Acute decrease of cerebrocortical microflow and lack of carbon dioxide reactivity following subarachnoid haemorrhage in the rat

Jarus-Dziedzic, Katarzyna; Czernicki, Z; Koźniewska, Ewa

doi:10.1007/978-3-7091-0651-8_97

Cited by 6 publications

(9 citation statements)

References 11 publications

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“…A lack of response to changes in PaCO 2 has also been observed during acute time periods (ie, minutes) after SAH. 42 In contrast, SAH attenuated CO 2 reactivity in other studies. 42,46 However, meaningful comparisons between the various studies can be problematic because of the various models of SAH used and the differences in post-SAH time period evaluations.…”

Section: Co 2 Reactivitymentioning

confidence: 43%

“…42 In contrast, SAH attenuated CO 2 reactivity in other studies. 42,46 However, meaningful comparisons between the various studies can be problematic because of the various models of SAH used and the differences in post-SAH time period evaluations. Although vasodilation to hypercapnia was not significantly altered after SAH in the present study, it is uncertain whether the phenomenon of reduced vasodilation is restricted to pathways associated with SNS-induced vasodilation.…”

Section: Co 2 Reactivitymentioning

confidence: 43%

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Time-Dependent Alterations in Functional and Pharmacological Arteriolar Reactivity After Subarachnoid Hemorrhage

Britz

Meno

Park

et al. 2007

Stroke

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Background and Purpose-Disturbances in cerebral arteriolar function, in addition to large vessel vasospasm, may be responsible for ischemia after subarachnoid hemorrhage. The purpose of this study was to test the hypothesis that subarachnoid hemorrhage alters cerebral microvascular reactivity. Methods-An endovascular filament model was used to induce subarachnoid hemorrhage in halothane-anesthetized male Sprague-Dawley rats. We evaluated pial arteriolar responses to sciatic nerve stimulation, topically applied vasoactive agents (adenosine or sodium nitroprusside), and CO 2 inhalation in rats subjected to subarachnoid hemorrhage at 1 to 5 days after insult. Results-In sham-operated rats, sciatic nerve stimulation evoked a 23.5Ϯ1.8% increase in arteriolar diameter, which was significantly attenuated to 13.7Ϯ0.9%, 12.8Ϯ2.5%, and 18.8Ϯ2.9% at 24, 48, and 72 hours after subarachnoid hemorrhage, respectively (PϽ0.05; nՆ7). At 96 and 120 hours after subarachnoid hemorrhage, sciatic nerve stimulation-induced dilation recovered to sham levels. Somatosensory-evoked potentials were unaltered by subarachnoid hemorrhage. Pial vasodilatation to adenosine (10 mol/L) and sodium nitroprusside (1 mol/L) were significantly impaired, by 47% and 41%, respectively, at 48 hours after subarachnoid hemorrhage (PϽ0.05; nϭ7). In contrast, CO 2 reactivity was unaffected by subarachnoid hemorrhage. Conclusions-Pial arteriolar responses to cortical activation may be decreased in the initial 2 to 3 days after experimental subarachnoid hemorrhage.

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Section: Co 2 Reactivitymentioning

confidence: 43%

Section: Co 2 Reactivitymentioning

confidence: 43%

Time-Dependent Alterations in Functional and Pharmacological Arteriolar Reactivity After Subarachnoid Hemorrhage

Britz

Meno

Park

et al. 2007

Stroke

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“…In addition, an increase of BBB permeability observed mainly ipsilaterally might raise question whether acute ischemia after SAH results in BBB disruption. Even though greater BBB permeability on the ipsilateral side may be accountable for a greater degree of CBF reduction ipsilaterally, as evidenced by others in the perforation SAH model (Jarus-Dziedzic et al, 2003), blood components including thrombin formation may contribute to BBB disruption after SAH. The role of blood components in BBB disruption after SAH has been examined previously (Sasaki et al, 1986).…”

Section: Early Brain Injury-brain Swelling Brain Edema and Blood-bramentioning

confidence: 82%

Mechanisms of Hyperbaric Oxygen-Induced Neuroprotection in a Rat Model of Subarachnoid Hemorrhage

Ostrowski

Colohan

Zhang

2005

J Cereb Blood Flow Metab

189

167

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Acute cerebral ischemia occurs after subarachnoid hemorrhage (SAH) because of increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). The effect of hyperbaric oxygen (HBO) on physiological and clinical outcomes after SAH, as well as the expressions of hypoxia-inducible factor-1alpha (HIF-1alpha) and its target genes, such as BNIP3 and VEGF was evaluated. Eighty-five male SD rats (300 to 350 g) were randomly assigned to sham, SAH, and SAH+HBO groups. Subarachnoid hemorrhage was induced by endovascular perforation. Cortical cerebral blood flow (CBF), ICP, brain water content, brain swelling, neurologic function, and mortality were assessed. HBO (100% O2, 2.8 ATA for 2 h) was initiated at 1 h after SAH. Rats were sacrificed at 24 h to harvest tissues for Western blot or for histology. Apoptotic morphology accompanied by strong immunostaining of HIF-1alpha, VEGF, and BNIP3 were observed in the hippocampus and the cortex after SAH. Increased expressions of HIF-1alpha, VEGF, and BNIP3 were quantified by Western blot. HBO reduced the expressions of HIF-1alpha, VEGF, and BNIP3, diminished neuronal damage and improved CBF and neurologic function. HBO reduced early brain injury after SAH, probably by inhibition of HIF-1alpha and its target genes, which led to the decrease of apoptosis and preservation of the blood-brain barrier function.

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“…The development of low cerebral oxygenation in 40% of our patients prior to drug treatment may be attributed to microvascular spasm and/or cerebral dysautoregulation related directly to the ictus. 27 The management of acute hypertension in acute cerebrovascular conditions is challenging, and consensus on optimal BP reductions or selection of pharmaceutical agent remains controversial. 9,10,22,43,48,59 On the one hand, treatment of BP may decrease the risk for further hemorrhage in patients with ICH, minimize the risk for rupture of cerebral aneurysms, and, in the acute postoperative period, prevent reperfusion bleeds after resection of an arteriovenous malformation.…”

Section: Discussionmentioning

confidence: 99%

Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation

Narotam

Roberts²,

Taylon³

et al. 2008

JNS

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Acute decrease of cerebrocortical microflow and lack of carbon dioxide reactivity following subarachnoid haemorrhage in the rat

Cited by 6 publications

References 11 publications

Time-Dependent Alterations in Functional and Pharmacological Arteriolar Reactivity After Subarachnoid Hemorrhage

Time-Dependent Alterations in Functional and Pharmacological Arteriolar Reactivity After Subarachnoid Hemorrhage

Mechanisms of Hyperbaric Oxygen-Induced Neuroprotection in a Rat Model of Subarachnoid Hemorrhage

Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation

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