Chapter 27: Age-related pathophysiology of the blood-brain barrier in heat stress

Sharma, H. S.; Kretzschmar, R.; Cervós-Navarro, J.; Ermisch, A.; Rühle, H; Dey, Prasanta Kumar

doi:10.1016/s0079-6123(08)62334-1

Cited by 59 publications

(23 citation statements)

References 8 publications

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“…Primary axonal damage induces changes in the fluid microenvironment of the central nervous system, to which in turn myelin is susceptible (21)(22)(23)(24). The moderate l ⊥ increases in our cardiac arrest patients are consistent with such secondary myelin damage (25).…”

Section: Neuroradiologysupporting

confidence: 61%

White Matter Changes in Comatose Survivors of Anoxic Ischemic Encephalopathy and Traumatic Brain Injury: Comparative Diffusion-Tensor Imaging Study

Eerden¹,

Khalilzadeh²,

Perlbarg³

et al. 2014

Radiology

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For the NICER (Neuro Imaging for Coma Emergence and Recovery) Consortium Purpose:To analyze white matter pathologic abnormalities by using diffusion-tensor (DT) imaging in a multicenter prospective cohort of comatose patients following cardiac arrest or traumatic brain injury (TBI). Materials and Methods:Institutional review board approval and informed consent from proxies and control subjects were obtained. DT imaging was performed 5-57 days after insult in 49 cardiac arrest and 40 TBI patients. To control for DT imagingprocessing variability, patients' values were normalized to those of 111 control subjects. Automated segmentation software calculated normalized axial diffusivity (l 1 ) and radial diffusivity (l ⊥ ) in 19 predefined white matter regions of interest (ROIs). DT imaging variables were compared by using general linear modeling, and sideto-side Pearson correlation coefficients were calculated. P values were corrected for multiple testing (Bonferroni). Results:In central white matter, l 1 differed from that in control subjects in six of seven TBI ROIs and five of seven cardiac arrest ROIs (all P , .01). The l ⊥ differed from that in control subjects in all ROIs in both patient groups (P , .01). In hemispheres, l 1 was decreased compared with that in control subjects in three of 12 TBI ROIs (P , .05) and nine of 12 cardiac arrest ROIs (P , .01). The l ⊥ was increased in all TBI ROIs (P , .01) and in seven of 12 cardiac arrest ROIs (P , .05). Cerebral hemisphere l 1 was lower in cardiac arrest than in TBI in six of 12 ROIs (P , .01), while l ⊥ was higher in TBI than in cardiac arrest in eight of 12 ROIs (P , .01). Diffusivity values were symmetrically distributed in cardiac arrest (P , .001 for side-to-side correlation) but not in TBI patients. Conclusion:DT imaging findings are consistent with the known predominance of cerebral hemisphere axonal injury in cardiac arrest and chiefly central myelin injury in TBI. This consistency supports the validity of DT imaging for differentiating axon and myelin damage in vivo in humans.q RSNA, 2013

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Section: Neuroradiologysupporting

confidence: 61%

White Matter Changes in Comatose Survivors of Anoxic Ischemic Encephalopathy and Traumatic Brain Injury: Comparative Diffusion-Tensor Imaging Study

Eerden¹,

Khalilzadeh²,

Perlbarg³

et al. 2014

Radiology

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“…In rats, global BBB opening appears to be negligible until a threshold core temperature of ∼40.0 • C (401), but this is highly variable and modified by a range of factors. Juvenile rats, for example, are far more susceptible to BBB opening to heat stress than their adult counterparts (410). The exposure time to high core temperature also appears to significantly affect BBB opening (401).…”

Section: Bbb Under Heat Stressmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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“…Immunohistochemistry analysis for albumin was performed on paraffin embedded (3-µm thick) sections using a sheep polyclonal anti-rat albumin antibody (Sigma, USA) and the streptavidin-HRP-biotin technique as described previously [129,130]. Brief-ly, the endogenous peroxidase activity was blocked with 3% H2O2 and 5% normal goat serum, followed by incubation with the primary antibodies (1:500 for albumin).…”

Section: Albumin Immunostainingmentioning

confidence: 99%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

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Chapter 27: Age-related pathophysiology of the blood-brain barrier in heat stress

Cited by 59 publications

References 8 publications

White Matter Changes in Comatose Survivors of Anoxic Ischemic Encephalopathy and Traumatic Brain Injury: Comparative Diffusion-Tensor Imaging Study

White Matter Changes in Comatose Survivors of Anoxic Ischemic Encephalopathy and Traumatic Brain Injury: Comparative Diffusion-Tensor Imaging Study

Cerebral Vascular Control and Metabolism in Heat Stress

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

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