Impaired cerebral circulation and the effect of glycerol infusion in the acute stage of hypertensive intracerebral hematoma

The purpose of the present study was to clarify the mechanism of reduction in cerebral blood flow (CBF) in the acute stage of hypertensive intracerebral hematoma and the effect of glycerol infusion on the reduced CBF. We examined 55 cases. Thirty-eight cases showed putaminal hematoma and 17 presented thalamic hematoma. The range of consciousness was from alert to stupor. CBF was measured by single photon emission CT with Xe-133 inhalation within five days after the onset of the hemorrhage. A CBF map was obtained at a slice 5 cm above the OM-line and mean CBF of the affected and non-affected hemispheres was calculated. In 20 of 55 cases, 500 ml of glycerol was intravenously infused for 60 minutes and thereafter CBF was measured again. Epidural pressure was also recorded at the affected frontal area during glycerol infusion in three of the 20 cases. CBF reduced more profoundly in the area around the hematoma on the CBF map. Mean CBF of the affected hemisphere was negatively correlated with the volume of hematoma by a quadratic regression. After glycerol infusion, 13 of 20 cases showed a significant increase in mean CBF of the affected hemisphere, while the other seven cases showed no increase. Mean CBF increased with a higher percentage in cases with ventricular hemorrhage than without ventricular hemorrhage. In three cases where epidural pressure was measured during glycerol infusion, mean CBF increased and epidural pressure decreased. The increase in mean CBF was proportional to a rise in perfusion pressure calculated as pressure difference between mean systemic arterial pressure and mean epidural pressure, indicating impaired autoregulation in these cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

Progressive lacunar infarction with demonstrated patency of the middle cerebral artery

Two cases of progressive hemiplegia were closely followed by daily clinical examination. In both, the CT scan and CSF were normal on admission. In both, objective aggravation occurred in three or more steps over four days, progressing from minor finger clumsiness to total paralysis of the arm. In both cases a second CT scan a day after appearance of hemiplegia demonstrated a lacune in the corona radiata just above the internal capsule. In one case an intravenous digital subtraction angiogram demonstrated patency of the middle cerebral artery during the course of the progression. In the other case, serial study with transcranial Doppler ultrasound documented the continued patency of the middle cerebral artery. These two cases demonstrate that it is not necessary to postulate transient occlusion of the middle cerebral artery as an essential mechanism for progressive lacunar infarction.     

Glycerol attenuates the adherence of leukocytes in rat pial venules after transient middle cerebral artery occlusion

Intravenous infusion of glycerol has been used in patients with a cerebral infarction, expecting improvement in brain edema and cerebral blood flow (CBF). However, the mechanism of the improvement of CBF has not been clearly demonstrated. The aim of this study in the rat pial microvasculature after transient middle cerebral artery occlusion (MCAO) is to examine the effects of glycerol on leukocyte-endothelium interaction, which plays a critical role in the pathogenesis of brain injury by ischemia/reperfusion and concerns induction of secondary brain damage. Rhodamine 6G-labeled leukocytes at the brain surface were visualized with intra-vital fluorescence videomicroscopy through a closed cranial window and an analysis was made of the number of adherent leukocytes and the centerline leukocyte velocity in the venule before MCAO, after reperfusion of MCAO and after infusion of glycerol (Group 1) or saline (Group 2). The number of adherent leukocytes decreased and the centerline leukocyte velocity increased statistically significantly immediately after the infusion of glycerol in Group 1, but there was no significant change in Group 2. The infusion of glycerol washes away the adherent leukocytes and prevents them from interfering with the blood cell and plasma flow. Furthermore, secondary brain damage may be relieved by decreasing the adherence of leukocytes. In conclusion, modulating the adherence of leukocytes is one of the important factors in the neuroprotective effect of glycerol.     

