Artery Mean Blood Flow Velocity Research Articles

Reduced Cerebrovascular CO 2 Reactivity in CADASIL

P1 Background and Purpose: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary angiopathy caused by mutations in Notch3 . Cerebral microvessels show an accumulation of granular osmiophilic material in the vicinity of degenerating vascular smooth muscle cells (VSMC). To study cerebrovascular function in CADASIL we performed measurements on cerebral hemodynamics using transcranial Doppler sonography (TCD). Methods: Middle cerebral artery (MCA) mean blood flow velocity (MFV), cerebrovascular CO 2 reactivity, and the resistance index (RI) were measured by bilateral TCD in 29 CADASIL individuals (mean age 49.0±2.4 years) and an equal number of age- and sex-matched controls. Results: Compared to controls, CO 2 reactivity was reduced in CADASIL (33.4±2.7% vs. 45.3±3.0%; p<0.01). This difference remained significant when non-disabled CADASIL individuals (Rankin=0) were compared to matched controls (36.8±3.4% vs. 48.6±3.9%; p<0.05). CO 2 reactivity was significantly lower in disabled than in non-disabled CADASIL individuals (24.5±2.7 vs. 36.8+3.4%; p<0.05). MCA MFV was reduced in CADASIL (45.6±2.2 vs. 54.2±2.4 cm/s; p<0.05) and correlated negatively with age both in affected individuals (r=-0.314; p<0.05) and controls (r=-0.339; p<0.05). RI was not significantly altered (59.0±1.0 vs. 57.7±1.2; p=0.42). Conclusions: In CADASIL there is a reduction of both CO 2 reactivity and basal MCA MFV, whereas vascular resistance appears to be normal. The reduced CO 2 reactivity suggests functional impairment of cerebral vasoreactivity probably related to VSMC dysfunction. The reduction of CO 2 reactivity in non-disabled CADASIL individuals suggests an early role of impaired cerebral vasoreactivity in the evolution of the disease.

Increased cerebral CO(2) reactivity after heparin-mediated extracorporal LDL precipitation (HELP) in patients with coronary heart disease and hyperlipidemia.

There is experimental and clinical evidence that hypercholesterolemia leads to an impairment of endothelial function in coronary and cerebral arteries. Using transcranial Doppler sonography, we examined CO(2) reactivity as a marker of cerebral vasoreactivity in patients with coronary heart disease and hyperlipidemia before and after drastic lowering of LDL cholesterol, lipoprotein(a) [Lp(a)], and fibrinogen levels by heparin-mediated extracorporal LDL precipitation (HELP). CO(2) reactivity was determined in 13 patients with coronary artery disease and hyperlipidemia undergoing regular HELP therapy. Middle cerebral artery mean blood flow velocity (MFV) was detected by transcranial Doppler. CO(2) reactivity was calculated as the percent change of MFV during hypercapnia, induced by ventilation of carbogene (5% CO(2), 95% O(2)), to normocapnia. Patients with extracranial or intracranial stenoses were excluded. Other parameters such as blood viscosity, heart rate, and blood pressure were measured to control hemorheologic and systemic influences on CO(2) reactivity. A single HELP treatment reduced total cholesterol, LDL cholesterol, Lp(a), triglycerides, and fibrinogen levels by >50% (P<0.001). Blood viscosity significantly decreased from 1.24+/-0.04 to 1.07+/-0.02 mPa (P<0.001). Blood pressure, heart rate, and MFV did not change significantly. CO(2) reactivity increased from 22% +/- 21% to 36% +/- 18% (P<0.05). Fast and drastic removal of LDL cholesterol, Lp(a), and fibrinogen from plasma results in an improvement of cerebrovascular reactivity in patients with coronary heart disease and hyperlipidemia. The clinical use of HELP in patients with impaired cerebrovascular reactivity might be promising.

