scholarly journals Increased Expression of Endothelin B Receptor mRNA following Subarachnoid Hemorrhage in Monkeys

1996 ◽  
Vol 16 (4) ◽  
pp. 688-697 ◽  
Author(s):  
Akihiko Hino ◽  
Yoshiharu Tokuyama ◽  
Masahiko Kobayashi ◽  
Mitsuo Yano ◽  
Bryce Weir ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Cerebral Arteries ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Receptor Mrna ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Receptor Mrnas

These studies tested the hypothesis that the cerebral vasospasm that follows subarachnoid hemorrhage (SAH) is due to alterations in endothelin (ET) and ET receptor expression. Eight monkeys underwent cerebral angiography and induction of SAH. Angiography was repeated 7 days later to confirm the presence of cerebral vasospasm, and animals were killed. RNA was isolated from right (vasospastic) and left (control) side middle cerebral arteries and surrounding cerebral cortex. The levels of prepro (PP) ET-1 (ppET-1) and ppET-3 and ETA and ETB receptor mRNAs were determined using a quantitative reverse transcriptase polymerase chain reaction-based assay. ET-1 peptide was also measured in CSF at baseline and after 7 days. Specific agonist binding to ETA and ETB receptors in both middle cerebral arteries and in surrounding brain cortex was measured in three animals by autoradiographic binding assays. Levels of ETB receptor mRNA were 3.4 ± 2.2-fold higher in the right than in the left cerebral arteries (p < 0.01). There were no significant differences in the levels of ppET-1, ppET-3, or ETA receptor mRNA in cerebral arteries. ET-1 peptide was not elevated in CSF. Levels of ETA and ETB receptor mRNAs were 2.6 ± 1.1- and 2.1 ± 1.3-fold higher, respectively, in the right than in the left cerebral cortex, while the level of ppET-3 mRNA was 2.1 ± 1.0-fold lower. There were no differences in ppET-1 mRNA levels between right and left cerebral cortex. Binding to ETA and ETB receptors in cerebral arteries and cortex did not differ significantly between right and left sides. These results do not support the hypothesis that overexpression of ET-1 is the principal cause of vasospasm, but rather they suggest that SAH causes complex changes in the ET system that together are responsible for the cellular response to SAH.

scholarly journals Time Course of Changes in Nitric Oxide Synthases Following Subarachnoid Hemorrhage in Primates

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 359-360
Author(s):  
Robert L Macdonald ◽  
Bak Yamini ◽  
Bryce K Weir ◽  
Shigeki Ono
Keyword(s):  
Nitric Oxide ◽  
Subarachnoid Hemorrhage ◽  
Time Course ◽  
Cerebral Arteries ◽  
Inflammatory Cells ◽  
Inos Mrna ◽  
Messenger Ribonucleic Acid ◽  
Fold Reduction ◽  
Middle Cerebral Arteries ◽  
The Right

P114 Nitric oxide (NO) may be important in vasospasm following subarachnoid hemorrhage (SAH). We evaluated the time course of changes in 3 isoforms of NO synthase (NOS) after SAH in monkeys. Right SAH was created and vasospasm was assessed on angiograms obtained at baseline and after 3, 7 and 14 days. Animals were euthanized at these times (n = 4 - 6 per time) and the right and left (control) middle cerebral arteries were removed. Levels of nNOS, eNOS and iNOS messenger ribonucleic acid (mRNA) and protein were measured by reverse transcriptase polymerase chain reaction and Western blotting. Angiography showed a 45 ± 13% (mean ± s.d., p < 0.05) decrease in middle cerebral artery diameter 3 days, a 41 ± 23% (p< 0.05) decrease 7 days and an insignificant 6 ± 14% decrease 14 days after SAH. The RNA for eNOS was significantly reduced (1.7 ± 0.5-fold) 7 days after SAH. There was a significant, 1.7 ± 0.2-fold reduction in eNOS protein on days 3 and 7 after SAH that returned to normal by day 14. There were no significant changes in nNOS mRNA or protein at any time after SAH. There were no significant changes in iNOS mRNA whereas iNOS protein increased on days 3 and 7 (7 ± 9 and 2.7 ± 2.8-fold, respectively, p > 0.05) and significantly decreased (2.7 ± 1.1-fold, p < 0.05) on day 14. Immunohistochemistry localized eNOS to endothelium, nNOS to brain and perivascular adventitia of the middle cerebral arteries and iNOS to inflammatory cells in the subarachnoid space. These results show a correlation between decreased eNOS and increased iNOS during vasospasm, suggesting a complex role for changes in NO in vasospasm.

