Acute reaction of arterial blood vessels after experimental subarachnoid hemorrhage – An in vivo microscopic study

Westermaier, Thomas; Stetter, Christian; Koehler, D.; Weiland, Judith; Lilla, Nadine

doi:10.1016/j.jns.2018.11.007

Cited by 7 publications

(4 citation statements)

References 25 publications

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“…Immediately after the rupture of the aneurysm, cerebral perfusion pressure (CPP) decreases due to a sudden increase of ICP resulting in a reduction of CBF and global ischemia. Simultaneously or shortly thereafter, diffuse early arterial vasoconstriction has been observed and contributes to the persistent perfusion deficit in the early stage of SAH 13 , 14 . Due to developments in emergency care, an increasing number of patients with poor-grade SAH can be adequately resuscitated and find their way to a specialized unit.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia

Stetter

Weidner

Lilla

et al. 2021

Sci Rep

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Temporary hypercapnia has been shown to increase cerebral blood flow (CBF) and might be used as a therapeutical tool in patients with severe subarachnoid hemorrhage (SAH). It was the aim of this study was to investigate the optimum duration of hypercapnia. This point is assumed to be the time at which buffer systems become active, cause an adaptation to changes of the arterial partial pressure of carbon dioxide (PaCO2) and annihilate a possible therapeutic effect. In this prospective interventional study in a neurosurgical ICU the arterial partial pressure of carbon dioxide (PaCO2) was increased to a target range of 55 mmHg for 120 min by modification of the respiratory minute volume (RMV) one time a day between day 4 and 14 in 12 mechanically ventilated poor-grade SAH-patients. Arterial blood gases were measured every 15 min. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary end points. Intracranial pressure (ICP) was controlled by an external ventricular drainage. Under continuous hypercapnia (PaCO2 of 53.17 ± 5.07), CBF was significantly elevated between 15 and 120 min after the start of hypercapnia. During the course of the trial intervention, cardiac output also increased significantly. To assess the direct effect of hypercapnia on brain perfusion, the increase of CBF was corrected by the parallel increase of cardiac output. The maximum direct CBF enhancing effect of hypercapnia of 32% was noted at 45 min after the start of hypercapnia. Thereafter, the CBF enhancing slowly declined. No relevant adverse effects were observed. CBF and StiO2 reproducibly increased by controlled hypercapnia in all patients. After 45 min, the curve of CBF enhancement showed an inflection point when corrected by cardiac output. It is concluded that 45 min might be the optimum duration for a therapeutic use and may provide an optimal balance between the benefits of hypercapnia and risks of a negative rebound effect after return to normal ventilation parameters.Trial registration: The study was approved by the institutional ethics committee (AZ 230/14) and registered at ClinicalTrials.gov (Trial-ID: NCT01799525). Registered 01/01/2015.

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Section: Discussionmentioning

confidence: 99%

Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia

Stetter

Weidner

Lilla

et al. 2021

Sci Rep

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“…In the setting of CV, the injured brain may be challenged to maintain cerebral perfusion, ultimately leading to the development of delayed cerebral ischemia. [69][70][71] The ideal treatment would cause dilation of the constricted vessels and restore cerebral perfusion. In this study, we demonstrate that pTNS evoked dose-dependent and highly reproducible increases in CBF and decreases in CVR in healthy rats, which is consistent with multiple previous studies in both animals 11,[19][20][21][22][23][25][26][27]29,30 and humans.…”

Section: Discussionmentioning

confidence: 99%

Percutaneous Trigeminal Nerve Stimulation Induces Cerebral Vasodilation in a Dose-Dependent Manner

White

Shah

et al. 2021

Neurosurg.

