Cerebral blood flow and CO2 reactivity in transient ischemic attacks: comparison between TIAs due to the ICA occlusion and ICA mild stenosis

Hemispheric mean cerebral blood flow (CBF), together with its CO2 reactivity in response to hyperventilation, was investigated in 18 patients with transient ischemic attacks (TIAs) by intraarterial 133Xe injection method in a subacute-chronic stage of the clinical course. In 8 patients, the lesion responsible for symptoms was regarded as unilateral internal carotid artery (ICA) occlusion, and in 10 patients, it was regarded as unilateral ICA mild stenosis (less than 50% stenosis in diameter). Resting flow values were significantly (P less than 0.05) decreased in the affected hemisphere of TIA due to the ICA occlusion as compared with the unaffected hemisphere of the same patient, regarded as the relative control. It was not decreased in the affected hemisphere of TIA due to the ICA mild stenosis as compared with the control. With respect to the responsiveness of CBF to changes in PaCO2, it was preserved in both TIAs, due to the ICA occlusion and ICA mild stenosis. Vasoparalysis was not observed in either types of TIAs in the subacute-chronic stage. However, in the relationship of blood pressure and CO2 reactivity, expressed as delta CBF(%)/delta PaCO2, pressure-dependent CO2 reactivity as a group was observed with significance (P less than 0.05) in 8 cases of TIA due to the ICA occlusion, while no such relationship was noted in 10 cases of TIA due to the ICA mild stenosis. Moreover, clinical features were different between TIAs due to the ICA occlusion and ICA mild stenosis, i.e., more typical, repeatable TIA (6.3 +/- 3.7 times) with shorter duration (less than 30 minutes) was observed in TIAs due to the ICA mild stenosis, while more prolonged, less repeatable TIA (2.4 +/- 1.4 times) was observed in TIAs due to fixed obstruction of the ICA. From these observations, two different possible mechanisms as to the pathogenesis of TIA might be expected, e.g., TIA of microembolic origin due to the ICA mild stenosis, and TIA of hemodynamic origin due to fixed obstruction of the ICA, for whom the bypass surgery might be beneficial, i.e., all TIAs are not based on the same mechanism.     

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.     

Does NO regulate the cerebral blood flow response in hypoxia?

Objectives –To study whether nitric oxide (NO) affects the CBF response to hypoxic and carbon monoxide (CO) hypoxia. Material and methods – We incrementally reduced arterial oxygen content in rats, by decreasing the concentration of inspired oxygen (20 rats) or by repeated CO inhalation (20 rats), and measured local CBF using the hydrogen clearance method. Ten animals of each group received 80 mg/kg NO synthase (NOS) inhibitor N-monomethyl-L-arginine intravenously prior to hypoxia, while 10 rats served as controls. Results – Inhibition of NOS decreased mean CBF by 30% and increased cerebrovascular resistance by 70%. Under hypoxic hypoxia, mean oxygen reactivity of CBF (relative change of CBF to a change of arterial oxygen content) was 7.8%/vol% in control animals and 3.3%/vol% after NOS inhibition ( P < 0.02). Under CO hypoxia, mean oxygen reactivity was 7.3%/vol% in control animals and 5.1%/vol% after NOS inhibition ( P < 0.05). Inhibition of NOS diminished significantly the cerebral vasodilatory response during hypoxic hypoxia ( P < 0.05) but only to a lesser extent during CO hypoxia. Conclusion – These observations suggest that NO is involved in cerebral oxygen vasoreactivity, particularly in severe hypoxia.     

Cerebrovascular CO2 reactivity in patients with dementia due to multiple infarction in the territory of the perforating artery]

In order to clarify the pathophysiology of dementia due to multiple infarction in the territory of the perforating artery, the reactivity of cerebral vessels to increased carbon dioxide tension was examined in patients with multiple cerebral infarction with or without dementia. The subjects studied were 11 patients with multi-infarct dementia (MID) (age 57-82 years old, mean +/- S.D. 72 +/- 8) and 16 patients with multiple infarction without dementia (MI) (age 51-81 years old, mean +/- S.D. 69 +/- 9). The diagnosis of cerebral infarction was based on the clinical signs and symptoms and findings of magnetic resonance imaging (MRI). Only patients with cerebral infarction located in the perforator territories were included in this study. Dementia was diagnosed by DSM-IIIR criteria. The extent of periventricular high intensity area (PVH) on the T2-weighted image of MRI was classified into 3 subgroups by the criteria of Gerard et al with some modifications. Cerebral blood flow (CBF) was measured by the 133Xe intravenous injection method using a Cerbrograph (Novo), and gray matter flow (F1) and initial slope index (ISI) were calculated. The cerebrovascular reactivity to CO2 was estimated as the increase in F1 or ISI per unit increase in PaCO2 (delta F1/delta PaCO2 or delta ISI/delta PaCO2, respectively) during inhalation of 5% CO2 and as %increase in F1 or ISI per unit increase in PaCO2 (delta F1%/delta PaCO2 or delta ISI%/delta PaCO2, respectively) during inhalation of 5% CO2. 1. CO2 reactivity in both groups. delta F1/delta PaCO2 in the MI and MID groups were 3.2 +/- 1.4 ml/100 g/min/mmHg and 2.0 +/- 1.4, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral blood flow responses to inhaled carbon dioxide in schizophrenia

