The Values of Cerebrovascular Pressure Reactivity and Brain Tissue Oxygen Pressure Reactivity in Experimental Anhepatic Liver Failure

Background

We investigated in a porcine model of anhepatic acute liver failure (ALF), the value of two parameters describing cerebrovascular autoregulatory capacity, pressure reactivity index (PRx) and brain tissue oxygen pressure reactivity (ORx), regarding their power to predict the development of intracranial hypertension.

Methods

In six pigs, hepatectomy was performed. Only one animal was sham operated. All animals received neuromonitoring including arterial blood pressure, intracranial pressure (ICP), and brain tissue partial oxygen pressure (P_brO₂). The average time of neuromonitoring was 31.0 h. Cerebral perfusion pressures (CPP), cerebrovascular pressure reactivity index (PRx) and brain tissue oxygen reactivity index (ORx) were calculated.

Results

Perioperative disturbance of AR improved within 4 h after surgery. From 6 to 16 h post hepatectomy, ICP did slowly increase by 4 mmHg from baseline; CPP remained stable around 40 mmHg. PRx and ORx, however, indicated in this period a progressive loss of AR, reflected in a decrease of P_brO₂ despite unchanged CPP. Beyond 16 h, ICP rose quickly. At CPP levels below 35 mmHg, P_brO₂ fell to ischemic levels.

Conclusions

The loss of cerebrovascular autoregulatory capacity, indicated by a rise of PRx and ORx precedes the final crisis of uncontrollable intracranial hypertension in this animal model by hours. During this phase cerebral blood flow, as reflected in tissue oxygenation, deteriorates despite unchanged CPP. Monitoring of AR during ALF therefore seems to carry the power to identify a risk for development of critical CBF and intracranial hypertension.

     

Association between intracranial,arterial pulse pressure amplitudes and cerebral autoregulation in head injury patients

Abstract

Objective: To explore whether intracranial pulse pressure amplitudes relate to arterial pulse pressure amplitudes and whether correlations between time-related changes in intracranial and arterial pulse pressure amplitudes associate with indices of cerebral autoregulation.

Methods: A total of 257 continuous and simultaneous intracranial pressure (ICP), arterial blood pressure (ABP) and middle cerebral artery (MCA) blood velocity recordings were obtained 1–14 days after ictus in 76 traumatic head injury patients and analysed retrospectively. Clinical outcome was assessed using the Glasgow outcome scale (GOS). Pulse pressure amplitudes of corresponding single ICP and ABP waves were correlated in consecutive 200 wave pairs. Mean ICP, mean ABP and mean ICP wave amplitudes, and mean and systolic MCA blood flow velocities, were computed in consecutive 6 second time windows. The indices of cerebral autoregulation PRx (moving correlation between mean ICP and mean ABP), and Mx and Sx (moving correlation between mean and systolic MCA blood velocity and cerebral perfusion pressure) were calculated over 4 minute periods and averaged over each recording.

Results: Intracranial pulse pressure amplitudes were not related to arterial pulse pressure amplitudes (mean of Pearson's correlations coefficients: 0.04). Outcome was related to mean ICP, PRx and Sx (p ≤ 0.04, multiple regression analysis). Correlations between intracranial and arterial pulse pressure amplitudes were weakly related to PRx (Pearson's correlation coefficient: 0.16; p=0.01), but were not related to the indices of cerebral autoregulation Mx (Pearson's correlation coefficient: 0.07) and Sx (Pearson's correlation coefficient: 0.04).

Conclusions: In this cohort of pressure recordings, we found no evidence of a correlation between intracranial and arterial blood pressure amplitudes. The correlation appeared not to be related to the state of cerebral autoregulation, although a weak correlation was found with pressure reactivity index PRx.     

