Assessment of cerebrovascular reserve in unilateral middle cerebral artery stenosis using perfusion CT and CO2 inhalation tests

Purpose/Aim of the study: Cerebrovascular reactivity (CVR) is an important marker for assessing cerebrovascular disease. This study assessed the CVR by perfusion computed tomography (CT) and CO₂ inhalation tests in patients with unilateral middle cerebral artery (MCA) stenosis disease. Materials and Methods: Thirty-one patients with unilateral MCA stenosis disease diagnosed by digital subtraction angiography were studied. Patients were divided into two groups according to the degree of stenosis: severe and moderate. The regional cerebral blood flow (CBF) before and after CO₂ inhalation was determined by perfusion CT. Regional CVR values were obtained by the following formula: increase (%) = (post-CBF) ? (pre-CBF)/(pre-CBF) × 100%. Results: No significant differences in the mean CBF in the MCA stenosis region were found between the affected and contralateral sides before the CO₂ inhalation test; after the test, CBF was more significantly decreased on the affected side than on the contralateral side. The changes in CBF on the affected side were categorized into three types: increased CBF (17 cases), decreased CBF (12 cases) and no change in CBF (2 cases). The rate of CVR impairment among severe stenosis patients (13/19) was higher than that among moderate stenosis patients (3/12). CVR was significantly correlated with the degree of stenosis (r = 0.423, P = 0.018). Conclusion: CVR impairment was found in approximately half of patients with unilateral MCA stenosis. Along with an increase in the degree of stenosis, patients with unilateral MCA stenosis were more likely to exhibit CVR impairment. It is important to assess the CVR in patients with unilateral MCA stenosis, especially those with severe stenosis.     

Role of nitric oxide in regulation of cerebral microvascular tone and autoregulation of cerebral blood flow in cats

The role of nitric oxide in the regulation of cerebrocortical microvascular tone and autoregulation of cerebral blood flow (CBF) was examined in 24 anesthetized cats. The local cerebral blood volume (CBV), mean transit time of blood (MTT), and CBF in the cortex were measured by our photoelectric method. CBV represents the cumulative dimensions of the cerebral microvessels. Intravenous injection of 0.35–0.7 mg/kg/minN^G-monomethyl-l-arginine (l-NMMA), an inhibitor of nitric oxide synthesis, significantly increased mean arterial blood pressure (MABP; 8.4–14.1%,P < 0.01), decreased CBV (15.2–28.7%,P < 0.01), and decreased CBF (20.0–29.8%,P < 0.01) in a dose-related manner. The changes in MABP, CBV, and CBF elicited byl-NMMA were inhibited (P < 0.05) by simultaneous infusion of 35 mg/kg/minl-arginine. Autoregulation of CBF was examined during controlled hypotension of −30 to −40 mmHg (artificial bleeding) and recovery of blood pressure (reinfusion of blood). Although CBF remained constant with blood pressure changes in the control state (ΔCBF/ΔMABP of 0.037±0.155 with hypotension), CBF became dependent on blood pressure changes (ΔCBF/ΔMABP of 0.478±0.135, P < 0.05) during infusion of 0.35 mg/kg/minl-NMMA. It is concluded that nitric oxide participates in both the regulation of basal tone of cerebral microvessels and the autoregulation of CBF.     

Effects of aging and hypertension on cerebral ischemic susceptibility: evidenced by MR diffusion-perfusion study in rat

Aging is the most significant non-modifiable risk factor and hypertension is the most significant modifiable risk factor for ischemic stroke. We used magnetic resonance imaging (MRI) to investigate the evidence of ischemic susceptibility after aging and hypertension. Four groups of rat were studied: young normotensive Wistar-Kyoto (WKY) rat, aged normotensive WKY rat, young spontaneously hypertensive rat (SHR) and aged SHR. Brain images were acquired at a 3.0T Tim-Trio MRI system. For diffusion-weighted images, apparent diffusion coefficient (ADC) was measured. Relative cerebral blood flow (CBF) was also calculated. Cerebral ischemic susceptibility was examined by using ischemic model of bilateral common carotid artery occlusion. In the MRI study of non-ischemic rat, aged SHR had significantly higher ADC (P < 0.01) and significantly lower CBF (P < 0.01) in the parietal cortex, but aged WKY rat had only significantly lower CBF (P < 0.01) when compared with young WKY rat. The ADC/CBF ratio in the parietal cortex was significantly higher in aged SHR when compared with young WKY rat, young SHR and aged WKY rat (P < 0.01, P < 0.05, P < 0.05, respectively) suggesting a significant diffusion–perfusion disparity in aged SHR. After bilateral common carotid artery occlusion, there was significantly larger damage in the parietal cortex of aged SHR when compared with young WKY rat, young SHR and aged WKY rat (all P < 0.05), but not in the hippocampus and thalamus (P > 0.05). Our study demonstrated a significantly increased ADC value and reduced CBF in the ischemia-vulnerable cortical area. This cerebral diffusion–perfusion disparity is seen mainly in aged rat and can be more evident if associated with hypertension indicating an increased susceptibility of brain tissue to ischemic injury.     