TMB—8对脑缺血大鼠脑血流量的作用

目的 研究8－（N，N－二乙胺）－n－辛基－3，4，5－三甲氧基苯甲酸酯（TMB－8）对局灶性脑缺血大鼠脑血流量（CBF）的作用。方法 用激光多谱勒血流仪测量大脑中动脉阻断（MCAO）大鼠脑血流量。分别于阻断前30分钟和阻断后20分钟给予TMB－8进行干预。结果 MCAO后，CBF迅速下降，维持恒定。阻断前30分钟给予TMB－8 0．5、1和2mg/kg，可剂量依赖性抑制CBF下降，阻断后20分钟给予TMB－8 1mg/kg，也能明显增加CBF。结论 TMB－8能预防和治疗MCAO局灶性脑缺血大鼠CBF减少，改善缺血区血供。     

Bi-hemispheric CBF and its CO2 reactivity of TIAs and completed strokes in ICA occlusions

Bi-hemispheric cerebral blood flow (CBF) measurements during rest and hyperventilation, with intra-arterial 133Xe injection method, were investigated in 19 cases, angiographically diagnosed as unilateral internal carotid artery (ICA) occlusion, including 8 cases with TIAs and 11 cases with completed strokes as the onset. Indices of cerebral vascular resistance and CO2 reactivity with decreasing arterial PCO2 were also investigated. A significant decrease (P less than 0.05) of hemispheric mean CBF was noted in the ischemic hemisphere, but normal flow values in the unaffected hemisphere and preserved CO2 responsiveness during hyperventilation were observed in both the affected and unaffected hemispheres in patients with TIAs. Moreover, a direct relationship between CBF and blood pressure, observed in 11 cases with completed strokes, was not recognized in 8 cases with TIAs. A degree of the abnormalities of the affected hemisphere in cerebral circulation was suggested to be somewhat different between TIAs and completed strokes in ICA occlusions, and bi-hemispheric CBF measurements would be an useful method for evaluating the various indices of the CBF in ICA occlusions.     

Effect of the kappa-1 opioid agonist CI-977 on ischemic brain damage and cerebral blood flow after middle cerebral artery occlusion in the rat

The effects of the kappa-1 opioid agonist CI-977 upon the volume of ischemic brain damage (defined using quantitative neuropathology) and local cerebral blood flow (CBF) (defined using quantitative [¹⁴C]iodoantipyrine autoradiography) have been examined at 4 h and 30 min, respectively, after permanent middle cerebral artery (MCA) occlusion in halothane-anesthetised rats. Treatment with CI-977 (0.3 mg/kg, s.c.) 30 min before and 30 min after occlusion of the MCA reduced the volume of infarction in the cerebral hemisphere (reduced by 27% when compared to vehicle;P<0.05) and cerebral cortex (reduced by 32%;P<0.05), despite a marked and sustained hypotension, with only minimal effect on damage in the caudate nucleus. In the hemisphere contralateral to the occluded MCA, treatment with CI-977 (0.3 mg/kg, s.c.) 30 min prior to the induction of ischemia failed to demonstrate any significant effect on either the level of local CBF in any of the 25 regions examined or on the volume of low CBF determined by frequency distribution analysis. In the hemisphere ipsilateral to MCA occlusion, CI-977 failed to produce statistically significant alterations in either the level of local CBF in 23 of the 25 regions or on the volume of low CBF, but areas of hyperemia were observed in both the medial caudate nucleus and lateral thalamus (local CBF increased by 65% and 86%, respectively, when compared to vehicle). The results of the present study indicate that the kappa-1 opioid agonist CI-977 is neuroprotective in a rat model of focal cerebral ischemia where key physiological variables have been assessed throughout the entire post-ischemic period, and fail to demonstrate that the neuroprotective effects of CI-977 in this model are due to improved blood flow to ischemic tissue.     

