Comparison of local cerebral blood flow determined by thermal and hydrogen clearance.

Gaines, Casey; Carter, L P; Crowell, Robert M.

doi:10.1161/01.str.14.1.66

Cited by 32 publications

(7 citation statements)

References 12 publications

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“…After placement of a catheter with its tip in the right ICA, a right temporal burr-hole craniectomy was performed using aseptic technique and a subdural CBF probe (Saber Thermomonitoring, Phoenix, AZ) was inserted over the right temporal lobe for continuous measurement of cortical CBF. 2,15 The position of the probe was verified using fluoroscopy and by rapidly injecting a bolus of saline (1 cc) through the right ICA catheter, which elicited a significant change in CBF and confirmed delivery of solution to the right temporal lobe in the distribution of the right MCA.…”

Section: Experimental Designmentioning

confidence: 97%

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

Afshar¹,

Pluta²,

Boock³

et al. 1995

Journal of Neurosurgery

129

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The continuous release of nitric oxide (NO) is required to maintain basal cerebrovascular tone. Oxyhemoglobin, a putative spasmogen, rapidly binds NO, implicating loss of NO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). If vasospasm is mediated by depletion of NO in the vessel wall, it should be reversible by replacement with NO. To investigate this hypothesis, the authors placed blood clots around the right middle cerebral artery (RMCA) of four cynomolgus monkeys; four unoperated animals served as controls. Arteriography was performed before and 7 days after surgery to assess the presence and degree of vasospasm, which was quantified in the anteroposterior (AP) projection by computerized image analysis. On Day 7, cortical cerebral blood flow (CBF) in the distribution of the right MCA was measured during four to six runs in the right internal carotid artery (ICA) of brief infusions of saline followed by NO solution. Arteriography was performed immediately after completing the final NO infusion in three of the four animals with vasospasm. Right MCA blood flow velocities were obtained using transcranial Doppler before, during, and after NO infusion in two vasospastic animals. After ICA NO infusion, arteriographic vasospasm resolved (mean percent of preoperative AP area, 55.9%); that is, the AP areas of the proximal portion of the right MCA returned to their preoperative values (mean 91.4%; range 88%-96%). Compared to ICA saline, during ICA NO infusion CBF increased 7% in control animals and 19% in vasospastic animals (p < 0.002) without significant changes in other physiological parameters. During NO infusion, peak systolic right MCA CBF velocity decreased (130 to 109 cm/sec and 116 to 76 cm/sec) in two vasospastic animals. The effects of ICA NO on CBF and CBF velocity disappeared shortly after terminating NO infusion. Intracarotid infusion of NO in a primate model of vasospasm 1) increases CBF, 2) decreases cerebral vascular resistance, 3) reverses arteriographic vasospasm, and 4) decreases CBF velocity in the vasospastic artery without producing systemic hypotension. These findings indicate the potential for the development of targeted therapy to reverse cerebral vasospasm after SAH.

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Section: Experimental Designmentioning

confidence: 97%

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

Afshar¹,

Pluta²,

Boock³

et al. 1995

Journal of Neurosurgery

129

View full text Add to dashboard Cite

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“…CBF of less than 10 mL/100 g of tissue per minute cannot be tolerated beyond a few minutes before infarction occurs, but between 10 and 20 mL · 100 g Ϫ1 · min Ϫ1 , cell death requires many minutes to hours. [21][22][23][24][25][26][27][28][29][30] Theoretically, tissues with flow values in this intermediate zone might be salvaged if flow restoration occurred quickly, either spontaneously by clot fragmentation and dissolution 31,32 or by therapeutic means such as arterial thrombolysis. While some tissues might be dead at the core of the ischemic process, the more peripheral tissues (the "penumbra") might still be salvageable.…”