Evaluation of Vasospasm after Subarachnoid Hemorrhage by Use of Multislice Computed Tomographic Angiography

Neurosurgery ◽  
2002 ◽  
Vol 51 (4) ◽  
pp. 939-943 ◽  
Author(s):  
Yasunari Otawara ◽  
Kuniaki Ogasawara ◽  
Akira Ogawa ◽  
Makoto Sasaki ◽  
Kei Takahashi
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Arteries ◽  
Computed Tomographic Angiography ◽  
Computed Tomographic ◽  
Tomography System ◽  
Middle Cerebral Arteries ◽  
Multislice Images ◽  
Tomographic Angiography

Abstract OBJECTIVE Multislice computed tomographic angiography (CTA) can provide clearer vascular images, even of the peripheral arteries, than conventional CTA. Multislice CTA was compared with digital subtraction angiography (DSA) for the detection of cerebral vasospasm in patients with acute aneurysmal subarachnoid hemorrhage (SAH) to analyze whether multislice CTA can replace DSA in the detection of vasospasm after SAH. METHODS Within 72 hours after the onset of symptoms, multislice CTA and DSA were performed in 20 patients with SAH. Multislice CTA and DSA were repeated on Day 7 to assess cerebral vasospasm. Regions of interest were established in the proximal and distal segments of the anterior and middle cerebral arteries on both multislice CTA and DSA images, and the agreement between the severity of vasospasm on multislice CTA and DSA images was statistically compared. The multislice Aquilon computed tomography system (Toshiba, Inc., Tokyo, Japan) used the following parameters: 1 mm collimation and 3.5 mm per rotation table increment (pitch, 3.5). RESULTS The degree of vasospasm as revealed by multislice CTA correlated significantly with the degree of vasospasm revealed by DSA (P &lt; 0.0001). The agreement between the severity of vasospasm on multislice images obtained via CTA and DSA in the overall, proximal, and distal segments of the cerebral arteries was 91.6, 90.8, and 92.3%, respectively. CONCLUSION Multislice CTA can detect angiographic vasospasm after SAH with accuracy equal to that of DSA.

Cerebrovascular ETB, 5-HT1B, and AT1 receptor upregulation correlates with reduction in regional CBF after subarachnoid hemorrhage

2007 ◽  
Vol 293 (6) ◽  
pp. H3750-H3758 ◽  
Author(s):  
Saema Ansar ◽  
Petter Vikman ◽  
Marianne Nielsen ◽  
Lars Edvinsson
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Molecular Mechanisms ◽  
Cerebral Arteries ◽  
Temporal Correlation ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Ang Ii ◽  
Contractile Responses ◽  
Protein Levels ◽  
Receptor Mrna

We hypothesize that cerebral ischemia leads to enhanced expression of endothelin (ET), 5-hydroxytryptamine (5-HT), and angiotensin II (ANG II) receptors in the vascular smooth muscle cells. Our aim is to correlate the upregulation of cerebrovascular receptors and the underlying molecular mechanisms with the reduction in regional and global cerebral blood flow (CBF) after subarachnoid hemorrhage (SAH). SAH was induced by injecting 250 μl blood into the prechiasmatic cistern in rats. The cerebral arteries were removed 0, 1, 3, 6, 12, 24, and 48 h after the SAH for functional and molecular studies. The contractile responses to ET-1, 5-carboxamidotryptamine (5-CT), and ANG II were investigated with myograph. The receptor mRNA and protein levels were analyzed by quantitative real-time PCR and immunohistochemistry, respectively. In addition, regional and global CBFs were measured by an autoradiographic method. As a result, SAH resulted in enhanced contractions to ET-1 and 5-CT. ANG II [via ANG II type 1 (AT1) receptors] induced increased contractile responses [in the presence of the ANG II type 2 (AT2) receptor antagonist PD-123319]. In parallel the ETB, 5-HT1B, and AT1 receptor, mRNA and protein levels were elevated by time. The regional and global CBF showed a successive reduction with time after SAH. In conclusion, the results demonstrate for the first time that SAH induces the upregulation of ETB, 5-HT1B, and AT1 receptors in a time-dependent manner both at functional, mRNA, and protein levels. These changes occur in parallel with a successive decrease in CBF. Thus there is a temporal correlation between the changes in receptor expression and CBF reduction, suggesting a linkage.