Regional cerebral blood flow in the acute stage with ischemic cerebrovascular disease studied by xenon-133 inhalation and single photon emission computerized tomography

The papers about cerebral blood flow (CBF) in patients with cerebrovascular diseases have been already reported by positron emission computerized tomography (PET), single photon emission computerized tomography (SPECT), Xray CT (CT) using cold Xe, and so on. However the literature about the CBF changes in acute stage is few. We studied CBF in 68 patients with ischemic cerebrovascular disease within 48 hours after the onsets from February 1984 through February 1985. CBF was measured by a rapidly rotating single photon emission computerized tomography (SPECT) using non-invasive Xenon-133 inhalation method. Our subjects included 51 cases with cerebral infarction (male 37, female 14, average 62.9 years) and 17 cases with TIA (male 13, female 4, average 60.5 years), the patients who had a past history of stroke were excluded from the subjects. The SPECT was performed with use of Tomomatic 64 developed by Dr. Lassen, et al, SPECT and carotid arteriography were simultaneously performed within 48 hours in all cases. CT we used were GE CT 9800 scanner and Hitachi HF CT. The following results have been obtained: 1) SPECT clearly showed an ischemic focus correlated with clinical symptom after the attack rather than CT, the positive finding by SPECT was 92.2% and that by CT was 62.7% within 48 hours after the onset. 2) The remote effect phenomenon so-called crossed cerebellar diaschisis was demonstrated in 7 of 14 cases (50%) with cerebral infarction due to internal carotid artery occlusion and in 9 of 26 cases (34.6%) with that due to middle cerebral artery occlusion. 3) SPECT and CT were performed within 8 hours after the onset in 20 cases with cerebral infarction. SPECT showed decreased CBF in all cases whereas the positive finding by CT was 40.0%. The area of decreased CBF was always larger than the low density area that CT demonstrated. Mean CBF value of the cerebral hemisphere in the cases with ICA occlusion within 8 hours after the onsets was 31.0 (ml/100 g/min), and that of MCA occlusion was 36.0 (ml/100 g/min), and that of MCA occlusion was 36.0 (ml/100 g/min). 4) The positive finding by SPECT on TIA cases was 47% and that by CT was 41.1%, SPECT usually did not demonstrate a small ischemic focus especially at the deep region (ie, basal ganglia region). 5) SPECT using Xe-123 inhalation was useful and non-invasive method for the diagnosis in acute stage with ischemic cerebrovascular disease.(ABSTRACT TRUNCATED AT 400 WORDS)     

Glycerol attenuates the adherence of leukocytes in rat pial venules after transient middle cerebral artery occlusion

Abstract

Intravenous infusion of glycerol has been used in patients with a cerebral infarction, expecting improvement in brain edema and cerebral blood flow (CBF). However, the mechanism of the improvement of CBF has not been clearly demonstrated. The aim of this study in the rat pial microvasculature after transient middle cerebral artery occlusion (MCAO) is to examine the effects of glycerol on leukocyte- endothelium interaction, which plays a critical role in the pathogenesis of brain injury by ischemia/ reperfusion and concerns induction of secondary brain damage. Rhodamine 6G-labeled leukocytes at the brain surface were visualized with intra-vital fluorescence videomicroscopy through a closed cranial window and an analysis was made of the number of adherent leukocytes and the centerline leukocyte velocity in the venule before MCAO, after reperfusion of MCAO and after infusion of glycerol (Croup 1) or saline (Croup 2). The number of adherent leukocytes decreased and the centerline leukocyte velocity increased statistically significantly immediately after the infusion of glycerol in Croup I, but there was no significant change in Croup 2. The infusion of glycerol washes away the adherent leukocytes and prevents them from interfering with the blood cell and plasma flow. Furthermore, secondary brain damage may be relieved by decreasing the adherence of leukocytes. In conclusion, modulating the adherence of leukocytes is one of the important factors in the neuroprotective effect of glycerol. [Neurol Res 1999; 21: 785-790]     

Pathophysiological study of corona radiata infarcts by clinically available diagnostic methods