Carbon dioxide (CO2) is a potent cerebrovasodilator; even mild changes in CO2 are associated with marked changes in cerebral blood flow (CBF). We measured CBF before and after 5% CO2 inhalation in 19 medicated patients with schizophrenia and 16 normal volunteers. Another group of 16 volunteers had 2 CBF measurements under resting conditions. Although both patients and controls showed marked CBF increase during CO2 inhalation, the CBF response was significantly less in the patients. Change in CBF per mm of CO2 was lower in the patients. The second group of controls did not show significant differences between the 2 resting CBF measurements.     

脑梗死、TIA与高同型半胱氨酸血症的关系分析

目的观察高同型半胱氨酸血症与脑梗死及TIA之间的关系。方法应用高压液相色谱法(HPLC)对脑梗死、TIA和对照组中的健康体检者进行血浆同型半胱氨酸测定。结果脑梗死组病人的血浆同型半胱氨酸水平明显高于对照组(P<0.01),而TIA组病人的血浆同型半胱氨酸水平高于对照组但无显著性差异(P>0.05)。结论高同型半胱氨酸血症主要损伤中等及大血管而不是小血管。     

L-arginine-mediated vasoreactivity in patients with a risk of stroke

OBJECTIVES:L-arginine is the substrate for nitric oxide (NO) production and has been shown to induce an endothelium-dependent increase in cerebral blood flow in humans. We studied the hypothesis that L-arginine-mediated vasoreactivity is impaired in patients with cardiovascular risk factors and a risk of stroke. METHODS: 55 patients with cardiovascular risk factors (mean age 63.0 +/- 8.5 years) were included in the study. 45 of them had a history of previous minor stroke or transient ischemic attack (TIA) while 10 patients had cardiovascular risk factors but no previous cerebral ischemic event. Endothelium-dependent changes in cerebral blood flow during the infusion of 30 g L-arginine were assessed by continuous transcranial Doppler sonography of both middle cerebral arteries, intima-media thickness (IMT) of the common carotid artery, by Duplex sonography. Associations between risk factors, IMT, L-arginine reactivity and previous cerebrovascular events were analyzed by stepwise multiple linear regression analysis and patient groups were compared. RESULTS: Normal young volunteers showed an L-arginine-mediated increase in mean flow velocity of 22 +/- 8%; L-arginine reactivity of the 55 patients was 28 +/- 10%. Patients with a history of stroke or TIA had significantly higher flow velocity responses to L-arginine (29 +/- 10%) than patients with cardiovascular risk factors but no previous cerebrovascular event (21 +/- 8%, p < 0.05). Stepwise multiple linear regression analysis showed a significant association of enhanced L-arginine reactivity with previous stroke/TIA (p < 0.001) and elevated fibrinogen levels (p < 0.05) but not with age, IMT, hypertension, cholesterol or other risk factors. The same regression model showed an association between IMT and previous stroke/TIA (p < 0.001) and serum cholesterol levels (p < 0.05) but not L-arginine reactivity. CONCLUSIONS: L-arginine reactivity of the cerebral vessels may be assessed by Doppler sonography and was enhanced in patients with a history of stroke or TIA. It was independent of IMT of the carotid arteries. We conclude that enhanced L-arginine reactivity is a potential marker for cerebral endothelial dysfunction and an independent indicator for an increased risk of stroke.     