Effects of porta-systemic shunting and ammonia infusion on cerebral blood flow autoregulation in the rat

Background: Portacaval shunting of blood, hyperammonemia, and impaired cerebral blood flow (CBF) autoregulation are assumed to be involved in the development of high intracranial pressure (ICP) in liver failure. In this study, we determined whether CBF autoregulation is impaired by portacaval anastomosis and hyperammonemia. Methods: Four groups of pentobarbital-sedated and mechanically ventilated rats were investigated after construction of a portacaval anastomosis or following sham operation. Half of the rats received either infusion of ammonia (55 μmol/kg/minute) or saline for 180 minutes. Arterial pressure and ICP was monitored, and lower limit of CBF autoregulation was determined. Results: Lower limit of autoregulation was preserved in all four groups of studied animals; vehicle lower limits were 40±2.3, 40±2, 54±1, and 51±3 mmHg in sham-operated rats, sham rats receiving ammonia infusion, portacaval anastomosis-vehicle animals, and portacaval anastomosis-hyperammonemia animals, respectively. The lower limit of auto-regulation was higher in portacaval anastomosis rats (p=0.01) compared to the sham-operated rats. Hyperammonemia in portacaval anastomosis rats did not aggravate this. Conclusion: Portacaval anastomosis and hyperammonemia does not impair the lower limit of CBF autoregulation. However, shunting of portal blood to the systemic circulation shifts the lower limit of autoregulation to higher blood pressure values, making the brain more sensitive to episodes of arterial hypotension.     

Comparison of transcranial Doppler ultrasonography and positron emission tomography using a three-dimensional template of the middle cerebral artery

Abstract

Objective: Transcranial Doppler (TCD) measures blood flow velocities (BFV) and is an indirect method of assessing cerebral blood flow (CBF). Positron emission tomography (PET) is a direct method to measure CBF. This study evaluates the correlations between TCD and PET findings

Methods: Nine patients with a symptomatic carotid artery stenosis, who underwent CEA, were studied pre- and post-operatively on the ipsi- and contralateral sides. Measurements of the BFV, CO₂ reactivity, CBF, cerebral blood volume (CBV) and mean vascular transit time (MVTT) were performed using a three-dimensional volume of interest (VOI) for the middle cerebral artery (MCA).

Results: CBF in the MCA region, as measured with PET, shows a good correlation with BFV, as measured with TCD, with similar pattern for total, gray and white matter MCA territory (Pearson's correlation coefficients: 0.751, 0.748 and 0.748, respectively). This correlation was found in the pre-operative as well as the post-operative state. No association could be demonstrated between CO₂ reactivity and CBV or (Pearson's correlation coefficients: 0.051 and 0.166, respectively).

Conclusion: With PET, it is possible to create three-dimensional VOI of arterial territories. CBF measured in these VOI seems to correlate with BFV before and after CEA on ipsi- and contralateral sides, while CBV shows no association with pre-operative CO₂ reactivity.     

Blood flow velocities during experimental intracranial hypertension in pigs

Abstract

Objectives: A purely hydraulic mechanism consisting in the pulsatile cuff-compression effect, by the cerebrospinal fluid displacement induced by the arterial pulsation, on the final portion of the bridging veins, has recently been hypothesized. This mechanism is able to maintain the constancy of cerebral blood flow (CBF) within the autoregulatory range, thus implying an exact balance between arterial inflow and venous outflow. In this study, we correlated arterial inflow and venous outflow during an experimentally induced condition of intracranial hypertension in pigs.

Methods: Mock cerebrospinal fluid (CSF) was progressively infused until a condition of brain tamponade was reached. Blood flow velocities at middle cerebral artery and sagittal sinus sites were evaluated simultaneously.

Results: Mean intracranial arterial blood flow velocity (IABFV), mean sagittal sinus blood flow velocity (SSBFV), and pulsatile-IABFV remained almost constant until cerebral perfusion pressure (CPP) dropped below 60–70 mmHg; then, a progressive decrease in mean IABFV and SSBFV, together with an increase in pulsatile-IABFV, was evident.