The authors evaluated 18 patients who presented with corona radiata infarction, one of the 'water-shed infarctions', on CT and/or MRI to determine its etiology and pathophysiology using cerebral angiography, single-photon emission computed tomography (SPECT), and tests of hemostatic function including hematocrit, platelet aggregation and adhesiveness. On angiography, 8 of these 18 patients had ulcerative lesions in the common carotid artery bifurcation with or without minimal stenosis and exhibited no or a minimal area of hypoperfusion localized to the corona radiata on SPECT. In these, microembolism from the lesions at the common carotid bifurcation seemed play an important role in the genesis of corona radiata infarction. In 7 of the remaining 10 patients, cerebral angiography showed occlusive lesions of the internal carotid artery around its origin in 3, more than 90% stenosis of the internal carotid artery in 1, severe stenosis of the M1 segment of the middle cerebral artery in 2, and M1 occlusion in 1. In 5 of these 7, SPECT demonstrated a larger area of hypoperfusion than the corona radiata in the involved hemisphere. In the remaining 2, SPECT demonstrated a hypoperfusion area localized to the corona radiata. In all 7, the hematocrit was elevated. A collateral blood supply was visualized in 5 of 7 on cerebral angiography. In these 7 patients, hemodynamic disturbance was considered to contribute to the pathogenesis of infarction in the corona radiata. In the final three patients, cerebral angiography showed significant occlusive lesions in the main trunk of the cerebral arteries.(ABSTRACT TRUNCATED AT 250 WORDS)     

Blood flow velocities of cerebral arteries in lacunar infarction and other ischemic strokes

Blood flow velocity is an important determinant of vascular hemodynamics. The aim of the present study was to determine the mean flow velocities (MFVs) of cerebral arteries in patients with ischemic stroke, comparing lacunar and nonlacunar infarctions. 388 consecutive patients were examined for lacunar infarction, other subtypes of ischemic stroke, and the presence of underlying internal carotid artery steno-occlusion (ICS). MFVs were measured using transcranial Doppler along the full segments of each cerebral artery including both right and left middle cerebral arteries, basilar artery, and both of the vertebral arteries. The patients were categorized into two major groups: lacunar infarction, and nonlacunar infarction with or without underlying ICS. The characteristics of patients with lacunar infarction (n=83, 21.4%) were significantly different from those with nonlacunar infarctions: younger age, lower prevalence of type 2 diabetes, and lower concentration of plasma total homocysteine. The patients with lacunar infarction had lower MFVs in cerebral arteries than the patients with nonlacunar infarctions, especially in the posterior circulation vessels such as the basilar artery and both vertebral arteries. Different hemodynamics might be pathophysiologically associated with the lacunar infarction, compared with the other subtypes of ischemic stroke.     

Fenofibrate improves cerebral blood flow after middle cerebral artery occlusion in mice

Fibrates, one group of peroxisome proliferator-activated receptor (PPAR) activators, are lipid lowering drugs. Fibrates have been shown to attenuate brain tissue injury after focal cerebral ischemia. In this study, we investigated the impact of fenofibrate on cerebral blood flow (CBF) in male wild type and PPARα-null mice. Animals were treated for 7 days with fenofibrate and subjected to 2 h of filamentous middle cerebral artery occlusion and reperfusion under isoflurane anesthesia. Cortical surface CBF was measured by laser speckle imaging. Regional CBF (rCBF) in nonischemic animals was measured by ¹⁴C-iodoantipyrine autoradiography. Fenofibrate did not affect rCBF and mean arterial blood pressure in nonischemic animals. In ischemic animals, laser speckle imaging showed delayed expansions of ischemic area, which was attenuated by fenofibrate. Fenofibrate also enhanced CBF recovery after reperfusion. However, such effects of fenofibrate on CBF in the ischemic brain were not observed in PPARα-null mice. These findings show that fenofibrate improves CBF in the ischemic hemisphere. Moreover, fenofibrate requires PPARα expression for the cerebrovascular protective effects in the ischemic brain.     

