Multiple territory watershed infarcts following spinal anaesthesia

Abkur, Tarig Mohammed; Mohamed, Mohamed Bakri; Peters, Catherine

doi:10.1136/bcr-2014-204995

Cited by 3 publications

(3 citation statements)

References 17 publications

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“…10,42,68 Hypoxia also caused a sustained increase in expression of Rabep2, a novel gene that is critical in the VEGFA!Flk1!Rabep2!Notch!ADAM10/ 17!Clic4 pathway that directs collaterogenesis during development. 10,12,69 Our observation that hypoxic NCF was blocked in Rabep2 À/À mice is consistent with evidence that reduced oxygen, which under baseline conditions in normoxia is lowest in the vessels within the watershed zone between adjacent arterial trees, [70][71][72][73][74][75] induces the same or a similar pathway in the adult.…”

Section: Durability Of Hypoxic Neo-collateral Formation Collateral Rsupporting

confidence: 88%

“… 11 , 12 Perfusion of the plexus by the adjacent arterial trees normally proceeds down the trees’ pressure gradients and venous outflow pathways. 87 – 89 At baseline, oxygen content within watershed capillaries is low because they are the “furthest away from the aorta,” which is consistent with the watershed stroke phenomenon 70 – 75 ; the above-mentioned negligible flow in collaterals at baseline would also favor their PO 2 values being closer to tissue PO 2 . In the case of systemic hypoxemia, the PO 2 in watershed capillaries declines further and activates the collaterogenesis signaling pathway.…”

Section: Discussionsupporting

confidence: 55%

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Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke

Zhang

Rzechorzek

Aghajanian

et al. 2020

J Cereb Blood Flow Metab

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Pial collaterals provide protection in stroke. Evidence suggests their formation late during gestation (collaterogenesis) is driven by reduced oxygen levels in the cerebral watersheds. The purpose of this study was to determine if collaterogenesis can be re-activated in the adult to induce formation of additional collaterals (“neo-collateral formation”, NCF). Mice were gradually acclimated to reduced inspired oxygen (FIO2) and maintained at 12, 10, 8.5 or 7% for two-to-eight weeks. Hypoxemia induced “dose”-dependent NCF and remodeling of native collaterals, and decreased infarct volume after permanent MCA occlusion. In contrast, no formation occurred of addition collateral-like intra-tree anastomoses, PComs, or branches within the MCA tree. Hypoxic NCF, remodeling and infarct protection were durable, i.e. retained for at least six weeks after return to normoxia. Hypoxia increased expression of Hif2α, Vegfa, Rabep2, Angpt2, Tie2 and Cxcr4. Neo-collateral formation was abolished in mice lacking Rabep2, a novel gene involved in VEGFA→Flk1 signaling and required for formation of collaterals during development, and inhibited by knockdown of Vegfa, Flk1 and Cxcr4. Rabep2-dependent NCF was also induced by permanent MCA occlusion. This is the first report that hypoxia induces new pial collaterals to form. Hypoxia- and occlusion-induced neo-collateral formation provide models to study collaterogenesis in the adult.

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Section: Durability Of Hypoxic Neo-collateral Formation Collateral Rsupporting

confidence: 88%

Section: Discussionsupporting

confidence: 55%

Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke

Zhang

Rzechorzek

Aghajanian

et al. 2020

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…It is generally considered that postoperative stroke is multifactorial, and intraoperative hypotension may aggravate the pathological process by increasing the infarction size 26,27 . Furthermore, a decrease of MAP by more than 30% from baseline is significantly associated with the occurrence of a postoperative stroke 34 , and watershed infarct is associated with hypotension following spinal anesthesia 35 . By postoperative MRI examination, we confirmed that watershed infarct is absent in the three patients.…”

Section: Discussionmentioning

confidence: 99%

Postoperative Stroke in Patients After Spinal Anesthesia and Disparate Response Patterns of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

Poon

Liu

Huang

et al. 2021

Preprint

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Spinal anesthesia is generally accepted as an effective and safe practice. Three rare incidents of postoperative cerebral infarction after surgery under spinal anesthesia with bupivacaine prompted us to assess whether spinal bupivacaine may impact carotid or cerebral blood flow and baroreflex functionality. We found that all three patients shared common pathology of stenosis or atheromatous lesions in the carotid or middle cerebral artery. In a companion animal study, we further observed that subarachnoid application of bupivacaine that reached low thoracic spinal cord in male Sprague‐Dawley rats elicited an initial (Phase I) reduction in mean arterial pressure (MAP), carotid blood flow (CBF) and baroreflexmediated sympathetic vasomotor tone, all of which returned to baseline in Phase II. Whereas heart rate (HR) exhibited sustained reduction, cardiac vagal baroreflex, baroreflex efficiency index (BEI) and tissue perfusion and oxygen in cerebral cortex supplied by middle cerebral artery remained unaltered during both phases. However, in one‐third of animals studied, Phase II gave way to a Phase III characterized by secondary hypotension and depressed baroreflex‐mediated sympathetic vasomotor tone, along with continuous decline in HR, sustained cardiac vagal baroreflex, decreased BEI, and reduction in CBF and tissue perfusion or oxygen in cerebral cortex. We conclude that carotid and cerebral blood flow can be compromised after spinal anesthesia, and impaired baroreflex‐mediated sympathetic vasomotor tone that leads to hypotension plays a contributory role.

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Postoperative Stroke after Spinal Anesthesia and Responses of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

Poon

Liu

Huang

et al. 2021

Biology

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Spinal anesthesia is generally accepted as an effective and safe practice. Three rare incidents of postoperative cerebral infarction after surgery under spinal anesthesia prompted us to assess whether spinal bupivacaine may compromise carotid or cerebral blood flow. Postoperative examination after the stroke incident revealed that all three patients shared a common pathology of stenosis or atheromatosis in the carotid or middle cerebral artery. In a companion study using 69 Sprague-Dawley rats, subarachnoid application of bupivacaine elicited an initial (Phase I) reduction in the mean arterial pressure, carotid blood flow (CBF) and baroreflex-mediated sympathetic vasomotor tone, all of which subsequently returned to baseline (Phase II). Whereas heart rate (HR) exhibited sustained reduction, cardiac vagal baroreflex, baroreflex efficiency index (BEI) and tissue perfusion and oxygen in the cerebral cortex remained unaltered. However, in one-third of the rats studied, Phase II gave way to Phase III characterized by secondary hypotension and depressed baroreflex-mediated sympathetic vasomotor tone, along with declined HR, sustained cardiac vagal baroreflex, decreased BEI, reduced CBF and waning tissue perfusion or oxygen in the cerebral cortex. We concluded that carotid and cerebral blood flow can indeed be compromised after spinal anesthesia, and an impaired baroreflex-mediated sympathetic vasomotor tone, which leads to hypotension, plays a contributory role.

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Multiple territory watershed infarcts following spinal anaesthesia

Cited by 3 publications

References 17 publications

Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke

Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke

Postoperative Stroke in Patients After Spinal Anesthesia and Disparate Response Patterns of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

Postoperative Stroke after Spinal Anesthesia and Responses of Carotid or Cerebral Blood Flow and Baroreflex Functionality to Spinal Bupivacaine in Rats

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