Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage.

Hatake, Kiyohiko; Wakabayashi, Ichiro; Kakishita, Eizo; Hishida, Shigeru

doi:10.1161/01.str.23.8.1111

Cited by 88 publications

(37 citation statements)

References 44 publications

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“…A number of studies suggest that nitric oxide (NO)-mediated vasodilation is impaired in large-diameter cerebral arteries in experimental models of SAH (5, 13). Similar findings have been reported in basilar arteries of SAH patients (23). However, the contribution of endothelial dysfunction to cerebral artery constriction is controversial, and others have reported that endothelium-dependent relaxation is unchanged after SAH (8,39).…”

Section: Discussionsupporting

confidence: 87%

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: 87%

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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“…22 Alternatively, endothelial dysfunction may also impose an increased vulnerability for DCI in patients early after SAH. 22,23 Furthermore, the increased incidence of DCI after concomitant early perfusion impairment and increased subarachnoid blood clot (high-risk group) in our study may reflect an exacerbation of SAH-related endothelial dysfunction. 24 Finally, our results reflect recent studies on the dissociation of angiographic vasospasm and poor neurological outcome and support the assumption that cerebral infarction might reflect the ultimate end point of different, proischemic pathomechanisms (eg, microthromboembolism, microvascular spasm, cortical spreading ischemia, impaired autoregulation).…”

Section: Discussionmentioning

confidence: 70%

Early Perfusion Computerized Tomography Imaging as a Radiographic Surrogate for Delayed Cerebral Ischemia and Functional Outcome After Subarachnoid Hemorrhage

Etminan

Beseoglu

Heiroth

et al. 2013

Stroke

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Background and Purpose-To date, there is no immediate radiographic surrogate to quantify primary cerebral injury to identify patients at risk for delayed cerebral ischemia and poor clinical outcome after aneurysmal subarachnoid hemorrhage. Therefore, we investigated the relation of early cerebral perfusion-computerized tomography and clot volume with radiological events of delayed cerebral ischemia and clinical outcome in patients with aneurysmal subarachnoid hemorrhage. Methods-Data from 2 cohorts of patients (51 in main, 28 patients in control cohort) with aneurysmal subarachnoid hemorrhage, receiving computerized tomography and perfusion-computerized tomography scanning <12 hours after ictus, were included. A risk group model for functional outcome was developed on the basis of early mean transit time (MTT) and volumetric blood clot measurements.

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“…Similarly, dilation of basilar arteries in response to thrombin was reduced after subarachnoid hemorrhage, and that in response to vasopressin was abolished (27). Reduced dilation of arteries to stimulation by thrombin, bradykinin, and Ca2+ ionophore A23187 has been reported, whereas relaxation to SNP was not affected in basilar artery from human patients after subarachnoid hemorrhage (28). The mechanism(s) by which cerebral vessels lose the ability to dilate in response to selective vasoactive stimuli after exposure to blood is not well understood.…”

Section: Discussionmentioning

confidence: 76%

Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

1994

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The effects of perivascular blood on pial arteriolar vasoreactivity to selected vasodilators and vasoconstrictors were examined in vivo in a newborn pig model. a-Chloraloseanesthetized newborn pigs were fitted with closed cranial windows 4 d after cortical subarachnoid injections of autologous blood. The responsiveness of pial arterioles to topical application of dilator agents [iloprost, prostaglandin E, (PGE,), histamine, and sodium nitroprusside (SNP)] and vasoconstrictor agents [leukotriene C4 and endothelin-1 (ET-1) in artificial cerebrospinal fluid was studied in control and blood-injected piglets. Pial arterioles dilated dose dependently in response to topical application of iloprost, PGE,, histamine, and SNP in the control group, with increases in diameter of 54,44,67, and 50% at lop8 M, lop5 M, lop5 M, and M, respectively. These dilations in response to iloprost, PG&, and histamine in the blood-injected piglets were significantly attenuated to 23, 18, and 34%, respectively, whereas the dilation in response to SNP was not changed (64%). Constrictions in response to lop8 M leukotriene C4 and ET-1 were 16 and 26% and were potentiated by hematoma to 36 and 43%, respectively. The lowest dose of ET-1 (10-l2 M) significantly dilated pial arterioles in the control but not in the blood-treated group. We conclude that prolonged exposure of pial arterioles to perivascular blood attenuates cerebrovascular dilation in response to selected vasoactive agents (iloprost, PGE;, and histamine) but not to SNP, suggesting that blood-induced attenuation of vasodilation and the generalized vasoconstriction may involve inhibiting the prostanoid/cAMP signaling pathway. Potentiation of vasoconstriction induced by ET-1 and leukotriene C, in the hematoma group could be due to loss of this dilator influence. (Pediatr Res 36: [589][590][591][592][593][594] 1994) Abbreviations aCSF, artificial cerebrospinal fluid ET-1, endothelin-1 LTC,, leukotriene C, PGF,, prostaglandin F,, PGE,, prostaglandin E, SNP, sodium nitroprusside Intraventricular and periventricular cerebral hemorrhages occur frequently in preterm babies, whereas subarachnoid hemorrhages occur in both term and preterm infants (1-3). In adults and children, subarachnoid hemorrhage can also result from trauma, asphyxia, brain injury, or rupture of an intracranial aneurysm (4-6). In adults, one of the major complications of cerebral hemorrhage is a delayed cerebral ischemia due to abnormal vasoconstriction of large cerebral arteries that usually presents itself 4-7 d after the hemorrhage. Alterations of cerebral circulation and metabolism can develop secondary to cerebral vasoconstriction, resulting in death or permanent cerebral dysfunction (4-8). Despite much research into the etiology of hemorrhage-induced vasoconstriction (4-8), our understanding of the mechanism by which cerebral arterial vasoconstriction occurs after cerebral hemorrhages is still limited. Much less information is available on the effects of hematoma on cerebral circulation in neonates.Vasodilator pr...

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Impairment of endothelium-dependent relaxation in human basilar artery after subarachnoid hemorrhage.

Cited by 88 publications

References 44 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

Early Perfusion Computerized Tomography Imaging as a Radiographic Surrogate for Delayed Cerebral Ischemia and Functional Outcome After Subarachnoid Hemorrhage

Subarachnoid Hematoma Attenuates Vasodilation and Potentiates Vasoconstriction Induced by Vasoactive Agents in Newborn Pigs

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