Characterization of an improved double hemorrhage rat model for the study of delayed cerebral vasospasm

Lee, Jin Yul; Huang, Dah Luen; Keep, Richard F.; Sagher, Oren

doi:10.1016/j.jneumeth.2007.10.029

Cited by 34 publications

(45 citation statements)

References 37 publications

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“…The basis for the observed differences between those studies and our present work is not readily apparent. However, in support of our present findings, histological studies have found evidence of increased constriction of intracerebral arterioles from SAH model animals (22,37,50).…”

Section: Discussionsupporting

confidence: 92%

“…A small (0.5-1.5 cm), longitudinal, midline suboccipital incision was centered over the foramen magnum, and the neck muscles were dissected until dura was visualized. Autologous unheparinized blood (0.5 ml) drawn from the tail artery was injected into the cisterna magna (day 0) with a 25-gauge butterfly needle (37). The animal was then positioned on an incline board at a 45°angle with the head down in neutral position for 30 min.…”

Section: Methodsmentioning

confidence: 99%

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Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization

Nystoriak¹,

O'Connor²,

Sonkusare³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

118

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Nystoriak MA, O'Connor KP, Sonkusare SK, Brayden JE, Nelson MT, Wellman GC. Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization. Am J Physiol Heart Circ Physiol 300: H803-H812, 2011. First published December 10, 2010 doi:10.1152 doi:10. /ajpheart.00760.2010 arterioles are morphologically and physiologically unique compared with pial arteries and arterioles. The ability of subarachnoid hemorrhage (SAH) to induce vasospasm in large-diameter pial arteries has been extensively studied, although the contribution of this phenomenon to patient outcome is controversial. Currently, little is known regarding the impact of SAH on parenchymal arterioles, which are critical for regulation of local and global cerebral blood flow. Here diameter, smooth muscle intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i), and membrane potential measurements were used to assess the function of intact brain parenchymal arterioles isolated from unoperated (control), sham-operated, and SAH model rats. At low intravascular pressure (5 mmHg), membrane potential and [Ca 2ϩ ]i were not different in arterioles from control, sham-operated, and SAH animals. However, raising intravascular pressure caused significantly greater membrane potential depolarization, elevation in [Ca 2ϩ ]i, and constriction in SAH arterioles. This SAH-induced increase in [Ca 2ϩ ]i and tone occurred in the absence of the vascular endothelium and was abolished by the L-type voltage-dependent calcium channel (VDCC) inhibitor nimodipine. Arteriolar [Ca 2ϩ ]i and tone were not different between groups when smooth muscle membrane potential was adjusted to the same value. Protein and mRNA levels of the L-type VDCC CaV1.2 were similar in parenchymal arterioles isolated from control and SAH animals, suggesting that SAH did not cause VDCC upregulation. We conclude that enhanced parenchymal arteriolar tone after SAH is driven by smooth muscle membrane potential depolarization, leading to increased L-type VDCC-mediated Ca 2ϩ influx.voltage-dependent calcium channels; vascular smooth muscle; cerebral blood flow; endothelium; ion channels CEREBRAL BLOOD FLOW IS REGULATED by the diameter of resistance arteries and arterioles both on the surface of the brain and within the brain parenchyma. Parenchymal arterioles, unlike pial arteries and arterioles, lack extrinsic innervation and are encased by astrocytic processes ("endfeet") (17, 27). The close association of this microvasculature with astrocytic endfeet is essential for functional hyperemia, whereby focal increases in neuronal activity are coupled to vasodilation of nearby arterioles and increased blood flow (6,14,27,45). In addition to their role in neurovascular coupling, parenchymal arterioles also contribute significantly to autoregulation of global cerebral blood flow and account for ϳ40% of total cerebral vascular resistance (12 (1,13,19,32,44). Recent work has established that pressuredependent constriction, or myogeni...

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Section: Discussionsupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization

Nystoriak¹,

O'Connor²,

Sonkusare³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

118

View full text Add to dashboard Cite

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“…Patients may experience a broad range of deficits involving memory, learning, attention, psychomotor speed, and emotional health [3][4][5]. Short-term rodent recovery models are often used to explore post-SAH mechanisms that result in neurologic deficits [6][7][8]. Only recently has this work been extended to examine cognitive deficits [9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

et al. 2016

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Background Cognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models. Methods Pilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days. Results DB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB. Conclusion Both SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.

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“…Including prechiasmatic cistern injection model, common mortality of experimental SAH rats were various from 9% to 100% (Gules, Satoh, Clower, Nanda, & Zhang, 2002; Lee, Huang, Keep, & Sagher, 2008; Lee, Sagher, Keep, Hua, & Xi, 2009; Park et al., 2008; Prunell, Mathiesen, & Svendgaard, 2002). In present study, the mortality of SAH and VEH group were 25% and 22%, respectively, which were similar to other studies using this injection model (Boettinger et al., 2017; Dou et al., 2017).…”

Section: Discussionmentioning

confidence: 99%

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

Cai

Bai

et al. 2017

Brain and Behavior

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Background and PurposeSubarachnoid hemorrhage (SAH)‐induced cerebral vasospasm and early brain injury is a fatal clinical syndrome. Cerebral vasospasm and early brain injury are associated with inflammatory response and oxidative stress. Whether curcumin, which plays important roles to regulate inflammatory cytokines and inhibit oxidative stress, inhibits SAH‐induced inflammation and oxidative stress are largely unknown.MethodsAdult male rats underwent autologous blood injection into prechiasmatic cistern to induce SAH. Curcumin (150 mg/kg) was administered at 0.5, 24 and 48 hr post‐SAH. Mortality calculation and neurological outcomes as well as morphological vasospasm of anterior cerebral artery were studied. Superoxide dismutase, lipid peroxidation, and inflammatory cytokines (MCP‐1 and TNF‐α) expression in prefrontal region were quantified. Furthermore, p65 and phosphor‐p65 were quantitatively analyzed.ResultsCurcumin remarkedly reduced mortality and ameliorated neurological deficits after SAH induction (p < .05); morphological results showed that cerebral vasospasm in curcumin‐treated group was mitigated (p < .05). SAH‐induced MCP‐1 and TNF‐α overexpression were inhibited in curcumin‐treated group (p < .05). Importantly, phosphor‐p65 was significantly inhibited after curcumin treatment (p < .05).ConclusionsCurcumin can inhibit SAH‐induced inflammatory response via restricting NF‐κB activation to alleviate cerebral vasospasm and early brain injury.

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Characterization of an improved double hemorrhage rat model for the study of delayed cerebral vasospasm

Cited by 34 publications

References 37 publications

Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization

Fundamental increase in pressure-dependent constriction of brain parenchymal arterioles from subarachnoid hemorrhage model rats due to membrane depolarization

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

Curcumin mitigates cerebral vasospasm and early brain injury following subarachnoid hemorrhage via inhibiting cerebral inflammation

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