Transcranial Doppler Ultrasonography for Diagnosis of Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage: Mean Blood Flow Velocity Ratio of the Ipsilateral and Contralateral Middle Cerebral Arteries

Neurosurgery ◽  
2011 ◽  
Vol 69 (4) ◽  
pp. 876-883 ◽  
Author(s):  
Ryuta Nakae ◽  
Hiroyuki Yokota ◽  
Daizo Yoshida ◽  
Akira Teramoto
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Flow Velocity ◽  
Cerebral Vasospasm ◽  
Transcranial Doppler ◽  
Blood Flow Velocity ◽  
Predictive Value ◽  
Cerebral Arteries ◽  
Absolute Flow ◽  
Middle Cerebral Arteries

Abstract BACKGROUND: Transcranial Doppler (TCD) is widely accepted to monitor cerebral vasospasm after subarachnoid hemorrhage (SAH); however, its predictive value remains controversial. OBJECTIVE: To investigate the predictive reliability of an increase in the mean blood flow velocity (mBFV) ratio of the ipsilateral to contralateral middle cerebral arteries (I/C mBFV) compared with the conventional absolute flow velocity. METHODS: We retrospectively investigated the clinical and radiologic data of consecutive patients with SAH admitted from July 2003 to August 2009 who underwent TCD ultrasonography. The highest mBFV value in bilateral middle cerebral arteries was recorded, while delayed cerebral ischemia (DCI) was defined as neurological deficits or computed tomographic evidence of cerebral infarction caused by vasospasm. The ipsilateral side was defined as the side with higher mBFV value when evaluating the I/C mBFV. We thus elucidated the reliability of this rate in comparison with the conventional method for predicting DCI with receiver operating characteristic (ROC) analysis. RESULTS: One hundred and forty-two patients were retrospectively analyzed with specific data from 1262 TCD studies. The ROC curve showed that the overall predictive value for DCI had an area under the curve of 0.86 (95% confidence interval: 0.76-0.96) when the I/C mBFV was used vs 0.80 (0.71-0.88) when the absolute flow velocity was used. The threshold value that best discriminated between patients with and without DCI was I/C mBFV of 1.5. CONCLUSION: In patients with SAH, the I/C mBFV demonstrated a more significant correlation to vasospasm than the absolute mean flow velocity.

scholarly journals Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

1991 ◽  
Vol 11 (1) ◽  
pp. 161-164 ◽  
Author(s):  
Mária Faragó ◽  
Csaba Szabó ◽  
Eörs Dóra ◽  
Ildikó Horváth ◽  
Arisztid G. B. Kovách
Keyword(s):  
Smooth Muscle ◽  
Vascular Reactivity ◽  
Calcium Influx ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Contractile Responses ◽  
Middle Cerebral Arteries ◽  
The Right ◽  
Endothelial Receptor