Feasibility and safety of intrathecal nimodipine on posthaemorrhagic cerebral vasospasm refractory to medical and endovascular therapy

OBJECTIVE: The effectiveness of balloon angioplasty and intra-arterial infusion of vasodilating agents for patients suffering from severe vasospasm following aneurysmal subarachnoid haemorrhage (SAH) is often unsatisfying and there is still demand for further last resort treatment strategies. In the current prospective study, we attempted the intrathecal lavage administration of nimodipine in cases of severe cerebral vasospasm that were refractory to medical and endovascular therapy. METHODS: Eight of 146 patients with aneurysmal SAH were included in the prospective study, which had been approved by the local ethics committee. Treatment was instituted by intraventricular nimodipine bolus (0.4mg), followed by a continuous lumbar intrathecal infusion (0.4mg/h). Effectiveness was monitored angiographically, with transcranial Doppler (TCD), perfusion CT (pCT), and by neurological examination during treatment course and follow-up. RESULTS: The neurological condition improved directly in three patients and remained unchanged in four patients. Seventeen (70.8%) CT perfusion analyses revealed improved perfusion. A reduction of vasospasm was seen angiographically by digital subtraction angiography (DSA) in seven (66.6%) investigations. Additional ischaemic infarction after onset of the intrathecal therapy was documented in two (25%) patients. There were no serious adverse effects observed. CONCLUSION: The present study has for the first time demonstrated the feasibility and safety of intrathecal nimodipine lavage in patients with severe vasospasm resistant to the established medical and endovascular treatment strategies. The results of the study are therefore encouraging, and further experimental and clinical trials should be carried out so as to investigate the efficacy of intrathecal nimodipine lavage in vasospasm therapy.     

尼莫地平灌洗对自发性蛛网膜下腔出血脑血流的影响

目的 已证实尼莫地平液灌洗可缓解蛛网膜下腔出血(SAH)后脑血流速度的异常增高,现拟研究其对SAH所致异常脑血流灌注的影响.方法 14头雄性小型实验猪随机分为假手术组、SAH组和灌洗组.开颅向鞍上池注入5 ml自体股动脉血制备SAH模型,4 d后用40 ml尼莫地平稀释液(0.04 mg/ml)灌洗灌洗组蛛网膜下腔.30 min后行CT/SPECT扫描,图像经重建断层、对齐及空间标准化后于CT模板绘制感兴趣区再与对应层面SPECT图像配准计算大脑小脑比(CCR)和相对离散度(RD)以半定量描述右侧大脑半球血流量和血流分布异质性.结果 假手术组、SAH组和灌洗组CCR分别为1.988±0.346、1.382±0.192和1.503±0.107;RD分别为0.389±0.015,0.417±0.015和0.425±0.018.SAH组CCR和RD与假手术组差异有统计学意义(P<0.05);灌洗组CCR和RD均与SAH组差异无统计学意义(P>0.05),提示尼莫地平灌洗对SAH所致的半球血流量下降及脑血流分布异质性增加无显著缓解作用.结论 尼莫地平灌洗不能缓解SAH后异常脑血流灌注的机制尚不明确,可能与难以缓解SAH引起的脑微循环障碍有关.     