Conclusion: The strict similarity between mean IABFV and SSBFV patterns suggests that CBF decrement is mainly due to a decrease in the venous outflow, which, in turn, produces an obstacle to the arterial inflow. The correspondent increase in pulsatile-IABFV confirms the presence of a distal outflow obstruction. All these findings point towards a purely hydraulic mechanism underlying the cerebral autoregulation which acts at the level of the so-called Starling resistor.     

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]     

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.     

The course of dynamic cerebral autoregulation during cervical internal carotid artery occlusion

Abstract

Objectives: The selection of patients with cervical internal carotid artery occlusion (ICAO) for extracranial-intracranial bypass surgery is based on exhausted cerebrovascular reactivity to vasodilatory stimuli. However, a spontaneous increase in this reactivity can occur with time, questioning the ideal time for bypass surgery. In contrast, the natural course of dynamic cerebral autoregulation is not known in these patients.

Methods: Patients with cervical ICAO were examined at baseline and after a mean interval of 15 months. Dynamic autoregulation was determined by transcranial Doppler sonography in both middle cerebral arteries via respiratory-induced 0·1-Hz oscillations (phase, available for n=47 patients) and correlation analysis between diastolic blood pressure and Doppler signal (index Dx, n=55 patients). Pre-defined cut-off values and repeatability measures of healthy controls were used to define significant individual changes in autoregulation.

Results: Group mean comparisons between studies were not significant for any autoregulation parameter. The intraclass correlation coefficient between studies was high for phase (ipsilateral: 0·83; contralateral: 0·74), and moderate for Dx (ipsilateral: 0·63; contralateral: 0·35). There was no clear trend for an improvement across cut-off values. A significant individual improvement/deterioration in autoregulation occurred in 6%/6% for phase and 13%/9% for Dx.

Discussion: Dynamic autoregulation only rarely improves during the course of ICAO. This finding should be considered when deciding for or against a policy of delaying extracranial-intracranial bypass surgery for reasons of a potentially improving hemodynamic status.     

Effects of High-frequency Oscillatory Ventilation on Systemic and Cerebral Hemodynamics and Tissue Oxygenation: An Experimental Study in Pigs

Background

In this study, we compare the effects of high frequency oscillatory ventilation (HFOV) with those of lung-protective volume-controlled ventilation (VCV) on cerebral perfusion, tissue oxygenation, and cardiac function with and without acute intracranial hypertension (AICH).

Methods

Eight pigs with healthy lungs were studied during VCV with low tidal volume (V_T: 6 ml kg⁻¹) at four PEEP levels (5, 10, 15, 20 cmH₂O) followed by HFOV at corresponding transpulmonary pressures, first with normal ICP and then with AICH.

Systemic and pulmonary hemodynamics, cardiac function, cerebral perfusion pressure (CPP), cerebral blood flow (CBF), cerebral tissue oxygenation, and blood gases were measured after 10 min at each level. Transpulmonary pressures (TPP) were calculated at each PEEP level. The measurements were repeated with HFOV using continuous distending pressures (CDP) set at TPP plus 5 cmH₂O for the corresponding PEEP level. Both measurement series were repeated after intracranial pressure (ICP) had been raised to 30–40 cmH₂O with an intracranial balloon catheter.

Results

Cardiac output, stroke volume, MAP, CPP, and CBF were significantly higher during HFOV at normal ICP. Systemic and cerebral hemodynamics was significantly altered by AICH, but there were no differences attributable to the ventilatory mode.

Conclusion

HFOV is associated with less hemodynamic compromise than VCV, even when using small tidal volumes and low mean airway pressures. It does not impair cerebral perfusion or tissue oxygenation in animals with AICH, and could, therefore, be a useful ventilatory strategy to prevent lung failure in patients with traumatic brain injury.