Influence of a central cholinergic mode of action on the regulation of the intact and disturbed cerebral blood flow (author's transl)]

Cerebral chemical vasomotor reactivity and autoregulation were tested in normal baboons before and after intravertebral, intravenous and (or) intracarotid infusion of atropine and neostigmine. Furthermore, disordered cholinergic neurotransmission and dysautoregulation after acute experimental cerebral infarction have also been investigated. Intravertebral injection of atropine suppressed the increase of CBF by inhalation of 5% CO2 and enhanced the decrease of CBF induced by hyperventilation, but did not appreciably affect autoregulatory response. On the other hand, cerebral autoregulatory vasoconstriction during increases of CPP was significantly reduced following both intravertebral and intracarotid neostigmine infusion. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced only following intravertebral neostigmine and cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. Following experimental cerebral infarction regional dysautoregulation was found in infarcted gray matter and correlated significantly with increased AChE levels in the same zones of cortex and basal ganglia. Intravenous infusion of scopolamine restored autoregulation to the ischemic zones. The results thus obtained support the view that central cholinergic cerebrovascular influences exist and are vasodilatory in nature. Furthermore, in acute experimental cerebral infarction disordered cholinergic neurotransmission seems to play a role in vasoconstrictive dysautoregulation.     

Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide.

To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone (VMRCO2), and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR (r = 0.69 in VMRTOT versus VMRACE and 0.79 in VMRCO2 versus VMRACE; P less than 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Severe haemodynamic stress in selected subtypes of patients with moyamoya disease: a positron emission tomography study

BACKGROUND: The optimum management of patients with moyamoya disease remains controversial. OBJECTIVES: To examine retrospectively the correlation between the degree of haemodynamic stress and the clinical presentation by measuring cerebral haemodynamics and metabolism using positron emission tomography (PET). METHODS: 57 patients with moyamoya disease (mean age 32 years, range 12 to 64), classified into five groups according to clinical manifestations, underwent PET measurement of cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMR(O2)), and oxygen extraction fraction (OEF) using (15)O labelled gases. The regional values in patient groups were compared with a normal group. RESULTS: CBF in non-symptomatic patients, patients presenting with transient ischaemic attacks (TIA), and patients with haemorrhagic onset (H) was not significantly lower than in normal controls in any region. CBV in the TIA group and in patients with infarction associated with TIA (I/TIA) was significantly higher than in the controls in most regions. OEF in the frontal, parietal, and temporal cortex was significantly higher in the I/TIA group than in the controls. Patients in the H group and those with a permanent deficit with infarction (PD group) had decreased metabolism with normal OEF. Multivariate analysis to test the distribution of the three dimensional vector (CBF, CBV, OEF) showed significant differences between every possible pair among the six groups except NS v H and H v PD in the frontal cortex. CONCLUSIONS: The haemodynamic status of moyamoya disease is not uniform, and severe haemodynamic stress occurs in selected subgroups of patients.     

Assessment of cerebral haemodynamic reserve: correlation between PET parameters and CO2 reactivity measured by the intravenous 133 xenon injection technique.

Regional cerebral blood flow (CBF), oxygen utilisation, fractional oxygen extraction (OER) and cerebral blood volume (CBV) were measured by positron emission tomography (PET) in 21 patients with occlusive carotid artery disease. In the same patients, measurements of cerebral CO2 reactivity were performed using the intravenous xenon-133 technique. A significant correlation was found in symptomatic hemispheres between the CBF/CBV ratio and CO2 reactivity. Four patients had significant increases in OER and this was associated with a reduction in CBF/CBV ratio implying exhaustion of haemodynamic reserve. CO2 reactivity was reduced below 1.5% mm Hg in all four cases with raised OER but only in two cases with normal OER. In patients with CO2 reactivities above 1.5% mm Hg, OER was normal in all cases. It is concluded that measurements of CO2 reactivity provide a satisfactory method for assessing cerebral haemodynamic reserve.     

Effect of labetalol on cerebral blood flow and middle cerebral arterial flow velocity in healthy volunteers.

The effect of labetalol, a combined alpha- and beta-adrenoceptor antagonist, on the cerebral circulation was investigated in 7 normotensive subjects. Cerebral blood flow (CBF) was measured with the intravenous 133Xe method and mean flow velocity (Vmean) in the middle cerebral artery was determined using transcranial Doppler (TCD) ultrasound. Examination was performed before and then 15, 60 and 120 min after 0.75 mg/kg i.v. labetalol. Reactivity to inhalation of 5% CO2 in air was studied before, and again 90 min after labetalol administration. Neither CBF nor Vmean changed following labetalol administration, whereas a marked increase occurred during inhalation of CO2. The median CO2 reactivity was 3.2%/mmHg (range: 1.8-4.0) for CBF and 4.4%/mmHg (1.5-5.6) for Vmean. These results indicate that labetalol, given in moderate but clinically relevant doses, does not affect the cerebral circulation in normotensive subjects. Neither does it affect CO2 reactivity. The uniform results obtained with the two methods suggest TCD as a usable alternative to conventional CBF technique in the assessment of cerebral vasoactivity of various drugs in subjects with a normal cerebral circulation.     