Early ischemic lesion demonstrated by ictal diffusion-weighted MRI during prior TIA in a patient with cerebral infarction]

We reported a patient with transient ischemic attack (TIA), subsequently evolving to a cerebral infarction, in whom ictal diffusion-weighted magnetic resonance imaging (MRI) detected early ischemic lesion in the left hemisphere. The patient was a 30-year-old right-handed male medical doctor, who had an in-hospital episode of TIA with obtundation and right hemiparesis, which lasted for 150 minutes. Ictal diffusion-weighted MRI obtained 110 minutes after symptom onset demonstrated an area of high signal intensity in the left striatum and corona radiata, whereas T 2-weighted and FLAIR images were entirely normal. Ictal magnetic resonance angiography (MRA) showed occlusive lesions in the M 2 branches of the left middle cerebral artery. The second MRA obtained 90 minutes after resolution of the symptoms showed nearly complete recanalization of the left middle cerebral artery, suggesting that the TIA was embolic mechanism. However the patient rapidly developed similar neurological symptoms again 58.5 hours after the TIA episode, evolving finally to a completed stroke. A brain CT obtained 1 hour after the second episode demonstrated diffuse hypodense lesions in the left basal ganglia and corona radiata, and in the left temporal lobe. MRIs 3 and 7 days later displayed completed infarcts, of which distribution was consistent with that of the hypodense lesions on the earlier CT. The left middle cerebral artery remained patent on the follow-up MRAs. The patient fairly recovered and returned to his premorbid position as medical doctor with a mild residual right hand clumsiness. In this patient, ictal and post-ictal MRAs documented an occlusion and a reopening of the middle cerebral artery. The embolic mechanism remains unknown despite detailed cardiac, vascular, and hematological examinations. In addition to recurrent embolism, we would like to point out that the reperfusion injury, secondary delayed neuronal death, and other factors may be involved in the second exacerbation evolving to the completed stroke.     

Time course of cerebral blood flow and histological outcome after focal cerebral ischemia in rats.

BACKGROUND AND PURPOSE: The relation between time-dependent changes in cerebral blood flow and the appearance of infarction after focal cerebral ischemia is still a matter for debate. The aim of this study was to measure perfusion after simultaneous occlusions of the left middle cerebral artery and ipsilateral common carotid artery in rats and correlate it with the timing and distribution of histological changes. METHODS: We studied histological and cerebral blood flow changes 5 minutes and 4, 24, and 48 hours after the onset of focal ischemia. Blood flow was determined autoradiographically using [14C]iodoantipyrine. A coronal template subdivided into regions of interest was applied to the autoradiographs and the histological data. RESULTS: In some regions of the nonoccluded hemisphere, cerebral blood flow 5 minutes after occlusion fell below 50% of normal. Many ischemic structures showed stable blood flow for 48 hours after occlusion, confirming that in this model reperfusion is minimal. Infarction occurred eventually in all areas in which blood flow at 5 minutes fell below 10% of that in control rats, but infarction appeared earlier in regions in which blood flow at 5 minutes was below 5% of that in control rats. When blood flow at 5 minutes rose above 12% of that in control rats, the occurrence of infarction became unpredictable. CONCLUSIONS: Despite the general dependence of infarction on perfusion levels, blood flow was not a reliable indicator of those regions committed to infarction.     

Effect of the NMDA antagonist MK-801 on local cerebral blood flow in focal cerebral ischaemia in the rat

