scholarly journals Role of Nitric Oxide in Regulation of Brain Stem Circulation during Hypotension

1997 ◽  
Vol 17 (10) ◽  
pp. 1089-1096 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Tetsuhiko Nagao ◽  
Takanari Kitazono ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Stem ◽  
Topical Application ◽  
Basilar Artery ◽  
Group Versus ◽  
Control Group ◽  
Cranial Window ◽  
Severe Hypotension ◽  
The Brain

We tested the hypothesis that nitric oxide (NO) plays a role in CBF autoregulation in the brain stem during hypotension. In anesthetized rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. During topical application of 10−5 mol/L and 10−4 mol/L Nω-nitro-L-arginine (L-NNA), a nonselective inhibitor of nitric oxide synthase (NOS), CBF started to decrease at higher steps of mean arterial blood pressure in proportion to the concentration of L-NNA in stepwise hypotension (45 to 60 mm Hg in the 10−5 mol/L and 60 to 75 mm Hg in the 10−4 mol/L L-NNA group versus 30 to 45 mm Hg in the control group). Dilator response of the basilar artery to severe hypotension was significantly attenuated by topical application of L-NNA (maximum dilatation at 30 mm Hg: 16 ± 8% in the 10−5 mol/L and 12 ± 5% in the 10−4 mol/L L-NNA group versus 34 ± 4% in the control group), but that of the branches was similar between the control and L-NNA groups. Topical application of 10−5 mol/L 7-nitro indazole, a selective inhibitor of neuronal NOS, did not affect changes in CBF or vessel diameter through the entire pressure range. Thus, endothelial but not neuronal NO seems to take part in the regulation of CBF to the the brain stem during hypotension around the lower limits of CBF autoregulation. The role of NO in mediating dilatation in response to hypotension appears to be greater in large arteries than in small ones.

scholarly journals Attenuation and Recovery of Brain Stem Autoregulation in Spontaneously Hypertensive Rats

1998 ◽  
Vol 18 (3) ◽  
pp. 305-310 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Takanari Kitazono ◽  
Tetsuhiko Nagao ◽  
...  
Keyword(s):  
Brain Stem ◽  
Basilar Artery ◽  
Antihypertensive Treatment ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Doppler Flowmetry ◽  
Spontaneously Hypertensive ◽  
Large Arteries ◽  
Cranial Window ◽  
Severe Hypotension

Cerebral large arteries dilate actively around the lower limits of CBF autoregulation, mediated at least partly by nitric oxide, and maintain CBF during severe hypotension. We tested the hypothesis that this autoregulatory response of large arteries, as well as the response of arterioles, is altered in spontaneously hypertensive rats (SHR) and that the altered response reverts to normal during long-term antihypertensive treatment with cilazapril, an angiotensin-converting enzyme inhibitor. In anesthetized 6- to 7-month-old normotensive Wistar-Kyoto rats (WKY), 4- and 6- to 7-month-old SHR without antihypertensive treatment, and 6- to 7-month-old SHR treated with cilazapril for 10 weeks, local CBF to the brain stem was determined with laser—Doppler flowmetry and diameters of the basilar artery and its branches were measured through a cranial window during stepwise hemorrhagic hypotension. The lower limit of CBF autoregulation shifted upward in untreated SHR to 90 to 105 mm Hg from 30 to 45 mm Hg in WKY, and it reverted to 30 to 45 mm Hg in treated SHR. In response to severe hypotension, the basilar artery dilated by 21 ± 6% (mean ± SD) of the baseline internal diameter in WKY. The vasodilation was impaired in untreated SHR (10 ± 8% in 4-mo-old SHR and 4 ± 5% in 6- to 7-month-old SHR), and was restored to 22 ± 10% by treatment with cilazapril ( P < 0.005). Dilator responses of branch arterioles to hypotension showed similar attenuation and recovery as that of the basilar artery. The data indicate that chronic hypertension impairs the autoregulatory dilation of the basilar artery as well as branch arterioles and that antihypertensive treatment with cilazapril restores the diminished dilation toward normal.

scholarly journals Role of Endogenous Nitric Oxide in the Brain Stem on the Rapid AdaptatKion of Baroreflex

Hypertension ◽  
1998 ◽  
Vol 31 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Kiyoshi Hironaga ◽  
Yoshitaka Hirooka ◽  
Isamu Matsuo ◽  
Miwako Shihara ◽  
Tatsuya Tagawa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Brain Stem ◽  
Endogenous Nitric Oxide ◽  
The Brain

scholarly journals Role of the basilar artery in regulation of blood flow to the brain stem in rats.