     

The Utility of Cerebral Blood Flow Assessment in TBI

Over the past few decades, intracranial monitoring technologies focused on treating and preempting secondary injury after traumatic brain injury (TBI) have experienced considerable growth. A physiological measure fundamental to the management of these patients is cerebral blood flow (CBF), which may be determined directly or indirectly. Direct measurement has proven difficult previously; however, invasive and non-invasive CBF monitors are now available. This article reviews the history of CBF measurements in TBI as well as the role of CBF in pathologies associated with TBI, such as cerebral autoregulation, hyperemia, and cortical spreading depression. The limitations of various CBF monitors are reviewed in order to better understand their role in TBI management.     

Impaired dynamic cerebral autoregulation in middle cerebral artery stenosis

Abstract

Background and purpose: Analysis of dynamic cerebral autoregulation during transient falls in blood pressure is considered a sensitive and convenient method for evaluating patients with carotid artery stenosis. To this point, there have been few reports on the efficacy of using the thigh cuffs technique to analyse middle cerebral artery (MCA) stenosis. If it could be determined whether cerebral blood flow can be maintained (autoregulated) during sudden falls in arterial blood pressure (ABP), then it might be possible to identify patients with MCA stenosis who are at risk of stroke.

Methods: We used the thigh cuff technique to estimate dynamic cerebral autoregulation in 57 patients with MCA stenosis and 72 normal controls. After a stepwise fall in arterial blood pressure, we determined the rate of the rise of MCA blood velocity and compared it with the rate of the rise of arterial blood pressure. In this manner, the dynamic cerbral autoregulation of 11 patients undergoing MCA M1 stent angioplasty was estimated both pre- and post-operation.

Results: The autoregulatory index (ARI) was significantly reduced in patients with stenosed/occluded MCA (3.24 ± 1.52), as compared with normal controls (5.25 ± 1.39; p<0.001) (results reported as mean ± SD). Poor ARI values are usually observed in patients with a higher degree of stenosis and particularly in patients with insufficient collateral compensation. ARI was significantly reduced in severe stroke patients (modified ranking scale≥1), as compared with asymptomatic or TIA patients (p<0.05). After MCA stent angioplasty was performed, there was a significant improvement in ARI in 11 subjects, which caused a mean increase in ARI from 2.08 ± 1.10 to 3.80 ± 1.36 (p=0.008).

Conclusions: Dynamic cerebral autoregulation is impaired in patients with middle cerebral artery stenosis. Assessing dynamic cerebral autoregulation may allow a subgroup of patients with MCA stenosis who are at risk of hemodynamic stroke to be identified. Dynamic cerebral disautoregulation in patients with severe MCA stenosis is mostly remedied by stent angioplasty.     

Acute hypercarbia increases the lower limit of cerebral blood flow autoregulation in a porcine model

Objectives: In the present study, our objective was to determine if hypercarbia would alter cerebral blood flow (CBF) autoregulation and reduce the ability of cerebrovascular reactivity monitoring to identify the lower limit of cerebrovascular autoregulation (LLA).

Methods: Anaesthetised juvenile pigs were assigned between two groups: normocarbia (control group, n?=?10) or hypercarbia [high carbon dioxide (CO₂) group, n?=?8]. Normocarbia subjects were maintained with an arterial CO₂ of 40?Torr, while the hypercarbia subjects had an increase of inspired CO₂ to achieve an arterial pCO₂ of >80?Torr. Gradual hypotension was induced by continuous haemorrhage from a catheter in the femoral vein, and the LLA was determined by monitoring cortical laser Doppler flux (LDF). Vascular reactivity monitoring was performed using the pressure reactivity index (PRx) and haemoglobin volume index (HVx).

Results: There were no sustained differences in ICP between groups. Autoregulation was present in both groups, despite elevation in pCO₂.The control group had an average LLA of 45?mmHg (95% CI: 43–47?mmHg) and the high CO₂ group had a LLA of 75?mmHg (95% CI: 73–77?mmHg). The detected LLA for each subject correlated with the level of pCO₂ (spearman R?=?0.8243, P?<?0.0001). Both the PRx and HVx accurately detected the LLA despite the presence of hypercarbia.