The effects of MK-801 upon local CBF after permanent middle cerebral artery (MCA) occlusion have been examined using [14C]iodoantipyrine autoradiography in halothane-anaesthetised rats. MK-801 (0.5 mg kg-1 i.v.) or saline was administered 30 min before MCA occlusion and CBF measured approximately 40 min after occlusion. In the hemisphere contralateral to the occluded MCA, MK-801 significantly reduced local CBF in 19 of the 22 regions examined from the levels in saline-treated rats. In the contralateral hemisphere, after treatment with MK-801, blood flow was reduced by an average of 37% with little variation in the magnitude of the reductions in different regions. In the hemisphere ipsilateral to MCA occlusion, MK-801 reduced CBF in almost every region located outside the territory of the occluded MCA. Within the territory of the occluded MCA, blood flow in the MK-801-treated rat did not significantly differ from values in vehicle-treated rats in any of the five cortical areas examined, although in the caudate nucleus there was a tendency for CBF to be lower in rats pretreated with MK-801. MK-801 had no effect on the amount of hypoperfused cerebral tissue (CBF less than 30 ml 100 g-1 min-1) in the ipsilateral hemisphere at any coronal plane examined; e.g., at coronal plane anterior 7.2 mm, 51 +/- 5% of the hemisphere displayed CBF of less than 30 ml 100 g-1 min-1 in saline-treated rats with MCA occlusion compared with 52 +/- 8% of the hemisphere in rats treated with MK-801 prior to MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bi-hemispheric CBF and Its CO2 Reactivity of TIAs and Completed Strokes in ICA Occlusions

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Bi-hemispheric cerebral blood flow (CBF) measurements during rest and hyperventilation, with intra-arteria1 ¹³³Xe injection method, were investigated in 19 cases, angiographically diagnosed as unilateral internal carotid artery (ICA) occlusion, including 8 cases with TIAs and 11 cases with completed strokes as the onset. Indices of cerebral vascular resistance and CO₂ reactivity with decreasing arterial\PCO₂ were also investigated.

A significant decrease (P < 0.05) of hemispheric mean CBF was noted in the ischemic hemisphere, but normal flow values in the unaffected hemisphere and preserved CO₂ responsiveness during hyperventilation were observed in both the affected and unaffected hemispheres in patients with TIAs. Moreover, a direct relationship between CBF and blood pressure, observed in 11 cases with completed strokes, was not recognized in 8 cases with TIAs.

A degree of the abnormalities of the affected hemisphere in cerebral circulation was suggested to be somewhat different between TIAs and completed strokes in ICA occlusions, and bi-hemispheric CBF measurements would be an useful method for evaluating the various indices of the CBF in ICA occlusions.     

Effect of perfluorochemicals on experimental cerebral ischemia

It has been noted that perfluorochemicals (PFC) which were developed as artificial blood substitutes, protect against ischemic brain injury by their ability to serve as oxygen carriers. It is also known that normovolemic hemodilution (HD) improves cerebral blood flow (CBF) and neurological symptoms in cerebral infarction. However, there are few reports concerning the effect of PFC on the collateral circulation via pial anastomoses in cases of middle cerebral artery (MCA) occlusion. The ability to record the pial arterial blood pressure (PAP) without interfering blood flow now makes it possible to measure the segmental resistance of cerebral vessels. By using this method, one can measure collateral vessel resistance through pial anastomoses following MCA occlusion. In this paper, we studied the protective effects of PFC combined with HD on ischemic brain injury with the focus on the collateral circulation via pial anastomoses following occlusion of the MCA. Twenty adult cats were studied: control, 8; HD, 5; Fluosol (Fluosol-DA), 7. The systemic arterial pressure (SAP) and PeCO2 were continuously monitored. Subsequently the MCA was occluded via the transorbital approach. CBF in the ectosylvian gyrus (central area of the ischemic lesion) was measured by the hydrogen clearance method. A small pial artery about 100 microns in diameter on the exposed ectosylvian gyrus was punctured nonocclusively with a micropipette filled with 2 M sodium chloride which was connected to a servo-null micropressure system (Model 900, W-P Instruments, Inc. U.S.A.). The electroencephalogram (EEG) was recorded from the ectosylvian gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Focal cerebral ischemia in the rat: topography of hemodynamic and histopathological changes