Xenon-enhanced computed tomography cerebral blood flow measurements in acute cerebral ischemia: Review of 56 cases

Objective: Ischemic stroke must be diagnosed promptly if patients are to be treated with thrombolytic therapy. The diagnosis of acute cerebral ischemia, however, is usually based on clinical and computed tomography (CT) scan findings. CT scans are often normal in the first few hours after stroke. The purpose of this study was to determine whether Xenon-enhanced CT (XeCT) cerebral blood flow (CBF) studies could increase the sensitivity of stroke detection in the acute stage. Methods: CBF studies performed within 8 hours of symptom onset were evaluated in 56 patients who presented with hemispheric stroke symptoms. Mean CBF in the symptomatic vascular territory was calculated and compared with the corresponding contralateral area. CBF values below 18 mL/100g/min on 2 adjacent regions of interest were considered ischemic lesions. CT scans and angiograms were compared with the XeCt findings. Neurological condition on admission and discharge was evaluated by using National Institutes of Health Stroke Scale (NIHSS) scores. Results: The mean NIHSS score on admission was 12+/-5. Early CT scans were abnormal in 28 (50%) patients. There were 9 (16%) patients who had normal XeCT scans because of spontaneous reperfusion of the ischemic area. XeCT studies showed an ischemic lesion in 47 (84%) patients. In these patients, the mean CBF in the affected vascular territory was 16+/-8 mL/100g/min compared with 35+/-13 mL/100g/min in the contralateral specular territory (P<0.001). There were no false positive or negative XeCT studies, and the location of the perfusion defect corresponded with the CT and/or angiographic findings in all cases. Eight patients died (14%), and the 48 survivors (86%) had a mean NIHSS score of 9+/-6 on discharge. Conclusions: CBF measurements were correlated with the CT and angiographic results and greatly assisted in the diagnosis of acute ischemic stroke. XeCT studies used for estimating the location and extent of cerebral ischemia may be important in the triage of patients for acute stroke therapy.     

The effects of ketamine–xylazine anesthesia on cerebral blood flow and oxygenation observed using nuclear magnetic resonance perfusion imaging and electron paramagnetic resonance oximetry

Ketamine–xylazine is a commonly used anesthetic for laboratory rats. Previous results showed that rats anesthetized with ketamine–xylazine can have a much lower cerebral partial pressure of oxygen (P_tO₂), compared to unanesthetized and isoflurane anesthetized rats. The underlying mechanisms for the P_tO₂ reduction need to be elucidated. In this study, we measured regional cerebral blood flow (CBF) using nuclear magnetic resonance (NMR) perfusion imaging and cortical P_tO₂ using electron paramagnetic resonance (EPR) oximetry in the forebrain of rats under isoflurane, ketamine, ketamine–xylazine and isoflurane–xylazine anesthesia. The results show that in ventilated rats ketamine at a dose of 50 mg/kg does not induce significant changes in CBF, compared to isoflurane. Ketamine–xylazine in combination causes 25–65% reductions in forebrain CBF in a region-dependent manner. Adding xylazine to isoflurane anesthesia results in similar regional reductions in CBF. EPR oximetry measurements show ketamine increases cortical P_tO₂ while xylazine decreases cortical P_tO₂. The xylazine induced reduction in CBF could explain the reduced brain oxygenation observed in ketamine–xylazine anesthetized rats.     

急性脑梗死的320排动态容积CT脑灌注成像研究

目的研究320排动态容积CT全脑灌注成像(CTP)在脑梗死患者中的价值。方法对2014-01—2016-01驻马店市中心医院收治的33例脑梗死患者采取CT全脑灌注成像检查,测量梗死核心区、缺血半暗带(IP)与健侧镜像区的脑血流量(CBF)、脑血容量(CBV)、达峰时间(TTP)及平均通过时间(MTT)值,计算梗死核心区及IP的相对脑血流量(rCBF)、相对脑血容量(rCBV)、相对达峰时间(rTTP)、相对平均通过时间(rMTT),并进行对比分析。结果 33例患者中,头颅平扫发现9例早期脑梗死征象,其余24例未发现异常。33例患者行CTP成像均发现异常灌注区,其中25例存在IP;与健侧镜像区对比,CBV无显著差异(P0.05),而TTP、MTT值明显延长,CBF显著降低,差异有统计学意义(P0.05);与梗死核心区对比,CBF、CBV升高,TTP缩短,MTT延长,差异均有统计学意义(P0.05)。IP区与梗死核心区rCBF、rCBV、rTTP、rMTT对比,差异有统计学意义(P0.05)。10例超急性期(发病6h以内)、15例急性期(发病6~72h)中11例、8例亚急性期(发病72h~14d)中4例存在IP。缺血半暗带分期:Ⅰ2期6例,Ⅱ1期12例,Ⅱ2期7例。结论 320排动态容积CT全脑灌注成像可通过注射一次对比剂获得常规CT、CTP、CTA数据,对脑梗死患者的病变部位、范围及有无IP等提供明确的影像学依据,且可对IP进行分期,为临床实现对患者的个体化治疗提供了可能,且显著降低了患者所受的辐射剂量,安全性高。     

