Journal articles: 'Vasomotor reactivity'

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Friedman, E. H. "Vasomotor reactivity." Neurology 45, no. 11 (November 1, 1995): 2115. http://dx.doi.org/10.1212/wnl.45.11.2115.

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Brothers, R. Matthew, Chansol Hurr, Kiyoung Kim, Joshua F. Lee, and Rong Zhang. "Cerebral Vasomotor Reactivity." Medicine & Science in Sports & Exercise 46 (May 2014): 13. http://dx.doi.org/10.1249/01.mss.0000493201.13477.46.

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Rogers, Robert L., John S. Meyer, Karl F. Mortel, Roderick K. Mahurin, and John Thornby. "Age-Related Reductions in Cerebral Vasomotor Reactivity and the Law of Initial Value: A 4-Year Prospective Longitudinal Study." Journal of Cerebral Blood Flow & Metabolism 5, no. 1 (March 1985): 79–85. http://dx.doi.org/10.1038/jcbfm.1985.11.

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A group of 51 neurologically normal, middle-aged and elderly volunteers (aged 35–86 years; mean age 63.24 years) with and without risk factors for stroke were given annual tests of cerebral vasomotor reactivity to assess any changes in the cerebral vascular capacitance associated with advancing age that might alter cerebral vasomotor reactivity. Cerebral vasomotor reactivity was estimated as the difference in bihemisphere gray matter CBF measured by the 133Xe inhalation method in the steady state breathing room air, followed by a second measurement during inhalation of 100% oxygen. There were significant and progressive reductions in cerebral vasomotor reactivity during the 4-year longitudinal study. Positive linear correlations were apparent between initial steady-state mean bihemisphere gray matter CBF levels and degrees of vasomotor reactivity, suggesting that the Law of Initial Value plays an important role. This should be borne in mind when analyzing scores of cerebral vasomotor reactivity. In the present communication, analysis of covariance was used to correct for influences of initial CBF levels on vasomotor responses tested while breathing pure oxygen.

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DENOVELLIS, V. "Aging and vasomotor reactivity." Pharmacological Research 26 (September 1992): 14. http://dx.doi.org/10.1016/1043-6618(92)90739-x.

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Ribigan, A. C., F. A. Antochi, E. O. Terecoasa, M. Popa, O. Rusu, C. Coclitu, A. Ciobotaru, C. Tiu, and O. A. Bajenaru. "CEREBRAL VASOMOTOR REACTIVITY IN PATIENTS WITH ARTERIAL HYPERTENSION AND COGNITIVE IMPAIRMENT." Romanian Journal of Neurology 15, no. 4 (December 31, 2016): 168–73. http://dx.doi.org/10.37897/rjn.2016.4.4.

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Objectives. The aim of our study is to determine whether cerebral vasomotor reactivity is impaired in patients with arterial hypertension and cognitive impairment and how this hemodynamic parameter is associated with different functions of cognition. Materials and methods. We included 87 patients with arterial hypertension divided into two groups, one with neurocognitive impairment ranging from mild to severe aged between 47 and 90 years (70.2 ± 11.4) and the second group without cognitive impairment aged between 41 and 86 years (60.1 ± 11.4). We excluded patients with significant hemodynamic cervico-cerebral arterial stenoses, arrhythmias and other diseases that may impair cerebral vasomotor reactivity. All the patients underwent assessment of vasomotor reactivity and neurocognitive functions. Results. BHI values were significantly lower in the first group of patients compared to the second one. The percent of patients with impaired cerebral vasomotor reactivity was significantly higher in the group of patients with cognitive impairment, as compared to the other group (54.35% vs 29.27%, p=0.01). There was a significant statistical difference between the MMSE, MOCA and clock test scores among patients with and without impaired vasomotor reactivity. This difference was also maintained for visuospatial/executive, naming and language domains of the MOCA test. Conclusions. Impaired cerebral vasomotor reactivity is more frequent in patients with arterial hypertension and cognitive impairment. Patients with arterial hypertension and impaired vasomotor reactivity have poorer cognitive performance, cognitive functions most affected in patients with impaired vasomotor reactivity being language, visuospatial and executive ones.

