Anesthetic Consideration for Descending Thoracic Aortic Aneurysm Repair

Kahn, Ronald A.; Stone, Marc E.; Moskowitz, David M.

doi:10.1177/1089253207306098

Cited by 42 publications

(27 citation statements)

References 95 publications

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“…As demonstrated in our previous study, increased BSCB leakage closely associated with invasion of exogenous ligands inducing immune and inflammatory responses were found during the course of spinal cord I/R injury, as evaluated by extravasation of EB dye [8,9]. Similarly, in this study, the bimodal distribution of EB extravasations was clearly observed as two phases, one stage from 6 to 18 h after surgery which continued for several hours, and the later one began at 36 h and peaked at 48 h (Figure 1), paralleling the clinical manifestation of an early ischemic phase with great risks of delayed and exacerbated injury, such as paralysis, two days after surgery [4,5]. …”

Section: Discussionsupporting

confidence: 70%

“…Spinal cord I/R injury after thoracic aortic surgery is invariably associated with dysfunction of the BSCB and plays a fundamental role in the progression of several unpredictable and disastrous complications, such as spinal cord swelling and secondary nerve injury, which account for much of the morbidity and mortality of this condition [4,5]. Spinal cord edema is often long lasting and resistant to therapeutic intervention.…”

Section: Discussionmentioning

confidence: 99%

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Role of the TLR4 pathway in blood-spinal cord barrier dysfunction during the bimodal stage after ischemia/reperfusion injury in rats

Tan

et al. 2014

J Neuroinflammation

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BackgroundSpinal cord ischemia-reperfusion (I/R) involves two-phase injury, including an initial acute ischemic insult and subsequent inflammatory reperfusion injury, resulting in blood-spinal cord barrier (BSCB) dysfunction involving the TLR4 pathway. However, the correlation between TLR4/MyD88-dependent and TLR4/TRIF-dependent pathways in BSCB dysfunction is not fully understood. The aim of this study is to characterize inflammatory responses in spinal cord I/R and the events that define its clinical progression with delayed neurological deficits, supporting a bimodal mechanism of injury.MethodsRats were intrathecally pretreated with TAK-242, MyD88 inhibitory peptide, or Resveratrol at a 12 h interval for 3 days before undergoing 14-minute occlusion of aortic arch. Evan’s Blue (EB) extravasation and water content were detected at 6, 12, 18, 24, 36, 48, and 72 h after reperfusion. EB extravasation, water content, and NF-κB activation were increased with time after reperfusion, suggesting a bimodal distribution, as maximal increasing were detected at both 12 and 48 h after reperfusion. The changes were directly proportional to TLR4 levels determined by Western blot. Double-labeled immunohistochemical analysis was also used to detect the relationship between different cell types of BSCB with TLR4. Furthermore, NF-κB and IL-1β were analyzed at 12 and 48 h to identify the correlation between MyD88-dependent and TRIF-dependent pathways.ResultsRats without functional TLR4 and MyD88 attenuated BSCB leakage and inflammatory responses at 12 h, suggesting the ischemic event was largely mediated by MyD88-dependent pathway. Similar protective effects observed in rats with depleted TLR4, MyD88, and TRIF receptor at 48 h infer that the ongoing inflammation which occurred in late phase was mainly initiated by TRIF-dependent pathway and such inflammatory response could be further amplified by MyD88-dependent pathway. Additionally, microglia appeared to play a major role in early phase of inflammation after I/R injury, while in late responding phase both microglia and astrocytes were necessary.ConclusionsThese findings indicate the relevance of TLR4/MyD88-dependent and TLR4/TRIF-dependent pathways in bimodal phases of inflammatory responses after I/R injury, corresponding with the clinical progression of injury and delayed onset of symptoms. The clinical usage of TLR4 signaling inhibitors at different phases may be a therapeutic option for the prevention of delayed injury.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Role of the TLR4 pathway in blood-spinal cord barrier dysfunction during the bimodal stage after ischemia/reperfusion injury in rats

Tan

et al. 2014

J Neuroinflammation

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“…Spinal cord ischemia/reperfusion (IR) injury is a well-recognized clinical problem resulting in motor and sensory dysfunction that is characterized as temporary or permanent ischemia of the spinal cord following reperfusion in a setting of shock or thoracoabdominal aorta surgery [1]. The blood brain barrier (BBB) is a well-known specialized structure that maintains brain tissue in an immune-privileged environment [1].…”