Dual role of cerebral blood flow in regional brain temperature control in the healthy newborn infant

Small shifts in brain temperature after hypoxia–ischaemia affect cell viability. The main determinants of brain temperature are cerebral metabolism, which contributes to local heat production, and brain perfusion, which removes heat. However, few studies have addressed the effect of cerebral metabolism and perfusion on regional brain temperature in human neonates because of the lack of non-invasive cot-side monitors. This study aimed (i) to determine non-invasive monitoring tools of cerebral metabolism and perfusion by combining near-infrared spectroscopy and echocardiography, and (ii) to investigate the dependence of brain temperature on cerebral metabolism and perfusion in unsedated newborn infants.Thirty-two healthy newborn infants were recruited. They were studied with cerebral near-infrared spectroscopy, echocardiography, and a zero-heat flux tissue thermometer. A surrogate of cerebral blood flow (CBF) was measured using superior vena cava flow adjusted for cerebral volume (rSVC flow). The tissue oxygenation index, fractional oxygen extraction (FOE), and the cerebral metabolic rate of oxygen relative to rSVC flow (CMRO₂ index) were also estimated.A greater rSVC flow was positively associated with higher brain temperatures, particularly for superficial structures. The CMRO₂ index and rSVC flow were positively coupled. However, brain temperature was independent of FOE and the CMRO₂ index. A cooler ambient temperature was associated with a greater temperature gradient between the scalp surface and the body core.Cerebral oxygen metabolism and perfusion were monitored in newborn infants without using tracers. In these healthy newborn infants, cerebral perfusion and ambient temperature were significant independent variables of brain temperature. CBF has primarily been associated with heat removal from the brain. However, our results suggest that CBF is likely to deliver heat specifically to the superficial brain. Further studies are required to assess the effect of cerebral metabolism and perfusion on regional brain temperature in low-cardiac output conditions, fever, and with therapeutic hypothermia.     

Effect of nimodipine on the autoregulation of cerebral blood flow studied by laser-Doppler flowmetry

The present work examines whether nimodipine impairs autoregulation of CBF during hypotension. The CBF of 16 anesthetized rabbits was measured with a laser-Doppler flowmetry probe placed on the external surface of a plexiglas window, chronically inserted in the skull. Autoregulation was triggered by aortic bleeding. First, the effects of three doses of nimodipine (1, 3 and 10 μg/kg) and the solvent were studied in 10 rabbits in which MABP was maintained at 50 mmHg for one minute. Second, 10 μg/kg i.v. nimodipine was administered to 6 rabbits in which MABP was kept at 30 mmHg for one minute. Before bleeding, the 10 μg/kg dose significantly decreased MABP (from 96 ± 11mmHg to 81 ± 11mmHg, P < 0.01) and increased CBF (from 104 ± 20%to147 ± 25%, P < 0.01) as compared to the solvent. In the first set of experiments, only the 10 μg/kg dose suppressed the autoregulatory vasodilation, but CBF was not different from control (84 ± 17%versus87 ± 12%), probably because of the previous induced vasodilation. In the second set of experiments, active vasodilation occurred and the CBF during hypotension was not different from control (72 ± 26%versus65 ± 11%). We conclude that under nimodipine the triggering of the active autoregulatory vasodilation is dependent on both the severity of hypotension and the previous nimodipine-induced vasodilation.     

Effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow and histopathology after middle cerebral artery occlusion

We used the [¹⁴C]iodoantipyrine autoradiography technique to study the effect of pretreatment with the calcium antagonist nimodipine on local cerebral blood flow (1CBF) in rats that underwent middle cerebral artery (MCA) occlusion. In untreated control animals there were profound localized reductions in 1CBF 30 minutes after MCA occlusion. These were most pronounced in neocortical areas and in the caudate nucleus ipsilateral to the MCA occlusion. In animals pretreated with nimodipine (1 μg · kg^?1 · min^?1 for 30 minutes before and 30 minutes after MCA occlusion), the ipsilateral decrease in 1CBF in cortical regions was significantly less than that in control animals. The drug did not appear to alter 1CBF in the ipsilateral caudate nucleus. Neuropathological quantification of the ischemic damage present 3 hours after occlusion showed thai: nimodipine pretreatment reduced the volume and extent of cellular damage in the periphery but not in the core of the lesion.     

Brain blood flow during hypercapnia in fish: no role of nitric oxide

Very little is known about the regulation of cerebral blood flow (CBF) in lower vertebrates, especially fish. In mammals, hypercapnia causes cerebral vasodilation and increased CBF through mechanisms that involve the production of nitric oxide (NO). We have used epi-illumination microscopy in vivo to observe effects of hypercapnia on venular erythrocyte velocity, used as an index of CBF velocity, in rainbow trout (Oncorhynchus mykiss) and crucian carp (Carassius carassius). Rainbow trout exposed to a pCO₂ of 7.5 mmHg displayed a small increase of CBF velocity in two out of five fishes, while dorsal aortic blood pressure (P_DA) did not change. Exposing trout to a pCO₂ of 22.5 mmHg, resulted in an 80% increase in CBF velocity and a 21% increase in P_DA. Trout exposed to a pCO₂ of 75 mmHg showed an additional increase in blood pressure, while no further increase was seen in CBF velocity compared to a pCO₂ of 22.5 mmHg. By contrast, no change in CBF velocity was seen in crucian carp, even at a pCO₂ of 75 mmHg. None of the circulatory changes seen in the trout could be blocked by superfusing the brain surface with the NO synthase blocker N^G-nitro- -arginine. The results point at striking species differences in the responses of CBF and P_DA to hypercapnia in fish, and that the hypercapnia induced increase in CBF velocity seen in rainbow trout is independent of NO production.     

Prognostic value of cerebral blood flow autoregulation in the long-term prognosis of ischemic cerebrovascular disease

The correlation between long-term prognosis, cerebral blood flow (CBF) and CBF autoregulation was studied in 34 patients with cerebral infarction (mean age, 64 years). CBF was measured by the nitrous oxide method 1–6 months (mean 87 days) after disease onset. CBF autoregulation was evaluated quantitatively from the Dysautoregulation Index (DI) (ΔCBF/Δeffective MABP). Reductions in effective MABP were induced with a tilt table. No significant correlation was noted among CBF, DI and activities of daily living at the time of measurement. The patients' physical condition was reevaluated by questionnaire 2 years or more (mean 32 months) later. Better functional state at follow-up was related to higher CBF and lower DI values although the differences were not significant. The relationships among CBF, DI and changes in physical condition during the period were evaluated. The mean CBF values in patients with a better prognosis exceeded those of poor prognosis patients. The CBF values in the group who became independent significantly exceeded those in the group that deteriorated (P < 0.05). The CBF values in the latter showed small but significant decreases during head-up tilting (P < 0.05). The DI in this group was significantly higher than in the groups with a less severe outcome (P < 0.01, P < 0.05, respectively).In conclusion, determinations of CBF autoregulation, together with flow values, in the chronic state may have some value in predicting the long-term prognosis in cerebral infarction.     

Nimodipine pretreatment improves cerebral blood flow and reduces brain edema in conscious rats subjected to focal cerebral ischemia

The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 micrograms/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a "vascular steal" and reduced the volume of the ischemic core (cortex with CBF of less than 25 ml/100 g/min) and accompanying edema by approximately 50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50-75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20-30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.     

Whole brain CT perfusion combined with CT angiography in patients with subarachnoid hemorrhage and cerebral vasospasm

Objective

To assess cerebral vasospasm (CVS) and monitor cerebral microcirculatory changes in patients with acute subarachnoid hemorrhage (SAH) via CT angiography (CTA) combined with whole-brain CT perfusion (CTP) techniques.