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Lucic-Prokin, Aleksandra, Petar Slankamenac, and Pavle Kovacevic. "Transcranial doppler methods in the assessment of cerebral vasomotor reactivity." Medical review 73, no. 1-2 (2020): 21–28. http://dx.doi.org/10.2298/mpns2002021l.

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Introduction. Transcranial Doppler is the only non-invasive neuroimaging modality in the diagnosis and monitoring of various neurovascular diseases. Apart from assessing cerebral hemodynamics of blood flow in the basal brain arteries, transcranial Doppler provides physiological data and anatomical images. Quantification analysis of vasomotor reactivity. Various transcranial Doppler methods evaluate cerebral vasomotor reactivity, providing important information on the properties of arterioles under induced hemodynamic conditions. Exogenous and endogenous vasoactive stimuli of different potency (apnea, acetazolamide, carbon dioxide, L-arginine) are most commonly used, making transcranial Doppler a prognostic indicator of future ischemic events. This article reviews principles of various transcranial Doppler methods in the evaluation of vasomotor reactivity, emphasizing their advantages and disadvantages. Transcranial Doppler in the field of reduced vasomotor reactivity. Evaluation of vasomotor reactivity has a role in the prediction of future ischemic events, evaluation of revascularization effect after carotid endarterectomy, but also in the increasingly significant choice of the right time to perform it. In recent years, transcranial Doppler methods have found application in other areas of dysfunctional cerebral hemodynamics: dementia, hypertension, migraines, and sepsis. Conclusion. Due to an excellent temporal resolution, non-invasive approach, good cost-benefit ratio, bedside monitoring, relative simplicity in terms of interpretation and performance, and portability, transcranial Doppler in vasomotor reactivity may be the ideal tool in the evaluation of cerebral hemodynamics, arterial perfusion integrity and collateral capacity.

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Carod-Artal, Francisco Javier. "Statins and Cerebral Vasomotor Reactivity." Stroke 37, no. 10 (October 2006): 2446–48. http://dx.doi.org/10.1161/01.str.0000239656.59618.d4.

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Kaşıkç, Mehmet Tayfun, and Güray Koç. "Vasomotor reactivity in the ophthalmic artery." Gulhane Medical Journal 62, no. 1 (March 13, 2020): 33–37. http://dx.doi.org/10.4274/gulhane.galenos.2019.784.

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Giannopoulos, S., B. Boden-Albala, J. H. Choi, E. Carrera, M. Doyle, T. Perez, and R. S. Marshall. "Metabolic syndrome and cerebral vasomotor reactivity." European Journal of Neurology 17, no. 12 (November 18, 2010): 1457–62. http://dx.doi.org/10.1111/j.1468-1331.2010.03087.x.

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Ameriso, S. F., J. G. Mohler, M. Suarez, and M. Fisher. "Morning reduction of cerebral vasomotor reactivity." Neurology 44, no. 10 (October 1, 1994): 1907. http://dx.doi.org/10.1212/wnl.44.10.1907.

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Lee, Soon-Tae, Keun-Hwa Jung, and Yong-Seok Lee. "Decreased Vasomotor Reactivity in Alzheimer's Disease." Journal of Clinical Neurology 3, no. 1 (2007): 18. http://dx.doi.org/10.3988/jcn.2007.3.1.18.

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Vernieri, Fabrizio, Giovanni Assenza, Paola Maggio, Francesco Tibuzzi, Filippo Zappasodi, Claudia Altamura, Marzia Corbetto, et al. "Cortical Neuromodulation Modifies Cerebral Vasomotor Reactivity." Stroke 41, no. 9 (September 2010): 2087–90. http://dx.doi.org/10.1161/strokeaha.110.583088.