Effect of hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebrovascular disorders

Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.     

The effect of low dose dopamine on CBF in patients with subarachnoid hemorrhage

Cerebral blood flow was measured in 10 patients with subarachnoid hemorrhage using the 133Xe inhalation methods. Regional cerebral blood flow (r-CBF) values were calculated with initial slope index, their values were compared with the blood flow response to the administration of low dose dopamine (DA). CBF values of just after and continuous administration of DA were compared with control values. The measurement of r-CBF was performed immediately after the infusion of 5 micrograms/kg/min DA for 30 min. The focal ischemic lesions decreased, bi-hemispheric mean CBF value (7 cases without A-Com patients) increased by 10.3% significantly (paired T test), affected hemispheric mean CBF value increased by 8.7% significantly and non-affected hemispheric mean CBF value increased by 16.6% significantly. The PaCO2 value didn't change but the mean systemic blood pressure increased by 5.1% significantly. The CBF values of continuous administration of DA for 10 days to 2 weeks were measured. The CBF values increased during the administration of DA. The mean CBF values increased without the steal phenomenon and the mean arterial blood pressure increased slightly after the administration of DA. These phenomena were observed more significantly in non affected side than affected side. We suggest that the administration of DA increase the CBF values in patients with subarachnoid hemorrhage due to the stimulation of DA receptor.     

Intra-aortic balloon counterpulsation: a treatment for ischaemic stroke?

Intra-aortic balloon counterpulsation (IABC) augments cardiac output (CO) and pulse pressure (PP) allowing patients with low output heart failure to be supported for a period of time. Augmentation of CO and PP may also be beneficial to the patient with acute cerebral ischaemia. In this paper we investigated the possibility of using IABC to increase local cerebral blood flow (CBF) in ischaemic brain. In 12 anaesthetized mongrel dogs, a canine stroke model was produced by occluding the left internal carotid and middle cerebral arteries with aneurysm clips. Six dogs were then treated with IABC for 2 h, and 6 other dogs acted as controls (no IABC). Haemodynamic data were measured continuously and CBF (microsphere technique) and CO measurements were performed pre- and post-occlusion, and then twice during the treatment period. In the IABC-treated animals, PP increased from 32 +/- 5.9 to 39 +/- 7.8 mmHg (p less than 0.01) but CO and local CBF in the ischaemic brain did not change significantly during IABC. However, in 4 dogs with significant increases in CO due to IABC [1.7 +/- 0.3 to 2.8 +/- 0.7 l/min (p less than 0.05)], local CBF in ischaemic brain also increased significantly from 22 +/- 12 to 26 +/- 11 cc/100 g/min (p less than 0.05). In the control animals, CO and local CBF did not change significantly during the observation period. These data suggest that augmentation of CO and PP by IABC results in an increase in local CBF in ischaemic brain. IABC may be an effective treatment for ischaemic stroke in those patients with compromised cardiac performance whose cardiac output and pulse pressure can be augmented by IABC.     

Cerebral blood flow changes induced by CO2 in anxiety

Cerebral blood flow (CBF) was measured twice with the 133Xenon inhalation technique, under resting conditions and during 5% CO2 inhalation, in 13 patients with generalized anxiety disorder and a group of normal volunteers of comparable age and sex distribution. CO2 inhalation was associated with similar increases in end-tidal CO2 (PECO2) and CBF. Neither group showed statistically significant increases in state anxiety. However, when subjects (both patients and controls) who became anxious during CO2 inhalation were compared with those who did not, on associated CBF changes, significant differences emerged. The former showed less marked CBF increase as compared to the latter in the absence of any significant differences between the two groups on PECO2 during the second measurement. Changes in state anxiety and CBF showed a statistically significant inverse correlation for the entire group.     

Noninvasive assessment of CO2-induced cerebral vasomotor response in normal individuals and patients with internal carotid artery occlusions