To clarify the effect of extracellular magnesium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2+ concentration on the contractile and endothelium-dependent dilatory responses were investigated in vitro. The contractions, induced by 10−8-10−5 M norepinephrine, were significantly potentiated at low Mg2+ (0.8 m M v. the normal, 1.2 m M). High (1.6 and 2.0 m M) Mg2+ exhibited an inhibitory effect on the contractile responses. No significant changes, however, in the EC50 values for norepinephrine were found. The endothelium-dependent relaxations induced by 108–10−5 M acetylcholine were inhibited by high (1.6 and 2.0 m M) Mg2+. Lowering of the Mg2+ concentration to 0.8 m M or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilatory responses also shifted the EC50 values for acetylcholine to the right. The present results show that the contractile responses of the cerebral arteries are extremely susceptible to the changes of Mg2+ concentrations. In response to contractile and endothelium-dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endothelial receptor. Since Mg2+ deficiency might facilitate the contractile but not the endothelium-dependent relaxant responses, the present study supports a role for Mg2+ deficiency in the development of the cerebral vasospasm.

scholarly journals A case of Young Stroke due to Moyamoya Disease

2020 ◽  
Vol 15 (1) ◽  
pp. 110-113
Author(s):  
Md Abdur Razzak ◽  
Ghulam Kawnayn ◽  
Fateha Naznin ◽  
Quazi Audry Arafat Rahman
Keyword(s):  
Moyamoya Disease ◽  
Past History ◽  
Cerebral Arteries ◽  
Armed Forces ◽  
Cerebral Angiogram ◽  
Medical College ◽  
Middle Cerebral Arteries ◽  
History Of ◽  
Collateral Vessels ◽  
The Right

Moyamoya disease is a disease in which certain arteries in the brain are constricted. Blood flow is blocked by the constriction, and also by blood clots (thrombosis). A collateral circulation develops around the blocked vessels to compensate for the blockage, but the collateral vessels are small, weak, and prone to bleeding, aneurysm and thrombosis which may result in TIA, recurrent ischemic or hemorrhagic stroke or seizure. The disease may manifest in pediatric age or young adults. In May 2019 we have diagnosed a young lady with Moyamoya disease who presented with right sided hemiplegia, motor aphasia and dysphagia. She was labeled as hypertensive 6 months prior to this event and used to take anti-hypertensive irregularly and gave past history of occasional headache. Her CT scan and MRI of brain revealed left sided ischemic infarct involving frontotemporoparietal region and cerebral angiogram revealed narrowing of left MCA and non-visualization of distal part. There is extensive fine collaterals (Moyamoya vessels) giving the appearance of puffed smoke. The right ACA and MCA were also narrowed with appearance of early collateral vessels. She was treated with aspirin, PPI, NG feeding, antihypertensive medication, physiotherapy, rehabilitation therapy and other supportive care. His condition gradually improved and discharged on 2.7.19. He was referred to Department of Neurosurgery for cerebral revascularization by STA-MCA (superficial temporal and middle cerebral arteries) bypass surgery after stabilization and MR perfusion study. Journal of Armed Forces Medical College Bangladesh Vol.15 (1) 2019: 110-113

Water deprivation upregulates ANG II AT1 binding and mRNA in rat subfornical organ and anterior pituitary

1997 ◽  
Vol 273 (1) ◽  
pp. E156-E163 ◽  
Author(s):  
G. L. Sanvitto ◽  
O. Johren ◽  
W. Hauser ◽  
J. M. Saavedra
Keyword(s):  
Paraventricular Nucleus ◽  
Median Eminence ◽  
Anterior Pituitary ◽  
Water Deprivation ◽  
Subfornical Organ ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Ang Ii ◽  
At1 Receptors ◽  
Receptor Mrna

We studied angiotensin II (ANG II) receptor subtype expression in selected brain nuclei and pituitary gland after water deprivation by in vitro receptor autoradiography using 125I-labeled [Sar1]ANG II and by in situ hybridization using 35S-labeled AT1A, AT1B, and AT2 receptor-specific riboprobes. In control rats we found binding to AT1 receptors in the subfornical organ, paraventricular nucleus, median eminence, and anterior pituitary; AT1A mRNA expression in the subfornical organ and paraventricular nucleus; and AT1B mRNA expression in the anterior pituitary. No receptor mRNA was found in the median eminence. AT1 receptors and AT1A receptor mRNA levels were increased in the subfornical organ, and, in the anterior pituitary, AT1 receptors and AT1B receptor mRNA were increased, only after 5 days of water deprivation. No significant changes occurred after 1 or 3 days of water deprivation, and no regulation of ANG II receptor expression was detected in other brain areas. Our results show that prolonged water deprivation selectively regulates AT1 receptor expression and AT1A and AT1B receptor mRNA levels in the subfornical organ and anterior pituitary, respectively, supporting a role for these receptors during sustained dehydration.