Methods

Sixty patients with SAH (SAH group) and 10 patients without SAH (control group) were selected for a prospective study. CTP combined with CTA and digital subtraction angiography (DSA) studies were performed on patients with initial onset of SAH less than three days. CTA and DSA as well as the CTP parameters such as cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT), and time-to-peak (TTP) were acquired and analyzed. The relationship of CTA and CTP measurements was assessed in these acute SAH patients.

Results

CTP techniques were used to achieve the perfusion maps of the whole brain in patients with acute SAH. Compared to the control group, mean CBF value was significantly lower while both MTT and TTP values were significantly higher in SAH group (all p < 0.05). Further analysis revealed that mean CBF in patients with CVS, sCVS, Fisher III–IV and Hunt–Hess III–V significantly decreased when compared to patients with nCVS, asCVS, Fisher I–II and Hunt–Hess I–II (p < 0.05). Furthermore both MTT and TTP values were also significantly reduced in patient with CVS, sCVS, Fisher III–IV and Hunt–Hess III–V (p < 0.05).

Conclusion

The study demonstrated that changes of microcirculation in patients with SAH could be assessed by whole-brain CTP. CTP combined with CTA could detect both macroscopic evident vasospasm on CTA and alterations of microcirculation on CTP. Mean CBF was significantly lower in patients with SAH.     

诱导升压对动脉瘤性蛛网膜下腔出血患者脑血流量的影响

目的本文旨在探讨对于动脉瘤性蛛网膜下腔出血患者,诱导升压对其脑血流量的影响。方法选取2015年1月至2018年12月在我院就诊的诊断为动脉瘤性蛛网膜下腔出血的患者,随机分为诱导组和对照组。分别对两组患者实行诱导升压以及无诱导操作,在24～36小时后,评估两组患者的脑血流量(CBF),同时评估两组患者的动脉血压。结果共有24名患者被纳入到本研究中,对照组和诱导组的临床资料无统计学的差异。在本研究中,在CTP1和CTP2两个时间点之间,诱导组患者的平均动脉血压为12 mmHg(95%置信区间,8.7～14.8 mm Hg),高于对照组。诱导组的所有患者在CTP2时间点时,仍然能够耐受诱导血压的升高。诱导组患者的总CBF变化为0.1(-31～43) ml/100g/min,而对照组为-8.3(-41～30) ml/100g/min,差异没有显著的统计学意义(P=0.24)。结论诱导升压对于动脉瘤性蛛网膜下腔出血患者的脑血流量无显著的统计学影响。     

Influence of body position on tissue-pO2, cerebral perfusion pressure and intracranial pressure in patients with acute brain injury

Abstract

ft is a common practice to position head-injured patients in bed with the head elevated above the level of the heart in order to reduce intracranial pressure OCP). This practice has been in vivid discussion since some authors argue a horizontal body position will increase the cerebral perfusion pressure (CPP) and therefore improve cerebral blood flow (CBF). However, ICP is generally significantly higher in the horizontal position. The aim of this study was to evaluate changes in regional microcirculation using tissue pO ² (ti-p0₂), as well as changes in cerebral perfusion pressure (CPP) and intracranial pressure induced by changes in body position in patients with head injury. The effect of 0° and 30° head elevation on ti-p0₂, CPp, ICP and arterial blood pressure (MABP) was studied in 22 head injured patients during day 0-12 after trauma. The mean ICP was significantly lower at 30° head elevation than at 00 (74.1 + 8.6 vs. 19.9+8.3 mmHg). While MABP was unaffected by head elevation, CPP was slightly higher at 300 than at 0° (76.5+ -13.5 vs. 71.5+ 13.2 mmHg). However, regional ti-p0₂ was unaffected by body position (30° vs. 0°: 24.9+73.1 vs. 24.7 + 12.9 mmHg). fn add~tion, there was no change in the time course after trauma concerning these findings in the individLfal pati,ents. The data indicate that a moderate head elevation of 300 reduces ICP without jeopardizing regional cerebral microcirculation as monitored using a polarographic ti-p0₂ microcatheter. [Neural Res 1997; 19: 249-253]     