The Effect of Clonidine on Cerebral Blood Flow Velocity, Carbon Dioxide Cerebral Vasoreactivity, and Response to Increased Arterial Pressure in Human Volunteers

BACKGROUND Because patients may be taking clonidine chronically or may be receiving it as a premedication before surgery, the authors investigated its effect on cerebral hemodynamics. METHODS In nine volunteers, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO2 vasoreactivity was measured before clonidine administration (preclonidine), 90 min after clonidine, 5 microg/kg orally, then following restoration of mean arterial pressure (MAP) to the preclonidine level. In addition, Vm was measured after a phenylephrine-induced 30-mmHg increase in MAP. RESULTS After clonidine administration, Vm decreased from 62 +/- 9 to 48 +/- 8 cm/s (P < 0.01), and MAP decreased from 86 +/- 10 to 63 +/- 5 mmHg (P < 0.01; mean +/- SD). Clonidine decreased the CO2 vasoreactivity slope from 2.2 +/- 0.4 to 1.2 +/- 0.5 cm x s(-1) x mmHg(-1) (P < 0.05); restoring MAP to the preclonidine level increased the slope to 1.60 +/- 0.5 cm x s(-1) x mmHg(-1), still less than the preclonidine slope (P < 0.05). CO2 vasoreactivity expressed as a percentage change in Vm, decreased after clonidine, 3.5 +/- 0.8 versus 2.4 +/- 0.8 %/mmHg (P < 0.05); this difference disappeared after restoration of MAP, 3.1 +/- 1.2 %/mmHg. With a 30-mmHg increase in MAP, Vm increased by 13% before and after clonidine (P < 0.05). CONCLUSIONS Clonidine, 5 microg/kg orally, decreases Vm and slightly attenuates cerebral CO2 vasoreactivity, therefore decreased cerebral blood flow and mildly attenuated CO2 vasoreactivity should be anticipated.

Cerebral blood flow velocity in patients with subclinical portal-systemic encephalopathy.

Alterations in cerebral blood flow (CBF) are implicated in the etiology of portal-systemic encephalopathy. We hypothesized that CO2 reactivity of the cerebral circulation may be impaired in subjects with chronic liver disease (CLD) who also had subclinical portal-systemic encephalopathy (SPSE). We compared the relationship between PETCO2 and cerebral blood flow velocity in 10 patients with CLD with those of 10 healthy control subjects. Middle cerebral artery mean blood flow velocity (MCAMFV) was measured using transcranial Doppler during rest, hyperventilation, and hypoventilation. The degree of SPSE was quantified by using psychometric testing. Patients with CLD had poorer psychometric test scores compared with control subjects. Patients with CLD had lower PETCO2, MCAMFV, and blood pressure values and higher heart rates, differing from control subjects in all ventilation states. However, CO2 reactivity, the rate of change in MCAMFV to changes in ventilation (expressed as percent change in CBF velocity per mm Hg change in PETCO2) was similar for both groups (4.6% +/- 0.6% vs 4.2% +/- 0.5% for patients with CLD versus control subjects, P = 0.15). Psychometric test scores in patients with chronic liver disease revealed subclinical impairment compared with control subjects. Transcranial Doppler measurements of middle cerebral artery blood flow with varying PETCO2 were conducted, but the CO2 response of patients with liver disease was within the range of control subjects.

Cerebral Blood Flow Velocity in Patients with Subclinical Portal-Systemic Encephalopathy

Alterations in cerebral blood flow (CBF) are implicated in the etiology of portal-systemic encephalopathy. We hypothesized that CO2 reactivity of the cerebral circulation may be impaired in subjects with chronic liver disease (CLD) who also had subclinical portal-systemic encephalopathy (SPSE). We compared the relationship between PETCO2 and cerebral blood flow velocity in 10 patients with CLD with those of 10 healthy control subjects. Middle cerebral artery mean blood flow velocity (MCAMFV) was measured using transcranial Doppler during rest, hyperventilation, and hypoventilation. The degree of SPSE was quantified by using psychometric testing. Patients with CLD had poorer psychometric test scores compared with control subjects. Patients with CLD had lower PETCO2, MCAMFV, and blood pressure values and higher heart rates, differing from control subjects in all ventilation states. However, CO2 reactivity, the rate of change in MCAMFV to changes in ventilation (expressed as percent change in CBF velocity per mm Hg change in PETCO2) was similar for both groups (4.6% +/- 0.6% vs 4.2% +/- 0.5% for patients with CLD versus control subjects, P = 0.15). Implications: Psychometric test scores in patients with chronic liver disease revealed subclinical impairment compared with control subjects. Transcranial Doppler measurements of middle cerebral artery blood flow with varying PETCO2 were conducted, but the CO2 response of patients with liver disease was within the range of control subjects. (Anesth Analg 1998;86:1005-9)

Complexity of middle cerebral artery blood flow velocity: effects of tilt and autonomic failure.

