic cholinergic blocker). Blood flow changes were largest when the tip of the electrode was located within the area containing cholinergic neurons shown by choline acetyltransferase-immunocytochemistry. These results suggest that cholinergic projections from basal forebrain neurons in mice cause vasodilation in the ipsilateral cerebral cortex by a combination of muscarinic and nicotinic mechanisms, as previously found in rats and cats.     

High (15 Hz) and low (1 Hz) frequency transcranial magnetic stimulation have different acute effects on regional cerebral blood flow in depressed patients

BACKGROUND: High and low frequency repetititve transcranial magnetic stimulation (rTMS) are both effective in treating depression but have contrary effects on motor cortical activity. This study aimed to understand further the mechanisms of action of high and low frequency rTMS by examining their acute effects on regional cerebral blood flow (rCBF) in depressed patients. METHOD: Eighteen depressed subjects underwent brain single photon emission computerized tomography (SPECT) scanning using split-dose 99mTc-HMPAO, and were examined during sham and active rTMS to the left prefrontal cortex, at 15 Hz or 1 Hz (N=9 each). Relative rCBF changes were examined by statistical parametric mapping and by regions of interest analysis. RESULTS: High (15 Hz) frequency rTMS resulted in relative rCBF increases in the inferior frontal cortices, right dorsomedial frontal cortex, posterior cingulate and parahippocampus. Decreases occurred in the right orbital cortex and subcallosal gyrus, and left uncus. Low (1 Hz) frequency rTMS led to increased relative rCBF in the right anterior cingulate, bilateral parietal cortices and insula and left cerebellum. High frequency rTMS led to an overall increase, whereas low frequency rTMS produced a slight decrease, in the mean relative rCBF in the left dorsolateral prefrontal cortex. CONCLUSIONS: High (15 Hz) and low (1 Hz) frequency rTMS led to different frontal and remote relative rCBF changes, which suggests different neurophysiological and possibly neuropsychiatric consequences of a change in frequency of rTMS.     

Propofol anesthesia and cerebral blood flow changes elicited by vibrotactile stimulation: a positron emission tomography study

We investigated the effects of the general anesthetic agent propofol on cerebral structures involved in the processing of vibrotactile information. Using positron emission tomography (PET) and the H(2)(15)O bolus technique, we measured regional distribution of cerebral blood flow (CBF) in eight healthy human volunteers. They were scanned under five different levels of propofol anesthesia. Using a computer-controlled infusion, the following plasma levels of propofol were targeted: Level W (Waking, 0 microg/ml), Level 1 (0.5 microg/ml), Level 2 (1.5 microg/ml), Level 3 (3.5 microg/ml), and Level R (Recovery). At each level of anesthesia, two 3-min scans were acquired with vibrotactile stimulation of the right forearm either on or off. The level of consciousness was evaluated before each scan by the response of the subject to a verbal command. At Level W, all volunteers were fully awake. They reported being slightly drowsy at Level 1, they had a slurred speech and slow response at Level 2, and they were not responding at all at Level 3. The following variations in regional CBF (rCBF) were observed. During the waking state (Level W), vibrotactile stimulation induced a significant rCBF increase in the left thalamus and in several cortical regions, including the left primary somatosensory cortex and the left and right secondary somatosensory cortex. During anesthesia, propofol reduced in a dose-dependent manner rCBF in the thalamus as well as in a number of visual, parietal, and prefrontal cortical regions. At Level 1 through 3, propofol also suppressed vibration-induced increases in rCBF in the primary and secondary somatosensory cortex, whereas the thalamic rCBF response was abolished only at Level 3, when volunteers lost consciousness. We conclude that propofol interferes with the processing of vibrotactile information first at the level of the cortex before attenuating its transfer through the thalamus.     

Cortical cerebral blood flow governed by the basal forebrain: age-related impairments.

This study sought to compare resting and evoked increases in cortical microvascular perfusion elicited by electrical microstimulation of the basal forebrain (BF) in young (4-6 months) and aged (22-26 months) Sprague-Dawley rats. Regional cerebral blood flow (rCBF) was measured in chloralose-anesthetized rats for twelve bilateral regions using 14C-iodoantipyrine with regional brain dissection, while second-to-second changes in tissue perfusion were concurrently assessed using laser-doppler flowmetry (LDF). In young animals, BF stimulation elicited significant ipsilateral increases in CBF in parietal (+123%) and frontal (+107%) cortices, caudate nucleus (+63%) and thalamus (+59%) (p less than 0.05). The BF-elicited increases were preserved in frontal cortex and thalamus, but not in parietal cortex or caudate nucleus of aged animals. No frequency- or current-specific attenuations were observed in the spared frontal cortex of aged animals. However, there was a significant (+70%) age-related increase in the latency to reach maximal blood flow increases (p less than 0.05), without any change in the total time of increased blood flow. These findings support the hypothesis that cortical CBF is in part governed by BF neurons, and suggest that regionally selective, age-related impairments of cortical coupling of neuronal to dynamic vascular responses exist. It remains to be determined whether the mechanism of this impairment relates to an age-related impairment in coupling of blood flow and metabolism.     

Single photon emission tomography with 99m Tc-HMPAO in Arab patients with depression

BACKGROUND: This study investigates the rate of cerebral blood flow (rCBF) in Arab patients wth depression. METHODS: Forty-four patients with DSM-III-R major depressive disorders were studied at rest using single photon emission computerized tomography (SPECT) with 99m Tc-HMPAO in comparison with 20 normal controls. All patients were assessed using the Hamilton Rating Scale for Depression (HRSD). RESULTS: The depressed group showed greater rCBF in left and right posterior frontal and parietal cortical regions than normal controls. Within the depressed group, patients with the least severe illness (HRSD < 20) had significantly lower rCBF than normal controls, whilst those with moderately severe (HRSD 20-29) and severe (HRSD > 30) had significantly greater rCBF in most cortical regions than normal controls. Symptom scores, derived from the HRSD were predicted by rCBF principally increased rCBF in the left frontal cortex. CONCLUSIONS: These results suggest a generalized cerebral activation principally in the frontal cortex which is in contrast to the results of most previous studies but more in line with the results of studies of induced affect and some studies of depression subsyndromes.