Stroke ◽  
1991 ◽  
Vol 22 (6) ◽  
pp. 763-767 ◽  
Author(s):  
K Fujii ◽  
D D Heistad ◽  
F M Faraci
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Basilar Artery ◽  
The Brain

scholarly journals The Role of Controlled Anticoagulation in Balloon Occluding Vertebral Arteries to Treat Giant Fusiform Aneurysms of the Basilar Artery

1999 ◽  
Vol 5 (2) ◽  
pp. 145-150
Author(s):  
F. Ling ◽  
H. Zhang ◽  
D. Wang ◽  
M. Li ◽  
Z. Miao ◽  
...  
Keyword(s):  
Brain Stem ◽  
Basilar Artery ◽  
Collateral Circulation ◽  
Anticoagulation Therapy ◽  
Balloon Occlusion ◽  
Vertebral Arteries ◽  
Aneurysm Wall ◽  
The Brain

We suggest and discuss the role of controlled anticoagulation therapy after the balloon occlusion of vertebral arteries to treat giant fusiform aneurysms in the basilar trunk. Two cases of giant fusiform aneurysms were treated with balloon occlusion of vertebral arteries. Both of these patients suffered severe brain stem ischaemia. Anticoagulants were used to adjust the PTT to 1.5–2.5 times the normal level to control the formation speed of thrombosis inside the aneurysms. Case 1 was obliged to suspend the anticoagulation therapy one week after occlusion because of digestive tract haemorrhage, and died of severe brain stem ischaemia. On autopsy, the sac of the aneurysm was totally occupied by the thrombus. Two perforating arteries feeding the brain stem arising from the wall of the aneurysm and infarction in the brain stem were found. Case 2 was anticoagulated strictly and progressively improved after three weeks. Anticoagulation was terminated after one month. Follow-up MRI showed the aneurysm had disappeared six months later. Giant fusiform aneurysms in the basilar artery trunk can be treated with the balloon occlusion of vertebral arteries which induces thrombosis in the sac of aneurysm. Controlled anticoagulation should be given to slow down the thrombotic obliteration in the perforators arising from the aneurysm wall to the brain stem and give the brain stem have enough time to establish the sufficient collateral circulation.

Role of ATP-sensitive potassium channels in brain stem circulation during hypotension

1997 ◽  
Vol 273 (3) ◽  
pp. H1342-H1346 ◽  
Author(s):  
K. Toyoda ◽  
K. Fujii ◽  
S. Ibayashi ◽  
T. Kitazono ◽  
T. Nagao ◽  
...  
Keyword(s):  
Brain Stem ◽  
Basilar Artery ◽  
Katp Channels ◽  
Vehicle Group ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Sprague Dawley Rats ◽  
The Brain

The basilar artery and its branch arterioles dilate actively in response to a marked decrease in blood pressure and maintain cerebral blood flow (CBF) to the brain stem. We tested the hypothesis that ATP-sensitive potassium (KATP) channels play a role in the autoregulatory responses of the brain stem circulation in vivo. In anesthetized Sprague-Dawley rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and branch arterioles were measured through a cranial window during stepwise hemorrhagic hypotension. During topical application of 10(-6) and 10(-5) mol/l of glibenclamide, a selective KATP-channel blocker, the lower limit of CBF autoregulation shifted upward to 60-75 from 30-45 mmHg in the vehicle group. Glibenclamide significantly impaired the dilator response of small arterioles (baseline diameter 45 +/- 2 microns) throughout hypotension (P < 0.03) but did not impair the dilatation of the basilar artery (247 +/- 3 microns) or large arterioles (99 +/- 4 microns). Thus KATP channels appear to play an important role in the regulation of CBF to the the brain stem during hypotension by mediating the compensatory dilatation of small arterioles. In contrast, these channels may not be a major regulator of the vascular tone of larger arteries during hypotension.

Changes in arterioles, arteries, and local perfusion of the brain stem during hemorrhagic hypertension

1996 ◽  
Vol 270 (4) ◽  
pp. H1350-H1354 ◽  
Author(s):  
K. Toyoda ◽  
K. Fujii ◽  
S. Ibayashi ◽  
S. Sadoshima ◽  
M. Fujishima
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Basilar Artery ◽  
Doppler Flowmetry ◽  
Large Arteries ◽  
Cerebrovascular Resistance ◽  
Cranial Window ◽  
Arterial Blood ◽  
The Brain