Evaluation of cerebral autoregulation following diffuse brain injury in rats

Abstract

The normal cerebral circulation has the ability to maintain a stable cerebral blood flow over a wide range of cerebral perfusion p(essures and this is known as cerebral autoregulation. This autoregulation may be impaired in the injured brain. Closed head injury was induced in 28 Sprague-Dawley rats weighing 400-450 g. Four groups were studied: control group, head injured rat from meter height using 350 g, 400 g and 450 g respectively. CBF, volume velocity was monitored using laser-Doppler flowmetry together with monitoring of ICP and arterial blood pressure. Correlation to assess the relationship between CBF and CPP was done in each animal every hour. If correlation coefficient was> 0.85 and CPP was within normal range, loss of autoregulation was hypothesized. Chi square test, ANOVA test and unpaired Studen(s t-test were done and significant level of p < 0.05 was established. Mean CBF in injured rats was significantly lower than controls (p = 0.028) at the fifth hour. CBV was lower in the group of 450 g 1 m impact than in controls at 3 h (p = 0.04). Velocity in the group ofall injured rats, was significantly lower than in controls at 3 h (p = 0.032) and at 4 h (p = 0.027). Loss ofautoregulation was seen during first four hours after trauma in all groups of rats who sustained injury. Statistical significant difference (p = 0.041) in loss of autoregulation between injured and control animals was seen. No loss of autoregulation was observed in the control group. In conclusion CBF and CPP provide information about loss of autoregulation in diffuse brain injury. Decrease in CBF and increase of ICP is observed as a result ofloss of cerebral autoregulation. Knowledge of loss of autoregulation could give important information and help in the management of head injured patients. [Neural Res 1997; 19: 393-402]     

Increased cerebral blood flow is correlated with neurocognitive impairment in long-term hemodialysis patients: an arterial spin labeling MRI study

The purpose of this study was to investigate cerebral blood flow (CBF) changes in hemodialysis patients with arterial spin labeling (ASL) and to correlate these changes with clinical risk factors and neurocognitive function. Thirty-two hemodialysis patients and 35 age-, sex-, and education-matched healthy controls (HCs) were recruited in this prospective study. The Mini-Mental State Examination (MMSE) was performed to evaluate neurocognitive function. Pulsed ASL was performed to measure CBF. Two independent sample t-test was used to explore the CBF difference between the patients and HCs. Multiple stepwise regression was used to investigate the risk factors for CBF in patients. Correlation analysis was used to explore the relationship between the MMSE scores and CBF changes with and without adjusting for anemia status. Compared to HCs, the hemodialysis patients showed significantly increased CBF in some neurocognition-related cerebral regions (all P < 0.001, Bonferroni corrected). Increased CBF in the right opercular and triangular part of the inferior frontal gyrus correlated with the poorer MMSE scores (r = -0.502, P = 0.004; r = -0.423, P = 0.018, FDR corrected) and these correlations still remained after adjusting for anemia status (r = -0.516, P = 0.005; r = -0.439, P = 0.019, FDR corrected). The increased dialysis duration, and decreased hemoglobin, hematocrit, and serum phosphorus were predictive risk factors for increased CBF (P < 0.05). In conclusion, long-term hemodialysis patients had increased CBF, which correlated with neurocognitive impairment, and after adjusting for the effect of anemia, the correlation still remained.

     

Regional cerebral blood flow in man at rest and during exercise

Summary Regional cerebral blood flow (rCBF) of the left hemisphere was measured in 12 healthy young men at rest and during physical work on a bicycle ergometer in the supine position at work-load levels of 25 W or 100 W using the intravenous ¹³³Xe method. Regional mean cerebral blood flow, regional gray-matter flow, and relative gray-matter weight was determined for six regions of interest. Arterial blood pressure, pulse frequency and expiratory CO₂ concentration were recorded. Cerebral blood flow in all regions was significantly (P<0.001) higher during exercise than at rest. The increase in the 100 W group (24.7%) was significantly (P<0.05) greater than in the 25 W group (13.5%), but resting blood flow levels and alveolar CO₂ concentrations were also different in both groups. Mean arterial blood pressure, pulse frequency and alveolar CO₂ concentrations, but not arterial pCO₂, were significantly higher during exercise and there was a faster washout of whole-body xenon. The CBF increase was interpreted as a combined effect of elevated systemic blood pressure and functionally activated brain metabolism. There was no evidence of impaired cerebral autoregulation.