Section: Roles Of Perfusion Imaging Acute Strokementioning

confidence: 99%

Guidelines and Recommendations for Perfusion Imaging in Cerebral Ischemia

Latchaw¹,

Yonas²,

Hunter³

et al. 2003

Stroke

274

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“…Through a craniectomy, a thermomonitoring probe (SABER; Flowtronics, Phoenix, AZ) was placed subdurally over the right parietal lobe in the arterial distribution of the right middle cerebral artery for continuous measurement of cortical CBF. 5,19 While continuously monitoring CBF, systematic alterations in the PaCO 2 (by ventilation) and then BP (using trimethaphan camsylate (Arfonad) and phenylephrine) were made in a controlled and graded manner to provide control and experimental curves of chemoregulation (CBF vs. PaCO 2 ) and autoregulation (CBF vs. MAP) during continuous intracarotid infusion of 1) saline and 2) an NOSI, either L-n-monomethyl arginine (LNMMA) or nitro-L-arginine (NLA) ( Table 1). To determine the maximum intracarotid NOSI doses that would not produce systemic hypertension, we established dose-response curves in five monkeys before beginning this study.…”

Section: Animal Preparationmentioning

confidence: 99%

Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates

Thompson

Pluta²,

Girton³

et al. 1996

Journal of Neurosurgery

101

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The authors sought to develop a model for assessing in vivo regulation of cerebral vasoregulation by nitric oxide (NO), originally described as endothelial-derived relaxing factor, and to use this model to establish the role of NO in the regulation of cerebral blood flow (CBF) in primates. By using regional intraarterial perfusion, the function of NO in cerebral vasoregulation was examined without producing confounding systemic physiological effects. Issues examined were: whether resting vasomotor tone requires NO; whether NO mediates vasodilation during chemoregulation and autoregulation of CBF; and whether there is a relationship between the degree of hypercapnia and hypotension and NO production. Twelve anesthetized (0.5% isoflurane) cynomolgus monkeys were monitored continuously for cortical CBF, PaCO2, and mean arterial pressure (MAP), which were systematically altered to provide control and experimental curves of chemoregulation (CBF vs. PaCO2) and autoregulation (CBF vs. MAP) during continuous intracarotid infusion of 1) saline and 2) an NO synthase inhibitor (NOSI), either L-n-monomethyl arginine or nitro L-arginine. During basal conditions (PaCO2 of 38-42 mm Hg) NOSI infusion of internal carotid artery (ICA) reduced cortical CBF from 62 (saline) to 53 ml/100 g/per minute (p<0.01), although there was no effect on MAP. Increased CBF in response to hypercapnia was completely blocked by ICA NOSI. The difference in regional (r)CBF between ICA saline and NOSI infusion increased linearly with PaCO2 when PaCO2 was greater than 40 mm Hg, indicating a graded relationship of NO production, increasing PaCO2, and increasing CBF. Diminution of CBF with NOSI infusion was reversed by simultaneous ICA infusion of L-arginine, indicating a direct role of NO synthesis in the chemoregulation of CBF. Hypotension and hypertension were induced with trimethaphan camsylate (Arfonad) and phenylephrine at constant PaCO2 (40 +/- 1 mm Hg). Autoregulation in response to changes in MAP from 50 to 140 mm Hg was unaffected by ICA infusion of NOSI. In primates, cerebral vascular tone is modulated in vivo by NO; continuous release of NO is necessary to maintain homeostatic cerebral vasodilation; vasodilation during chemoregulation of CBF is mediated directly by NO production; autoregulatory vasodilation with hypertension is not mediated by NO; and increasing PaCO2 induces increased NO production.

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Comparison of local cerebral blood flow determined by thermal and hydrogen clearance.

Cited by 32 publications

References 12 publications

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

Effect of intracarotid nitric oxide on primate cerebral vasospasm after subarachnoid hemorrhage

Guidelines and Recommendations for Perfusion Imaging in Cerebral Ischemia

Nitric oxide mediation of chemoregulation but not autoregulation of cerebral blood flow in primates

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