Section: Introductionmentioning

confidence: 99%

“…The blood brain barrier (BBB) is a well-known specialized structure that maintains brain tissue in an immune-privileged environment [1]. The spinal cord, as a part of the central nervous system (CNS), connects the brain and the peripheral nervous system.…”

Section: Introductionmentioning

confidence: 99%

Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

Cao

Wang

et al. 2014

Mol Brain

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BackgroundMicroglia are the primary immune cells of the spinal cord that are activated in response to ischemia/reperfusion (IR) injury and release various neurotrophic and/or neurotoxic factors to determine neuronal survival. Among them, matrix metalloproteinase-9 (MMP-9), which cleaves various components of the extracellular matrix in the basal lamina and functions as part of the blood spinal cord barrier (BSCB), is considered important for regulating inflammatory responses and microenvironmental homeostasis of the BSCB in the pathology of ischemia. Sevoflurane has been reported to protect against neuronal apoptosis during cerebral IR. However, the effects of sevoflurane preconditioning on spinal cord IR injury remain unclear. In this study, we investigated the role of sevoflurane on potential genetic roles of microglial MMP-9 in tight junction protein breakdown, opening of the BSCB, and subsequent recruitment of microglia to apoptotic spinal cord neurons.ResultsThe results showed significant upregulation of MMP-9 in rats with IR-induced inflammation of the BSCB compared to that of the sham group, manifested as dysfunctional BSCB with increased Evans blue extravasation and reduced expression of occludin protein. Increased MMP-9 expression was also observed to facilitate invasion and migration of activated microglia, imaging as high Iba-1 expression, clustered to neurons in the injured spinal cord, as shown by double immunofluorescence, and increased proinflammatory chemokine production (CXCL10, CCL2). Further, sevoflurane preconditioning markedly improved motor function by ameliorating neuronal apoptosis, as shown by reduced TUNEL-positive cell counts and expression of cleaved caspase-3. These protective effects were probably responsible for downregulation of MMP-9 and maintenance of normal expression of occludin protein indicating BSCB integrity from inflammatory damage, which was confirmed by decreased protein levels of Iba-1 and MMP-9, as well as reduced production of proinflammatory chemokines (CXCL10, CCL2) and proinflammatory cytokines (IL-1β). Intrathecal injection of specific siRNAs targeting MMP-9 had similar protective effects to those of sevoflurane preconditioning.ConclusionsPreconditioning with 2.4% sevoflurane attenuated spinal cord IR injury by inhibiting recruitment of microglia and secretion of MMP-9; thus inhibiting downstream effects on inflammatory damage to BSCB integrity and neuronal apoptosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13041-014-0069-7) contains supplementary material, which is available to authorized users.

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“…6 Lung isolation is also beneficial as it reduces contamination of the dependent lung from blood and/or secretions. 7 A DLT presents several advantages for achieving OLV in TAA repair. It is relatively reliable to place, allows easy suctioning of both lungs, is unlikely to migrate during surgery, and in the case of migration can be repositioned with the use of a fiber-optic bronchoscope.…”

Section: Intraoperative Managementmentioning

confidence: 99%

One-Lung Ventilation for Surgical Repair of Thoracic Aortic Aneurysm

Goodwin

Blasius

Brand

et al. 2013

Semin Cardiothorac Vasc Anesth

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Advances in the surgical approach to thoracic aortic aneurysm repairs have led to the increasing use of one-lung ventilation. Today's practice of cardiothoracic and vascular anesthesia requires a clear understanding of the techniques available for lung separation and the technical skills necessary to employ them. In this article, we discuss and evaluate the options for one-lung ventilation in thoracic aortic aneurysm repair with regard to preoperative, intraoperative, and postoperative management.

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Anesthetic Consideration for Descending Thoracic Aortic Aneurysm Repair

Cited by 42 publications

References 95 publications

Role of the TLR4 pathway in blood-spinal cord barrier dysfunction during the bimodal stage after ischemia/reperfusion injury in rats

Role of the TLR4 pathway in blood-spinal cord barrier dysfunction during the bimodal stage after ischemia/reperfusion injury in rats

Sevoflurane preconditioning ameliorates neuronal deficits by inhibiting microglial MMP-9 expression after spinal cord ischemia/reperfusion in rats

One-Lung Ventilation for Surgical Repair of Thoracic Aortic Aneurysm

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