To evaluate the CO2-induced vasomotor reactivity of the cerebral vasculature, relative changes of blood flow velocity within the middle cerebral artery were measured by transcranial Doppler ultrasonography during normocapnia and various degrees of hypercapnia and hypocapnia. We studied 40 normal individuals and 40 patients with unilateral and 15 patients with bilateral internal carotid artery occlusions. When blood flow velocity changes as percent of normocapnic values were plotted against end-tidal CO2 volume percent, a biasymptotic curve (a tangent-hyperbolic function) gave the best fit of the scattergram. The distance between the upper and lower asymptotes was defined as cerebral vasomotor reactivity. In the normal individuals, mean +/- SD vasomotor reactivity was 85.63 +/- 15.96%. In patients with internal carotid artery occlusions, vasomotor reactivity was significantly lower than normal on both the occluded (mean 45.2%, median 50.4%; p less than 0.0001) and the nonoccluded (mean +/- SD 67.7 + 13.3%, p less than 0.01) sides in the unilateral group and on both sides (mean +/- SD 36.6 +/- 15.9% and 44.9 +/- 24.6%, p less than 0.0001) in the bilateral group. The difference between vasomotor reactivity for symptomatic and asymptomatic unilateral occlusions was also highly significant (mean 37.6% and 62.9%, p less than 0.006). Vasomotor reactivity was also significantly lower in patients with low-flow infarctions on computed tomography than in patients with normal scans (mean +/- SD 36.7 +/- 25% and 60.2 +/- 16.9%, p less than 0.008). A striking association of low-flow infarctions, ischemic ophthalmopathy, and hypostatic transient ischemic attacks was found with vasomotor reactivities of less than 34% or even paradoxical reactions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Age-related reductions in cerebral vasomotor reactivity and the law of initial value: a 4-year prospective longitudinal study

A group of 51 neurologically normal, middle-aged and elderly volunteers (aged 35-86 years; mean age 63.24 years) with and without risk factors for stroke were given annual tests of cerebral vasomotor reactivity to assess any changes in the cerebral vascular capacitance associated with advancing age that might alter cerebral vasomotor reactivity. Cerebral vasomotor reactivity was estimated as the difference in bihemisphere gray matter CBF measured by the 133Xe inhalation method in the steady state breathing room air, followed by a second measurement during inhalation of 100% oxygen. There were significant and progressive reductions in cerebral vasomotor reactivity during the 4-year longitudinal study. Positive linear correlations were apparent between initial steady-state mean bihemisphere gray matter CBF levels and degrees of vasomotor reactivity, suggesting that the Law of Initial Value plays an important role. This should be borne in mind when analyzing scores of cerebral vasomotor reactivity. In the present communication, analysis of covariance was used to correct for influences of initial CBF levels on vasomotor responses tested while breathing pure oxygen.     

CBF and transcranial Doppler sonography during vasodilatory stress tests in patients with common carotid artery occlusion.

Cerebral blood flow (CBF) and the cerebral vasoreactivity was measured in patients with cerebrovascular disease and longstanding occlusion of the common carotid artery (CCA). In addition, regional CBF was correlated with transcranial doppler (TCD) measurements at baseline and during 6% CO2 inhalation and after intravenous administration of 1 g of acetazolamide. Twelve patients with a mean age of 62 years (range 45 to 71 years) were included, and the data compared to age-matched healthy controls. CBF was measured by intravenous injection of xenon-133 and SPECT (Tomomatic 564). TCD of the middle cerebral artery (MCA) was done by EME TC-64B. A very low global CBF value of 28 +/- 5 (SD) ml 100 g-1 min-1 was found at baseline as compared to 55 +/- 5 ml 100 g-1 min-1 in the normal controls. During 6% CO2-inhalation and after acetazolamide administration, CBF increased by 58 +/- 24% and 51 +/- 21%, respectively, indicating substantial collateral supply. Correlative analysis of CBF in the MCA territory and TCD in the MCA showed statistical significance only for the pooled data, i.e. compiling the data obtained during baseline and the two vasodilatory tests, and then only for the mean and peak TCD velocity (e.g. r = 0.59, p less than 0.002, n = 35, mean velocity, right side). We conclude that TCD measurements do not predict regional CBF in patients with CCA occlusion. The study emphasizes that these two methods yield supplementary information, with TCD measurements providing information of the circle of Willis and CBF studies of the flow distribution.     

Cerebral blood flow and cerebral hematocrit in patients with cerebral ischemia measured by single-photon emission computed tomography

Abstract– Single-photon emission computed tomography (SPECT) was used for the measurement of regional cerebral blood flow (CBF), cerebral blood volume (CBV) and cerebral hematocrit (Hct). CBF was measured using N-isopropyl-p-I-123-Iodoamphetamine. CBV was measured by both RBC tracer (Tc-99m RBC) and plasma tracer (Tc-99m human serum albumin) and cerebral hematocrit (Hct) was calculated. In normals, the cerebral-to-large vessel Hct ratio was 75.9%. Isovolemic hemodilution in patients with high Hct tended to increase the cerebral-to-large vessel Hct ratio. Low CBF, high CBV and slow cerebral blood mean transit time (MTT by dynamic CT scanning) was seen during the acute stage of completed infarction and during the symptom-free interval of TIA. Cerebral Hct was increased in the ischemic region of poor prognosis.