We examined spectral fractal characteristics of middle cerebral artery (MCA) mean blood flow velocity (MFV) and mean arterial blood pressure adjusted to the level of the brain (MAPbrain) during graded tilt (5 min supine, -10 degrees, 10 degrees, 30 degrees, 60 degrees, -10 degrees, supine) in eight autonomic failure patients and age- and sex-matched controls. From supine to 60 degrees, patients had a larger drop in MAPbrain (62 +/- 4.7 vs. 23 +/- 4.5 mmHg, P < 0.001; means +/- SE) and MFV (16.4 +/- 3.8 vs. 7.0 +/- 2.5 cm/s, P < 0.001) than in controls. From supine to 60 degrees, there was a trend toward a decrease in the slope of the fractal component (beta) of MFV (MFV-beta) in both the patients and the controls, but only the patients had a significant decrease in MFV-beta (supine: patient = 2.21 +/- 0.18, control = 1.99 +/- 0.60; 60 degrees: patient = 1.46 +/- 0.24, control = 1.62 +/- 0.19). The beta value of MAPbrain (MAPbrain-beta; 2.19 +/- 0.05) was not significantly different between patients and controls and did not change with tilt. High and low degrees of regulatory complexity are indicated by values of beta close to 1.0 and 2.0, respectively. The increase in fractal complexity of cerebral MFV in the patients with tilt suggests an increase in the degree of autoregulation in the patients. This may be related to the drop in MAPbrain. The different response of MFV-beta compared with that of MAPbrain-beta also indicates that MFV-beta is related to the regulation of cerebral vascular resistance and not systemic blood pressure.

The Effect of Clonidine on Cerebral Blood Flow Velocity, Carbon Dioxide Cerebral Vasoreactivity, and Response to Increased Arterial Pressure in Human Volunteers

Because patients may be taking clonidine chronically or may be receiving it as a premedication before surgery, the authors investigated its effect on cerebral hemodynamics. In nine volunteers, middle cerebral artery mean blood flow velocity (Vm) was measured using transcranial Doppler ultrasonography (TCD). CO2 vasoreactivity was measured before clonidine administration (preclonidine), 90 min after clonidine, 5 microg/kg orally, then following restoration of mean arterial pressure (MAP) to the preclonidine level. In addition, Vm was measured after a phenylephrine-induced 30-mmHg increase in MAP. After clonidine administration, Vm decreased from 62 +/- 9 to 48 +/- 8 cm/s (P < 0.01), and MAP decreased from 86 +/- 10 to 63 +/- 5 mmHg (P < 0.01; mean +/- SD). Clonidine decreased the CO2 vasoreactivity slope from 2.2 +/- 0.4 to 1.2 +/- 0.5 cm x s(-1) x mmHg(-1) (P < 0.05); restoring MAP to the preclonidine level increased the slope to 1.60 +/- 0.5 cm x s(-1) x mmHg(-1), still less than the preclonidine slope (P < 0.05). CO2 vasoreactivity expressed as a percentage change in Vm, decreased after clonidine, 3.5 +/- 0.8 versus 2.4 +/- 0.8 %/mmHg (P < 0.05); this difference disappeared after restoration of MAP, 3.1 +/- 1.2 %/mmHg. With a 30-mmHg increase in MAP, Vm increased by 13% before and after clonidine (P < 0.05). Clonidine, 5 microg/kg orally, decreases Vm and slightly attenuates cerebral CO2 vasoreactivity, therefore decreased cerebral blood flow and mildly attenuated CO2 vasoreactivity should be anticipated.

Relationships between cerebral regional blood flow velocities and volumetric blood flows and their respective reactivities to acetazolamide.

