Cerebrovascular Response to Dynamic Changes in pCO&lt;sub&gt;2&lt;/sub&gt;

Garnham, J.; Panerai, Ronney B.; Naylor, A.R.; Evans, David H.

doi:10.1159/000015944

Cited by 40 publications

(43 citation statements)

References 16 publications

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“…The reduction of CPPe due to hyperventilation in our patients was clinically relevant, which is in accordance with previous findings. 2,[5][6][7]40 When using TCD, an estimate of vascular resistance can be derived from the ratio between blood pressure and blood flow velocity, which equals the product of the peripheral resistance and the cross-sectional area of the vessel at the site of insonation, the RAP. 10 Up to now, there is no investigation that compared measurements of global CBF and V MCA compare changes in CVR with RAP.…”

Section: Discussionmentioning

confidence: 99%

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Grüne

Kazmaier

Stolker

et al. 2015

J Cereb Blood Flow Metab

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In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO 2 -induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO 2 levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure-flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean V MCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39%; despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak (r = 0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP.

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Section: Discussionmentioning

confidence: 99%

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Grüne

Kazmaier

Stolker

et al. 2015

J Cereb Blood Flow Metab

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“…The underlying pathophysiology for the impairment in dynamic CA was not under test in this study but could potentially result from abnormalities in metabolic, myogenic, neurogenic and endothelial mechanisms, including nitric oxide (NO) [15], although differences in pCO 2 which are known to dramatically affect CA [16]cannot account for these changes. Furthermore, these changes cannot be accounted for by previous antihypertensive medication, other workers have found antihypertensive medication does not appear to significantly affect CA [17], and none of the subjects at the follow-up study had received blood pressure lowering therapy since stroke onset.…”

Section: Discussionmentioning

confidence: 99%

Serial Changes in Static and Dynamic Cerebral Autoregulation after Acute Ischaemic Stroke

Dawson

Panerai²,

Potter³

2003

Cerebrovasc Dis

177

133

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Background: The longitudinal changes in static and dynamic cerebral autoregulation (CA) following acute ischaemic stroke are unknown and were assessed in this study. Methods: Fifty-four ischaemic stroke patients were studied within 96 h of ischaemic stroke and again 7–14 days later, using transcranial Doppler techniques to measure CA. Results were compared to an age-, sex- and blood pressure (BP)-matched control group. Static BP pressor stimulus was produced by thigh cuff inflation and dynamic stimulus by rapid thigh cuff release. Results: Dynamic, but not static, CA was globally impaired at initial (mean dynamic CA index 3.9 ± 3.1 vs. 6.2 ± 2.3, p < 0.005) and follow-up studies (dynamic CA 3.9 ± 2.8 vs. 6.2 ± 2.3, p < 0.01) in stroke patients compared to controls. Static CA was similar in stroke patients and controls and was unchanged during follow-up. Conclusions: Dynamic, but not static, CA is impaired after acute ischaemic stroke and remains abnormal for at least 1–2 weeks post ictus. These changes are present in both the affected and non-affected hemispheres and are unrelated to previous antihypertensive treatment, baseline BP levels or BP changes after stroke, age or stroke type.

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“…Although vasoactive dysfunction may partly underlie both cerebrovascular reactivity and autoregulation, it has been suggested that each reflects a different mechanism controlling cerebral blood flow [5]. Consistent with this is evidence that the pathophysiological bases of the hypercapnic and autoregulatory responses differ [14,16].…”

Section: Introductionmentioning

confidence: 88%

Cerebrovascular reactivity and dynamic autoregulation in nondemented patients with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)

Singhal

Markus

2005

J Neurol

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Reduced cerebrovascular reactivity has been reported in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and the measurement has been suggested as a useful surrogate marker of disease progression. Previous studies have not determined whether cerebral autoregulation is also impaired. We measured dynamic cerebral autoregulation and carbon dioxide reactivity in 24 nondemented CADASIL patients and 20 controls, using transcranial Doppler ultrasound (TCD). No impairment in either measure was found in the CADASIL group. We conclude that either cerebrovascular reactivity and autoregulation are not impaired in early disease, or that TCD may not be a sufficiently sensitive tool to detect haemodynamic changes in early disease. TCD is unlikely to be useful for disease monitoring in patients without advanced disease.

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Cerebrovascular Response to Dynamic Changes in pCO<sub>2</sub>

Cited by 40 publications

References 16 publications

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Serial Changes in Static and Dynamic Cerebral Autoregulation after Acute Ischaemic Stroke

Cerebrovascular reactivity and dynamic autoregulation in nondemented patients with CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)

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