Discussion: Hypercarbia without acidosis increases the observed LLA independent of alterations in ICP. Elevations in CO₂ can impair cerebrovascular autoregulation, but if there is a sufficient increase in blood pressure above the CO₂ altered LLA, then autoregulation persists.     

Significance of a reduced cerebral blood flow during the first 12 hours after traumatic brain injury

Background: It is controversial whether a low cerebral blood flow (CBF) simply reflects the severity of injury or whether ischemia contributes to the brain’s injury. It is also not clear whether posttraumatic cerebral hypoperfusion results from intracranial hypertension or from pathologic changes of the cerebral vasculature. The answers to these questions have important implications for whether and how to treat a low CBF. Methods: We performed a retrospective analysis of 77 patients with severe traumatic brain injury who had measurement of CBF within 12 hours of injury. CBF was measured using xenon-enhanced computed tomography (XeCT). Global CBF, physiological parameters at the time of XeCT, and outcome measures were analyzed. Results: Average global CBF for the 77 patients was 36±16 mL/100g/minutes. Nine patients had an average global CBF <18 (average 12±5). The remaining 68 patients had a global CBF of 39±15. The initial ICP was >20 mmHg in 90% and >30 mmHg in 80% of patients in the group with CBF<18, compared to 33% and 16%, respectively, in the patients with CBF≥18. Mortality was 90% at 6 months postinjury in patients with CBF<18. Mortality in the patients with CBF>18 was 19% at 6 months after injury. Conclusion: In patients with CBF<18 mL/100 g/minutes, intracranial hypertension plays a major causative role in the reduction in CBF. Treatment would most likely be directed at controlling intracranial pressure, but the early, severe intracranial hypertension also probably indicates a severe brain injury. For levels of CBF between 18 and 40 mL/100 g/minutes, the presence of regional hypoperfusion was a more important factor in reducing the average CBF.     

The vascular steal phenomenon is an incomplete contributor to negative cerebrovascular reactivity in patients with symptomatic intracranial stenosis

‘Vascular steal'' has been proposed as a compensatory mechanism in hemodynamically compromised ischemic parenchyma. Here, independent measures of cerebral blood flow (CBF) and blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) responses to a vascular stimulus in patients with ischemic cerebrovascular disease are recorded. Symptomatic intracranial stenosis patients (n=40) underwent a multimodal 3.0T MRI protocol including structural (T₁-weighted and T₂-weighted fluid-attenuated inversion recovery) and hemodynamic (BOLD and CBF-weighted arterial spin labeling) functional MRI during room air and hypercarbic gas administration. CBF changes in regions demonstrating negative BOLD reactivity were recorded, as well as clinical correlates including symptomatic hemisphere by infarct and lateralizing symptoms. Fifteen out of forty participants exhibited negative BOLD reactivity. Of these, a positive relationship was found between BOLD and CBF reactivity in unaffected (stenosis degree<50%) cortex. In negative BOLD cerebrovascular reactivity regions, three patients exhibited significant (P<0.01) reductions in CBF consistent with vascular steal; six exhibited increases in CBF; and the remaining exhibited no statistical change in CBF. Secondary findings were that negative BOLD reactivity correlated with symptomatic hemisphere by lateralizing clinical symptoms and prior infarcts(s). These data support the conclusion that negative hypercarbia-induced BOLD responses, frequently assigned to vascular steal, are heterogeneous in origin with possible contributions from autoregulation and/or metabolism.     