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Smoliński, Łukasz, and Anna Członkowska. "Cerebral vasomotor reactivity in neurodegenerative diseases." Neurologia i Neurochirurgia Polska 50, no. 6 (November 2016): 455–62. http://dx.doi.org/10.1016/j.pjnns.2016.07.011.

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Terborg, Christoph, Felix Gora, Cornelius Weiller, and Joachim Röther. "Reduced Vasomotor Reactivity in Cerebral Microangiopathy." Stroke 31, no. 4 (April 2000): 924–29. http://dx.doi.org/10.1161/01.str.31.4.924.

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Bek, Semai, Tayfun Kaşikçi, Güray Koç, Gençer Genç, Şeref Demirkaya, Zeki Gökçil, and Zeki Odabaşi. "Cerebral vasomotor reactivity in epilepsy patients." Journal of Neurology 257, no. 5 (December 27, 2009): 833–38. http://dx.doi.org/10.1007/s00415-009-5428-4.

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Sharma, Vijay K., Hock Luen Teoh, and Bernard P. L. Chan. "Cerebral vasomotor reactivity in epilepsy patients." Journal of Neurology 257, no. 9 (March 26, 2010): 1565. http://dx.doi.org/10.1007/s00415-010-5542-3.

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Milošević, Dušanka, Ljiljana Janošević, Slobodanka Janošević, Zoran Invanković, and Ranko Dergenc. "Skin reactivity to vasomotor agents in non-eosinophilic and eosinophilic non-allergic rhinitis." Journal of Laryngology & Otology 116, no. 7 (July 2002): 519–22. http://dx.doi.org/10.1258/002221502760132386.

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The aim of this prospective study was to examine skin reactivity to four vasomotor agents and to determine whether non-eosinophilic rhinitis patients differ from patients with eosinophilic rhinitis. Nasal cytology enabled us to classify 74 rhinitis patients into a non-eosinophilic (n = 63) and an eosinophilic group (n = 11). Skin reactivity to intradermal tests with papaverine, metacholine, histamine and compound 48/80 was measured. No significant difference for papaverine, metacholine, histamine and compound 48/80, singly, was found between the non-eosinophilic and eosinophilic group. The frequency of the total pathological skin reactivity to vasomotor agents, singly and in combinations, was greater in the eosinophilic (91 per cent) then in the non-eosinophilic group (78 per cent) but intergroup difference was not significant. These findings suggest that pathologic skin reactivity to vasomotor agents is a feature of non-eosinophilic as well as eosinophilic non-allergic rhinitis patients and indicate that no difference is noticed in the skin reactivity between these groups.

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Gongora-Rivera, Fernando, Adolfo Cordero-Perez, Alejandro Gonzalez-Aquines, Antonio Anaya-Escamilla, Eduardo Villarreal-Garza, Meztli Espinosa-Ortega, Mario C. Salinas-Carmona, and Xochilt Ortiz-Jimenez. "Impaired Cerebral Vasomotor Reactivity in Alzheimer’s Disease." International Journal of Alzheimer's Disease 2018 (September 9, 2018): 1–5. http://dx.doi.org/10.1155/2018/9328293.

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Background. Recent studies have shown that cerebral vascularity may be impaired in Alzheimer’s disease. Cerebral vasomotor reactivity could be an important biomarker for this pathology.Aims. The aim of this study was to investigate the alterations in cerebral vascular motor reactivity in Alzheimer’s disease subjects and to associate these changes with their cognitive scores.Methods. We recruited subjects with a diagnosis of Alzheimer’s disease and healthy controls. Demographic, clinical, imaging, and cognitive test were obtained. Then all participants performed a cerebral vascular motor reactivity test with 7% CO2 and cerebral blood flow velocities (CBFV) were recorded with transcranial doppler ultrasound before and after the test.Results. We recruited 45 subjects, 26 (21 female) Alzheimer’s disease participants and 19 (15 female) healthy controls. There were no differences in baseline cerebral blood flow velocities between the groups. After the cerebral vasomotor reactivity test, absolute mean difference in mean CBFV (ΔCBFV-m) was 8.70±4.14 versus 4.81±6.96 (p<0.01), respectively. Calculated percentage of change (%CVMR) was lower in the AD group 7.45±18.25 versus 23.29±17.48, and there was a positive but weak correlation with mini-mental scores (ρ=0.337, p=0.023).Conclusions. In this study, Alzheimer’s disease subjects showed significant changes in all absolute cerebral blood flow velocities after the cerebral vasomotor reactivity test with CO2, but only diastolic phase responses were statistically significant. There was a positive but weak correlation between cerebral vasomotor reactivity and cognitive scores. Further studies are needed to investigate these effects in larger Latin-American samples.

