Changes in Brain Stem Blood Flow under Various Grades of Brain Stem Ischemia.

Shiroyama, Yujiro; Nagamitsu, Tsutomu; Yamashita, Katsuhiro; Yamashita, Tetsuo; Abiko, Seisho; Ito, Hiroki

doi:10.1620/tjem.164.237

Cited by 9 publications

(7 citation statements)

References 11 publications

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“…A decreased VR to acetazolamide was shown in an animal model, where the median and paramedian branches of the BA were occluded [26]. In our study BLI patients showed a slight, insignificant decrease of the RVC.…”

Section: Discussionsupporting

confidence: 65%

Impaired Vasoreactivity of the Basilar Artery System in Patients with Brainstem Lacunar Infarcts

Pánczél

Bönöczk²,

Vokó³

et al. 1999

Cerebrovasc Dis

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Background and Purpose: Diminished vasoreactivity (VR) has been evidenced in patients with hemispheric small vessel disease, however, there is no data regarding vertebrobasilar (VB) territory VR changes in patients with subcortical vascular encephalopathy located in the brainstem. Therefore, we compared the cerebral blood flow velocity (CBFV) responses of the VB system during different vasoregulatory challenges in healthy volunteers to those in patients with brainstem lacunar infarcts. Methods: In 20 patients with brainstem lacunar infarcts and in 10 healthy volunteers the VR of the VB system was measured by analyzing the CBFV changes during different stimulation paradigms (ventilation, tilting and acetazolamide tests). During transcranial Doppler registration the systemic blood pressure and the expiratory partial CO₂ pressure were monitored. Results: During hypercapnia the VR was significantly higher in the control group than in the patient group (10.1 ± 4.9 vs. 3.4 ± 5.0 cm/s/kPa, p = 0.0025). In a subgroup of patients with mean baseline CBFV <25 cm/s the VR was 1.5 ± 2.4 cm/ s/kPa, while patients with mean baseline CBFV >25 cm/s showed a significantly higher value (7.8 ± 6.9 cm/s/kPa). Furthermore, in patients with mean baseline CBFV <25 cm/s the pulsatility index was significantly higher than in patients with mean baseline CBFV >25 cm/s (1.11 ± 0.26 vs. 0.86 ± 0.19, p = 0.0325), reflecting significantly higher vascular resistance in the former group. Although CBFV measurements during tilting and acetazolamide tests tended to support these findings, they showed no significant differences between patients and controls. Conclusion: Patients with cerebral microangiopathy involving the brainstem showed impaired VR in the VB flow territory in association with baseline CBFV.

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Section: Discussionsupporting

confidence: 65%

Impaired Vasoreactivity of the Basilar Artery System in Patients with Brainstem Lacunar Infarcts

Pánczél

Bönöczk²,

Vokó³

et al. 1999

Cerebrovasc Dis

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“…The mechanism by which the inhibition of 20-HETE synthesis prevents the observed hyperperfusion following cerebral ischemia in SHR and SHRSP cannot be determined by the present results. However, 20-HETE has recently been shown to stimulate formation of ROS by interactions with NADPH oxidase and uncoupling of NO synthase (NOS) (4,39,62), and there is evidence that the phenomenon of postischemic hyperperfusion may be associated with impairment of vascular reactivity by the elevated production of ROS in cerebral ischemia and reperfusion (27,34,48,58). This suggests that the effect of the 20-HETE inhibitor on postischemic cerebral hyperperfusion and on infarct size in SHR and SHRSP may be due to a reduction in cerebral ROS production, which may in itself be neuroprotective, and also may reduce secondary neural damage associated with vascular leakage and cerebral edema and inflammation.…”

Section: Discussionmentioning

confidence: 99%

Elevated production of 20-HETE in the cerebral vasculature contributes to severity of ischemic stroke and oxidative stress in spontaneously hypertensive rats

Dunn¹,

Renić²,

Flasch³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

127

132

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Dunn KM, Renic M, Flasch AK, Harder DR, Falck J, Roman RJ. Elevated production of 20-HETE in the cerebral vasculature contributes to severity of ischemic stroke and oxidative stress in spontaneously hypertensive rats. Am J Physiol Heart Circ Physiol 295: H2455-H2465, 2008. First published October 17, 2008 doi:10.1152/ajpheart.00512.2008.-Hypertension is a major risk factor for stroke, but the factors that contribute to the increased incidence and severity of ischemic stroke in hypertension remain to be determined. 20-hydroxyeicosatetraenoic acid (20-HETE) has been reported to be a potent constrictor of cerebral arteries, and inhibitors of 20-HETE formation reduce infarct size following cerebral ischemia. The present study examined whether elevated production of 20-HETE in the cerebral vasculature could contribute to the larger infarct size previously reported after transient middle cerebral artery occlusion (MCAO) in hypertensive strains of rat [spontaneously hypertensive rat (SHR) and spontaneously hypertensive stroke-prone rat (SHRSP)]. The synthesis of 20-HETE in the cerebral vasculature of SHRSP measured by liquid chromatography-tandem mass spectrometry was about twice that seen in Wistar-Kyoto (WKY) rats. This was associated with the elevated expression of cytochrome P-450 (CYP)4A protein and CYP4A1 and CYP4A8 mRNA. Infarct volume after transient MCAO was greater in SHRSP (36 Ϯ 4% of hemisphere volume) than in SHR (19 Ϯ 5%) or WKY rats (5 Ϯ 2%). This was associated with a significantly greater reduction in regional cerebral blood flow (rCBF) in SHR and SHRSP than in WKY rats during the ischemic period (78% vs. 62%). In WKY rats, rCBF returned to 75% of control following reperfusion. In contrast, SHR and SHRSP exhibited a large (166 Ϯ 18% of baseline) and sustained (1 h) postischemic hyperperfusion. Acute blockade of the synthesis of -formamidine (HET0016; 1 mg/kg) reduced infarct size by 59% in SHR and 87% in SHRSP. HET0016 had no effect on the fall in rCBF during MCAO but eliminated the hyperemic response. HET0016 also attenuated vascular O2•Ϫ formation and restored endothelium-dependent dilation in cerebral arteries of SHRSP. These results indicate the production of 20-HETE is elevated in the cerebral vasculature of SHRSP and contributes to oxidative stress, endothelial dysfunction, and the enhanced sensitivity to ischemic stroke in this hypertensive model. 20-hydroxyeicosatetraenoic acid; middle cerebral artery occlusion; cytochrome P-450A; N-hydroxy-N'-(4-butyl-2-methylphenyl)-formamidine HYPERTENSION IS A MAJOR RISK factor for stroke, but the factors that contribute to the increased incidence and severity of ischemic stroke in hypertension remain to be determined (46). Previous studies have indicated that arachidonic acid (AA) is released into cerebrospinal fluid following cerebral ischemia (1,31,42,56). AA is converted by cytochrome P-450 (CYP) enzymes in cerebral arteries to a potent vasoconstrictor, 20-hydroxyeicosatetraenoic acid (20-HETE) (15,16,32). 20-HETE has been reported to play an important...

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“…Hyperperfusion occurring in the brainstem is rare 1,2 . Brainstem hyperperfusion as a result of intravenous thrombolysis has not been reported.…”

Section: Introductionmentioning

confidence: 99%

“…Hyperperfusion occurring in the brainstem is rare. 1,2 Brainstem hyperperfusion as a result of intravenous thrombolysis has not been reported. Intravenous thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) is currently the only approved treatment for acute ischemic stroke when given within 3 hours after the stroke onset.…”

Section: Introductionmentioning

confidence: 99%