The technique of transcranial Doppler ultrasonography (TCD) is widely used for assessment of cerebral blood flow velocity. Whether measurement of changes in TCD velocity can be used for studying volumetric cerebral blood flow variations remains a matter of debate. We therefore investigated the relationship between flow velocity and volumetric cerebral blood flow before and during acetazolamide-induced vasodilation. The middle cerebral artery mean blood flow velocity (MV) measured by TCD and the corresponding regional and hemispheric cerebral blood flows assessed with 133Xe single-photon emission CT were measured in 52 unselected patients. Absolute values of flow and velocity before and after stimulation and their reactivity to acetazolamide were compared. When the correlation was statistically significant, the linearity of the relationship was tested. Absolute values of hemispheric cerebral blood flow were correlated with MV both before (r = .315, P = .02) and after acetazolamide (r = .436, P = .001), whereas regional cerebral blood flow was correlated with MV only after acetazolamide (before, r = .262, P = .06; after, r = .446, P = .001). All these relationships fitted a linear model. In contrast, there was no correlation between acetazolamide-induced relative increments of flow and velocity. Our results support a linear model describing the relationship between absolute values of flow and velocity when arterial section is the slope and anastomotic blood flow is the intercept. In contrast, relative increments in volumetric flow and velocity may be proportional only if anastomotic flow is negligible, ie, in subjects without cerebrovascular disease. We conclude that, for patients with cerebrovascular disease, TCD does not satisfactorily model cerebral vasoreactivity in terms of volumetric cerebral blood flow.

Acetazolamide-induced vasodilation in the carotid vascular bed in healthy volunteers.

Acetazolamide (ACTZ) vasodilating properties are used for the assessment of cerebral vasodilatory reserve not only in cerebral pathology investigation, but also in clinical pharmacology studies. However, the kinetics of these vasodilating properties are not clearly established; moreover, the cerebral selectivity of ACTZ-induced vasodilation has not been demonstrated. To address these issues, we performed an ACTZ test in 9 healthy volunteers and measured noninvasively the effects exerted by the drug simultaneously on common carotid artery blood flow (CCABF), middle cerebral artery mean blood flow (BF) velocity (MV) (transcranial Doppler technique), and facial cutaneous BF (CutBF). The time of the peak increase in MV was variable, occurring between 20 and 40 min after ACTZ, and brief. In addition, simultaneous increases (with variable mean peak times) occurred in flows in the CCA (+11% at 20 min) and in its intracranial (+25% at 30 min) and extracranial (+134% at 50 min) branches. The first finding suggests that the cerebral effects of ACTZ should be measured repeatedly to detect in each individual subject the time of MV peak increase; the transcranial Doppler is particularly suitable for such an approach. The second finding suggests that, especially in patients, extracranial actions of ACTZ must be taken into account for estimation of the cerebral vasodilatory reserve.

The effects of midazolam and sufentanil sedation on middle cerebral artery blood flow velocity in awake patients.

Midazolam and sufentanil are commonly used for sedation. Cerebrovascular effects of low-dose midazolam have not been studied previously, and cerebrovascular effects of sufentanil remain controversial. Forty ASA I and II patients were studied preoperatively. These patients were given midazolam (20 or 40 micrograms/kg) or sufentanil (0.1 or 0.2 micrograms/kg) i.v. Transcranial Doppler recordings of middle cerebral artery mean blood flow velocity (Vm) were recorded before administration of the study drug and for the 5-min investigation period. Mean arterial pressure, heart rate, and end-tidal CO2 remained constant during the investigation and did not vary between treatment groups. Vm decreased 17 to 21% with both midazolam doses (p < 0.05), returning to baseline within 5 min. Vm did not change with either sufentanil dose. These results suggest that midazolam decreases cerebral blood flow (CBF) by increasing cerebral vascular resistance (CVR). The low sedative doses of sufentanil used in this study did not affect Vm over 5 min in unanesthetized patients.

Transcranial colour coded sonography as an aid to measurement of blood flow velocity in the basal cerebral arteries

Unlike conventional transcranial Doppler, transcranial colour coded sonography allows imaging of the basal cerebral arteries. We used this technique to determine blood flow velocities, with compensation for the angle of insonation, in the anterior and posterior cerebral circulation of 60 volunteers categorised by age (20–39, 40–59, > 60 years). Successful vessel insonation declined with increasing age: 40/40 middle cerebral arteries insonated 20–39 y, 31/40 insonated >60 y. Peak, mean and end diastolic blood flow velocities also decreased with age in all arteries: 20–39 y middle cerebral artery mean velocity = 72 cm/s; > 60 y middle cerebral artery mean blood flow velocity = 58 cm/s; p < 0.0001. The pulsatility index increased significantly with age in the middle, posterior cerebral (P2 segment) and vertebral arteries ( p < 0.05-0.005), however the resistance index increased significantly with age in all vessels ( p < 0.05-0.0001).