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Hassler, Werner, and Helmuth Steinmetz. "Cerebral hemodynamics in angioma patients: an intraoperative study." Journal of Neurosurgery 67, no. 6 (December 1987): 822–31. http://dx.doi.org/10.3171/jns.1987.67.6.0822.

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✓ Local hemodynamics were investigated during 33 operations for cerebral arteriovenous malformation (AVM). In all cases, microvascular Doppler sonography was used to measure flow velocities and vasomotor reactivity to CO2 changes. Intravascular pressure recordings were performed in six patients. The AVM feeders had low intravascular pressure, high flow velocity, low peripheral stream resistance, and very poor vasomotor reactivity. Remote brain arteries showed no abnormalities. Doppler findings in arterial branches of AVM feeders that supplied normal brain indicated arteriolar dilation in their peripheral distribution. On removal of the angiomas, the arteries that formerly supplied them showed a return to normal intravascular pressure, whereas flow velocities dropped far below normal in these vessels. Remote arteries and branches of the former AVM feeders supplying the brain did not show any signs of impaired vasomotor reactivity following angioma removal. The results are in contrast to the normal perfusion pressure breakthrough theory.

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Suarez, Jose, and Osama O. Zaidat. "Cerebral vasomotor reactivity in brain dead patients." Stroke 32, suppl_1 (January 2001): 350. http://dx.doi.org/10.1161/str.32.suppl_1.350-a.

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P61 Background: Cerebral vasomotor reactivity (CVMR) is a measure of the changes in arteriolar resistance in response to changes in arterial C0 2 concentration. CMVR is easily performed at the bedside using transcranial Doppler ultrasound (TCD). CVMR has not been studied in brain death. Methods: Patients with a clinical diagnosis of brain death, confirmed by a neurointensivist, were studied. CVMR was determined at the time of the apnea test. An experienced sonographer used a Pioneer TC 2020 (Nicolette) with a 2 MHz probe to insonate a middle cerebral artery of these patients. Continuous middle cerebral artery blood flow velocity (MCAV), systolic blood pressure (SBP), heart rate (HR), body temperature, oxygen saturation, and end-tidal C0 2 was performed during the procedure.A confirmatory arterial blood gas was obtained at baseline, five and ten minutes into the apnea test, and three minutes after hyperventilation. CMVR was calculated as follows: (MCAV at hypercapnia/MCAV at baseline)x100 - (MCAV at hypocapnia/MCAV at baseline)x100.(Normal in adults: 86±16%) CMVR was then divided by the absolute change in C0 2 to yield the percentage change (%Δ) in MCAV per mmHg C0 2 (Normal in adults: 2–4%). Results: Ten patients were studied (8 men) with a mean age 47±16 years.Their underlying disease varied: 3 ischemic strokes, 3 ICH, 2 SAH and 2 anoxic encephalopathy. Values of parameters monitored during the apnea test for this population: SBP:140±25 mmHg, HR:90.6±31/min, temperature: 35.8±2, PC0 2 at baseline: 40.6±9, at end of test: 74.6±13, at hyperventilation: 33.3±5. CMVR was 43.5±20% and %Δ was 1.3±0.4. All these patients had MCAV patterns compatible with brain death. Conclusion: CMVR is severely reduced or exhausted in brain dead patients. This test should be considered when TCD is used as a confirmatory tool in clinically brain dead patients.