scholarly journals Expression of leptin and β3-adrenergic receptors in rat adipose tissue in altered thyroid states

1997 ◽  
Vol 322 (1) ◽  
pp. 145-150 ◽  
Author(s):  
John N. FAIN ◽  
Elizabeth C. CORONEL ◽  
Michael J. BEAUCHAMP ◽  
Suleiman W. BAHOUTH
Keyword(s):  
Adipose Tissue ◽  
Adrenergic Receptor ◽  
Male Rats ◽  
Epididymal Adipose Tissue ◽  
Mrna Levels ◽  
Receptor Mrna ◽  
Cl 316,243 ◽  
Altered Thyroid ◽  
Rat Adipose Tissue ◽  
Receptor Mrnas

The level of leptin [the obese (ob) gene product] mRNA is markedly elevated in hypothyroid male rats. The administration of tri-iodothyronine (T3) to hypothyroid rats resulted in a 40% decrease in leptin mRNA at 8 h. This decrease in leptin mRNA was associated with a parallel decline in circulating leptin levels of about 50% at 24 h. Conversely, β3-adrenergic receptor mRNA levels were markedly decreased in epididymal adipose tissue from hypothyroid rats. T3 administration resulted in a 147% increase at 12 h in β3-adrenergic receptor mRNA. There was a corresponding increase due to T3 in the lipolytic response to the specific β3-adrenergic agonist CL 316,243 that paralleled the increase in β3-adrenergic receptor mRNA. T3-mediated changes in leptin and β3-adrenergic receptor mRNAs were blocked by cycloheximide, suggesting the involvement of short-lived proteins in these effects. The present results indicate that T3 has opposite effects to those of insulin on the white adipose tissue of rats with respect to leptin mRNA expression.

Equal contribution of increased intracranial pressure and subarachnoid blood to cerebral blood flow reduction and receptor upregulation after subarachnoid hemorrhage

2009 ◽  
Vol 111 (5) ◽  
pp. 978-987 ◽  
Author(s):  
Saema Ansar ◽  
Lars Edvinsson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Pressure ◽  
Sham Group ◽  
Cerebral Arteries ◽  
Mrna Levels ◽  
Saline Injection ◽  
Receptor Upregulation ◽  
Subarachnoid Blood

Object Cerebral ischemia remains the key cause of disability and death in the late phase after subarachnoid hemorrhage (SAH), and its pathogenesis is still poorly understood. The purpose of this study was to examine whether the change in intracranial pressure or the extravasated blood causes the late cerebral ischemia and the upregulation of receptors or the cerebral vasoconstriction observed following SAH. Methods Rats were allocated to 1 of 3 experimental conditions: 1) cisternal injection of 250 μl blood (SAH Group), 2) cisternal injection of 250 μl NaCl (Saline Group), or 3) the same procedure but without fluid injection (Sham Group). Two days after the procedure, the basilar and middle cerebral arteries were harvested, and contractile responses to endothelin (ET)–1 and 5-carboxamidotryptamine (5-CT) were investigated by means of myography. In addition, real-time polymerase chain reaction was used to determine the mRNA levels for ETA, ETB, and 5-HT1 receptors. Regional and global cerebral blood flow (CBF) were quantified by means of an autoradiographic technique. Results Compared with the sham condition, both SAH and saline injection resulted in significantly enhanced contraction of cerebral arteries in response to ET-1 and 5-CT. Regional and global CBF were reduced both in the Saline and SAH groups compared with the Sham Group. The mRNA levels for ETB and 5-HT1B receptors were upregulated after SAH and saline injection compared with the sham procedure. The effects in all parameters were more pronounced for SAH than for saline injection. Conclusions This study revealed that both the elevation of intracranial pressure and subarachnoid blood per se contribute approximately equally to the late CBF reductions and receptor upregulation following SAH.

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