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BACKGROUND The trigeminal nerve directly innervates key vascular structures both centrally and peripherally. Centrally, it is known to innervate the brainstem and cavernous sinus, whereas peripherally the trigemino-cerebrovascular network innervates the majority of the cerebral vasculature. Upon stimulation, it permits direct modulation of cerebral blood flow (CBF), making the trigeminal nerve a promising target for the management of cerebral vasospasm. However, trigeminally mediated cerebral vasodilation has not been applied to the treatment of vasospasm. OBJECTIVE To determine the effect of percutaneous electrical stimulation of the infraorbital branch of the trigeminal nerve (pTNS) on the cerebral vasculature. METHODS In order to determine the stimulus-response function of pTNS on cerebral vasodilation, CBF, arterial blood pressure, cerebrovascular resistance, intracranial pressure, cerebral perfusion pressure, cerebrospinal fluid calcitonin gene-related peptide (CGRP) concentrations, and the diameter of cerebral vessels were measured in healthy and subarachnoid hemorrhage (SAH) rats. RESULTS The present study demonstrates, for the first time, that pTNS increases brain CGRP concentrations in a dose-dependent manner, thereby producing controllable cerebral vasodilation. This vasodilatory response appears to be independent of the pressor response induced by pTNS, as it is maintained even after transection of the spinal cord at the C5-C6 level and shown to be confined to the infraorbital nerve by administration of lidocaine or destroying it. Furthermore, such pTNS-induced vasodilatory response of cerebral vessels is retained after SAH-induced vasospasm. CONCLUSION Our study demonstrates that pTNS is a promising vasodilator and increases CBF, cerebral perfusion, and CGRP concentration both in normal and vasoconstrictive conditions.

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“…Immediately after the rupture of the aneurysm, cerebral perfusion pressure (CPP) decreases due to a sudden increase of ICP resulting in a reduction of CBF and global ischemia. Simultaneously or shortly thereafter, diffuse early arterial vasoconstriction has been observed and contributes to the persistent perfusion de cit in the early stage of SAH (12,13). Due to developments in emergency care, an increasing number of patients with poor-grade SAH can be adequately resuscitated and nd their way to a specialized unit.…”

Section: Discussionmentioning

confidence: 99%

Dose Optimization Study of Therapeutic Hypercapnia for Prevention of Secondary Ischemia After Severe Subarachnoid Hemorrhage

Stetter

Weidner

Lilla

et al. 2021

Preprint

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BackgroundAim of this study was to investigate the time point at which the cerebral blood flow (CBF) enhancing effect of controlled hypercapnia in patients with severe aneurysmal subarachnoid hemorrhage (SAH) starts to extenuate. This point is assumed to be the time at which buffer systems become active and annihilate a possible therapeutic effect. MethodsIn this prospective interventional study in a neurosurgical ICU the arterial partial pressure of carbon dioxide (PaCO2) was increased to a target range of 50 - 55 mmHg for 120 minutes by modification of the respiratory minute volume (RMV) one time a day between day 4 and 14 in 12 mechanically ventilated poor-grade SAH-patients. Arterial blood gases were measured every 15 minutes. CBF and brain tissue oxygen saturation (StiO2) were the primary and secondary end points. Intracranial pressure (ICP) was controlled by an external ventricular drainage. ResultsUnder continuous hypercapnia (PaCO2 of 53.17 ± 5.07), CBF was significantly elevated between 15 and 120 minutes after the start of hypercapnia. During the course of the trial intervention, cardiac output also increased significantly. To assess the direct effect of hypercapnia on brain perfusion, the increase of CBF was corrected by the parallel increase of cardiac output. The maximum direct CBF enhancing effect of hypercapnia of 31% was noted at 45 minutes after the start of hypercapnia. Thereafter, the CBF enhancing slowly declined. No relevant adverse effects were observed. Conclusion CBF and StiO2 reproducibly increased by controlled hypercapnia in all patients. After 45 minutes, the curve of CBF enhancement showed an inflection point when corrected by cardiac output. Temporary hypercapnia of 45 minutes is, thus, likely to be the optimum duration for a therapeutic use and for a controlled comparative trial. Longer intervals bear the risk of a negative rebound effect after return to normal ventilation parameters and may be counterproductive inducing ischemia in a state of critical perfusion after SAH. Trial registrationThe study was approved by the institutional ethics committee (AZ 230/14) and registered at ClinicalTrials.gov (Trial-ID: NCT01799525). Registered 01 January 2015. Retrospectively registered.

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Acute reaction of arterial blood vessels after experimental subarachnoid hemorrhage – An in vivo microscopic study

Cited by 7 publications

References 25 publications

Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia

Therapeutic hypercapnia for prevention of secondary ischemia after severe subarachnoid hemorrhage: physiological responses to continuous hypercapnia

Percutaneous Trigeminal Nerve Stimulation Induces Cerebral Vasodilation in a Dose-Dependent Manner

Dose Optimization Study of Therapeutic Hypercapnia for Prevention of Secondary Ischemia After Severe Subarachnoid Hemorrhage

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