Indomethacin: A review of its cerebral blood flow effects and potential use for controlling intracranial pressure in traumatic brain injury patients

Abstract

Traumatic brain injury (TBI) causes about 75,000 deaths and leaves approximately 200,000 people disabled in USA each year. Brain swelling and increased intracranial pressure (ICP) contribute to this morbidity and mortality. Aggressive management protocols,including ICP control, have been shown to reduce the overall mortality from 50% to 36% following severe head injury. Despite these encouraging results, new and improved pharmacologic strategies to control ICP are required. Indomethacin (IND) is a non-steroidal anti-inflammatory agent with unique effects on cerebral blood flow physiology which may be of benefit in reducing elevated ICP in TBI patients. Data from animal models and randomized, controlled studies with pre-term infants have shown that i.v. IND produces rapid, significant reductions in cerebral blood flow (CBF). Controlled studies of I.v. IND in normal volunteers show a reduction In CBF from 26%-40%. Case series involving severe TBI patients suggest that IND i.v. boluses of 30-50mg reduce ICP by 37%-52%, reduce CBF by 22%-26%, with a modest 14% increase in cerebral perfusion pressure (CPP). Despite these encouraging results, i.v. IND should only be considered an experimental treatment for control of refractory ICP in TBI patients. Larger, well-designed randomized trials in TBI patients will provide more efficacy and safety data and delineate the effects of IND alone or in combination with other proven, effective, or experimental therapies. Once these concerns have been addressed, larger outcome studies will ultimately be needed to determine the role of IND for ICP control in TBI patients. [Neurol Res 1999; 21: 491-499]     

The contribution of arterial blood gases in cerebral blood flow regulation and fuel utilization in man at high altitude

The effects of partial acclimatization to high altitude (HA; 5,050 m) on cerebral metabolism and cerebrovascular function have not been characterized. We hypothesized (1) increased cerebrovascular reactivity (CVR) at HA; and (2) that CO₂ would affect cerebral metabolism more than hypoxia. PaO₂ and PaCO₂ were manipulated at sea level (SL) to simulate HA exposure, and at HA, SL blood gases were simulated; CVR was assessed at both altitudes. Arterial–jugular venous differences were measured to calculate cerebral metabolic rates and cerebral blood flow (CBF). We observed that (1) partial acclimatization yields a steeper CO₂-H⁺ relation in both arterial and jugular venous blood; yet (2) CVR did not change, despite (3) mean arterial pressure (MAP)-CO₂ reactivity being doubled at HA, thus indicating effective cerebral autoregulation. (4) At SL hypoxia increased CBF, and restoration of oxygen at HA reduced CBF, but neither had any effect on cerebral metabolism. Acclimatization resets the cerebrovasculature to chronic hypocapnia.     

Endoscopic technique: A new model of subarachnoid hemorrhage in rats

Abstract

It has become increasingly evident that the pathophysiology of cerebral vasospasm following subarachnoid hemorrhage (SAH) which described the ischemic consequences of cerebral arterial constriction is complex and multifactorial. In an attempt to study cerebral vasospasm, numerous investigators have used experimental animal models that resemble cerebral vasospasm in humans. No ideal model for SAH has been found as yet, and hence the quest for such a model continues. We developed an endoscopic technique that permits a direct vision of internal carotid artery and puncturing the artery to provoke SAH. This model will closely reflect the clinical setting of an aneurysm rupture. The onset of SAH was characterized by a sudden decrease of cerebral blood flow (CBF) and cerebral blood volume (CBV) by at least 40% in the first 20 min. Following this initial drop, there was an increase in the CBF and the CBV, however, they remained significantly below the base line values, at the end of 1 h. This study describes a new model of SAH in rat that simulates the clinical phenomenon of ruptured intracranial aneurysm that also produces cerebral vasospasm. [Neurol Res 2001; 23: 627-630]     

Vascular reactivity in the primate brain after acute cryogenic injury.