We studied local cerebral blood flow, as measured by autoradiography with digital image processing and by tissue morphology, in six rats 4 hours after occlusion of the proximal middle cerebral artery. A consistent, three-dimensional pattern of graded reductions in local cerebral blood flow involved the affected hemisphere, with a densely ischemic zone (local cerebral blood flow less than 3 ml/100 gm/min) in the dorsolateral caudate putamen and the adjacent frontoparietal cortex. In the frontoparietal cortex, the normal laminar pattern of local cerebral blood flow was disrupted, and there was a transcortical gradient in flow, with pronounced ischemia in deeper layers and relatively preserved superficial flow. Comparisons of autoradiographic findings with histopathological abnormalities in adjacent frozen sections showed that the region of ischemic damage corresponded closely with the area of greatest reduction in blood flow. Although around this region local cerebral blood flow increased centrifugally, a striking finding was that flow density changed abruptly (a tenfold variation in flow within a 1 to 2 mm interval) at the edge of the pathological lesion. Penumbral conditions may therefore exist in only a very narrow zone 4 hours after onset of focal ischemia. After occlusion of a major cerebral artery, the pattern of local cerebral blood flow changes appears to depend on interactions among vascular architecture, reductions in perfusion pressure, alterations in metabolic demands, and variations in local vascular resistance.     

利用激光散斑成像技术观察尤瑞克林对脑梗死大鼠脑血流的影响

目的 利用激光散斑成像技术研究尤瑞克林对大鼠脑梗死后局部脑血流的影响.方法 成年雄性SD大鼠24只,线栓法制备大鼠永久性大脑中动脉梗死模型.激光散斑成像系统观测缺血半球皮质及大脑中动脉供血区血流,2,3,5-三苯基氯化四氮唑(TTC)染色法测定脑梗死体积,并进行神经功能评分.结果 皮质及大脑中动脉供血区血流在大剂量组第1天及第2天给药后均有明显改善,部分大脑皮质血管增粗,血流速度加快,小剂量组及生理盐水组无明显变化,脑缺血48 h后,大、小剂量尤瑞克林组及生理盐水组的梗死体积分别为10.14%±3.02%,25.99%±3.90%,27.10%±3.32%,大剂量组与生理盐水组比较差异有统计学意义(F=61.14,P<0.01),小剂量组与生理盐水组比较差异无统计学意义.缺血后4 h,大剂量组神经功能损伤明显改善,小剂量组及生理盐水组无明显改变,36 h各组间的神经功能评分差异无统计学意义.结论 尤瑞克林可以减少大鼠局灶性脑缺血后梗死体积,延缓神经功能损伤,其作用可能与促进侧支循环的开放,增加大脑皮质和缺血区血流有关.     

No intracerebral steal phenomenon in the ischemic brain following papaverine administration

The steal phenomenon due to a vasodilator was investigated in 6 cats in which cerebral ischemia had been produced by left middle cerebral artery (MCA) occlusion. The photoelectric method was employed for continuous recording of the cerebral blood volume together with frequent determinations of the cerebral blood flow (CBF) through the ischemic cerebral tissue at the following four stages: before MCA occlusion, 2 hours after MCA occlusion before the injection of papaverine, after the injection of papaverine, and when the systemic arterial blood pressure (SABP) was adjusted non-pharmacologically to the control level using a "vasculator". The administration of the vasodilator produced conflicting results for the CBF changes in the ischemic area with a decrease in SABP as reported previously in the literature. However, when the SABP was corrected to the control level, the CBF in the ischemic region became increased in all 6 cases to above the control ischemic flow values. It is concluded that the decreased CBF in the ischemic tissue after vasodilator administration was not due to the steal phenomenon, but simply to a fall in SABP.     

Regional cerebral blood flow, diaschisis, and steal after stroke

Regional CBF was measured by 133Xe inhalation in unilateral cerebral infarction, carotid TIAs, and normal volunteers. Regional CBF values were bilaterally and symmetrically reduced in patients measured within 3 weeks after stroke. Later, rCBF values returned toward normal in the contralateral hemisphere of patients with infarction and in both hemispheres with carotid TIAs. In cases with carotid occlusive disease, flow reduction was seen in the contralateral posterior cerebral artery distribution, with hyperemia in ipsilateral occipital lobe caused by interhemispheric steal. Brainstem-cerebellar flow values were increased following acute cerebral infarction if patients were alert but reduced if consciousness was impaired.