Cerebral arterioles have been regarded as the primary sites of autoregulatory responses, whereas the role of large arteries in the cerebral autoregulation is poorly understood. The goal of this study was to determine in vivo whether the basilar artery and its primary branches act as resistance vessels under hypotensive conditions by simultaneously measuring their diameters and local brain stem blood flow with laser-Doppler flowmetry. In 10 anesthetized rats, blood flow to the brain stem was well maintained during stepwise hemorrhagic hypotension when mean arterial blood pressure fell from 116 +/- 3 to 50 mmHg and decreased gradually between 50 and 30 mmHg. Diameter of the basilar artery (n = 10) and its large branches (n = 22), measured through an open cranial window, increased by 10% from the baseline value at 50 mmHg and reached their maximum at 30 mmHg (314 +/- 9 from 244 +/- 6 mum, and 149 +/- 4 from 117 +/- 3 mum, respectively). Small branches (n = 15) dilated to a larger extent compared with the larger arteries throughout hypotension and reached the maximum at 30 mmHg (69 +/- 3 from 48 +/- 2 mum). Below 30 mmHg, there was a steep fall in blood flow and reduction in diameter of all-sized arteries. Thus small vessels contribute to reductions in cerebrovascular resistance throughout the entire autoregulatory-range in the brain stem circulation. Large arteries, such as the basilar artery and its branches, also contribute to reductions in cerebrovascular resistance around the lower limits of cerebral blood flow autoregulation and may thus play a significant role in maintaining blood flow to the brain stem during severe systemic hypotension.

Effect of Aging on Regulation of Brain Stem Circulation During Hypotension

1997 ◽  
Vol 17 (6) ◽  
pp. 680-685 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Yutaka Takata ◽  
Setsuro Ibayashi ◽  
Megumi Fujikawa ◽  
...  
Keyword(s):  
Brain Stem ◽  
Basilar Artery ◽  
Aged Rats ◽  
Adult Rats ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Large Branch ◽  
Small Branch ◽  
Age Related ◽  
The Brain

This study was designed to determine age-related changes in autoregulatory responses of the brain stem circulation in vivo. In anesthetized adult (4 to 6 months, n = 8) and aged (24 to 26 months, n = 7) Sprague-Dawley rats, local CBF to the brain stem was determined with laser-Doppler flowmetry and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. In aged rats, the lower limit of CBF auto-regulation shifted upward to 60 to 75 mm Hg from 30 to 45 mm Hg in adult rats. Dilator responses of the basilar artery (baseline diameter: 254 ± 15 μm), large branch (109 ± 23 μm), and small branch (44 ± 10 μm) to hypotension were much smaller in aged rats than in adult rats. The maximum change in diameter of the basilar artery during profound hypotension was significantly smaller in aged rats (11 ± 8%) than that in adult ones (23 ± 12%, P < 0.05); that of the large branch was 12 ± 8% versus 33 ± 17% ( P < 0.005); and that of the small branch was 17 ± 7% versus 40 ± 13% ( P < 0.0005), suggesting greater attenuation of the responses in the smaller vessels. Thus, this study provides direct evidence that aging diminishes the compensatory dilatation of brain stem arterioles and arteries during hypotension and modifies the autoregulatory plateau of CBF, which seems to increase the risk of the brain stem ischemia during hypotensive conditions.

Role of nitric oxide in regulation of basilar artery tone in vivo

1990 ◽  
Vol 259 (4) ◽  
pp. H1216-H1221 ◽  
Author(s):  
F. M. Faraci
Keyword(s):  
Nitric Oxide ◽  
Basilar Artery ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Cranial Window ◽  
Enzymatic Formation ◽  
Basal Tone ◽  
Resting Tone

Previous studies have suggested that nitric oxide (NO) may be a major endothelium-derived relaxing factor in peripheral blood vessels. This study tested the hypotheses that 1) formation of NO from L-arginine contributes to basal tone of cerebral arteries in vivo and 2) dilator responses of cerebral arteries to acetylcholine are dependent on formation of NO. Diameter of the basilar artery was measured through a cranial window in anesthetized rats. Under control conditions, topical application of 10 microM NG-monomethyl-L-arginine (L-NMMA, an arginine analogue that inhibits enzymatic formation of NO), constricted the basilar artery by 11 +/- 1% (means +/- SE). L-Arginine (100 microM), which had no effect on baseline diameter, abolished vasoconstriction in response to L-NMMA. L-Arginine did not alter vasodilation during acetylcholine (1 microM) (11 +/- 2 vs. 12 +/- 2%) or vasoconstriction during serotonin (1 nM) (-15 +/- 3 vs. -16 +/- 2%). L-NMMA (5-10 microM) abolished the dilator response of the basilar artery to acetylcholine but did not alter responses to nitroglycerin (0.01 microM) (24 +/- 4 vs. 20 +/- 3%). The inhibitory effect of L-NMMA on the vasodilator response to acetylcholine was prevented by L-arginine. These studies suggest that synthesis of NO from L-arginine influences resting tone of the basilar artery in vivo. Dilatation of the basilar artery to acetylcholine in vivo appears to be dependent on formation of NO from L-arginine.

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