The effects of an acute cryogenic injury on cerebral flow (CBF) and cerebral vascular reactivity were studied in 12 anaesthetised, ventilated baboons. Autoregulation, defined in this study as intact with a greater than 20% change in cerebrovascular resistance in response to a change in cerebral perfusion pressure, was tested before the lesion by arterial hypotension. Intact autoregulation was found in half the animals, but all animals showed an increase in CBF with hypercarbia. The cryogenic lesion was followed by a marked rise in intracranial pressure, and a fall in CBF which was only partly related to the status of autoregulation beforehand. After injury, arterial hypertension caused an increase in cerebrovascular resistance of more than 20% in half the animals. This response was not related to the presence of autoregulation before the lesion, and was accompanied by a greater impairment of the cerebrovascular response to carbon dioxide, more severe brain oedema, and lower cerebral oxygen consumption, than in the remaining baboons which had a pressure passive response to arterial hypertension. This study confirms that the failure of CBF to increase with arterial hypertension may indicate severe brain damage rather than intact physiological autoregulation.     

Slow oscillations in middle cerebral artery cerebral blood flow velocity and aging

Abstract

Objective: A recent study using near infrared spectroscopy (NIRS) showed that low frequency oscillations of regional cerebral blood flow (CBF) decline with age. Using transcranial Doppler ultrasound (TCD), it is possible to monitor similar fluctuations in cerebral blood velocity (CBV) in basal cerebral vessels. Such oscillations have been used widely in the assessment of cerebral autoregulation. We postulated that it should be possible to observe similar age related reductions in the amplitude of slow waves recorded using TCD.

Methods: We studied 187 patients with head injury, who were admitted to Addenbrooke's Neuro Critical Care unit between 1992 and 1998. Intermittent recordings of CBV were undertaken using TCD, which were subsequently analysed using software developed in-house. Power spectra were computed in the very low frequency (VLF: 0.01–0.05 Hz) and low frequency (LF: 0.07–0.11 Hz) ranges for all signals and a regression analysis was performed to assess the correlation between power in each frequency band and age.

Results: No significant correlation was found between VLF or LF power and age (VLF: r=0.037; p=0.63; LF: r=?0.05, p=0.517).

Discussion: While remaining cogniscent of the complex nature of our patient group, we find that age dependent reductions in CBF oscillations seen using NIRS do not translate to recordings of CBV in the middle cerebral artery in patients with head injury.     

Cerebral vasomotor reactivity testing in head injury: the link between pressure and flow

BACKGROUND: It has been suggested that a moving correlation index between mean arterial blood pressure and intracranial pressure, called PRx, can be used to monitor and quantify cerebral vasomotor reactivity in patients with head injury. OBJECTIVES: To validate this index and study its relation with cerebral blood flow velocity and cerebral autoregulation; and to identify variables associated with impairment or preservation of cerebral vasomotor reactivity. METHODS: The PRx was validated in a prospective study of 40 head injured patients. A PRx value of less than 0.3 indicates intact cerebral vasomotor reactivity, and a value of more than 0.3, impaired reactivity. Arterial blood pressure, intracranial pressure, mean cerebral perfusion pressure, and cerebral blood flow velocity, measured bilaterally with transcranial Doppler ultrasound, were recorded. Dynamic cerebrovascular autoregulation was measured using a moving correlation coefficient between arterial blood pressure and cerebral blood flow velocity, the Mx, for each cerebral hemisphere. All variables were compared in patients with intact and impaired cerebral vasomotor reactivity. RESULTS: No correlation between arterial blood pressure or cerebral perfusion pressure and cerebral blood flow velocity was seen in 19 patients with intact cerebral vasomotor reactivity. In contrast, the correlation between these variables was significant in 21 patients with impaired cerebral vasomotor reactivity, whose cerebral autoregulation was reduced. There was no correlation with intracranial pressure, arterial blood pressure, cerebral perfusion pressure, or interhemispheric cerebral autoregulation differences, but the values for these indices were largely within normal limits. CONCLUSIONS: The PRx is valid for monitoring and quantifying cerebral vasomotor reactivity in patients with head injury. This intracranial pressure based index reflects changes in cerebral blood flow and cerebral autoregulatory capacity, suggesting a close link between blood flow and intracranial pressure in head injured patients. This explains why increases in arterial blood pressure and cerebral perfusion pressure may be useful for reducing intracranial pressure in selected head injured patients (those with intact cerebral vasomotor reactivity).