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Portegies, Marileen L. P., Renée F. A. G. de Bruijn, Albert Hofman, Peter J. Koudstaal, and M. Arfan Ikram. "Cerebral Vasomotor Reactivity and Risk of Mortality." Stroke 45, no. 1 (January 2014): 42–47. http://dx.doi.org/10.1161/strokeaha.113.002348.

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Bornstein, Natan M., Alexander Y. Gur, Edward G. Shifrin, and Baruch A. Morag. "Does Carotid Endarterectomy Modify Cerebral Vasomotor Reactivity?" Cerebrovascular Diseases 7, no. 4 (1997): 201–4. http://dx.doi.org/10.1159/000108191.

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Ducrocq, J., A. De Broca, M. Abdiche, S. Scaillet, L. Leke, and V. Bach. "Vasomotor Reactivity in Premature Neonates at Term." Neonatology 82, no. 1 (2002): 9–16. http://dx.doi.org/10.1159/000064146.

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Tsubokawa, Takashi, and Yoichi Katayama. "Cerebral vasomotor reactivity in head-injured patients." Critical Reviews in Neurosurgery 8, no. 2 (April 1998): 112–21. http://dx.doi.org/10.1007/s003290050068.

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Lee, Y., and B. Kim. "Cerebral vasomotor reactivity in small vessel disease." Journal of the Neurological Sciences 283, no. 1-2 (August 2009): 279. http://dx.doi.org/10.1016/j.jns.2009.02.151.

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Lee, Jee-Young, and Yong-Seok Lee. "Vasomotor reactivity in middle cerebral artery stenosis." Journal of the Neurological Sciences 301, no. 1-2 (February 2011): 35–37. http://dx.doi.org/10.1016/j.jns.2010.11.008.

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Heun, R., V. A. Knappertz, and And G. Krämer. "Vasomotor reactivity in dementia of alzheimer type." International Journal of Geriatric Psychiatry 9, no. 11 (November 1994): 913–18. http://dx.doi.org/10.1002/gps.930091108.

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Uzuner, N., S. Ozkan, and N. Cinar. "Cerebrovascular reactivity in multiple sclerosis patients." Multiple Sclerosis Journal 13, no. 6 (February 9, 2007): 737–41. http://dx.doi.org/10.1177/1352458506074645.

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A close relationship between multiple sclerosis (MS) lesions and the cerebral vasculature has long been recognised. Some studies have suggested that vascular endothelial cell activation might be an early event in the evolution of MS, and demyelisation may have an ischemic basis in this condition. Hypoxia caused by breath holding (BH) results in autoregulatory vasodilatation, and an increase in CBF to the cortex. The increased CBF can be evaluated by transcranial Doppler (TCD), and can provide information about the vascular integrity. In this study, we aimed to examine the vascular integrity and assess the vasomotor reactivity of MS patients in response to BH in different activation phases of the disease by means of TCD. We studied 12 patients with clinically diagnosed relapsing remitting (RR) MS, according to the Poser criteria. The initial TCD examination was performed in the first two days of an acute exacerbation of disease and prior to any treatment. The second test was performed just after iv methylprednisolone (IVMP) treatment, and the third examination occurred one month later, when the patient was in the remission phase. A group of 11 healthy subjects was also examined by TCD as control. Blood flow velocities were recorded during 30 seconds of normal breathing and 15 seconds BH. Vasomotor reactivity was calculated as a ratio of difference of cerebral flow velocities during BH. There were no significant vasomotor reactivity differences between the controls (55.7%) and the patients during attacks (46.5%), as well as after treatment (48.3%) and during attack free periods (50.9%). There were also no significant changes amongst the patients groups throughout the study. In this study, in different disease activity stages, we observed non-significant cerebrovascular vasomotor reactivity difference between the RRMS patients and the healthy controls, although it was slightly lower in the MS patients. This observation suggests that cerebrovascular reactivity is normal in different disease activity levels. Multiple Sclerosis 2007; 13: 737-741. http://msj.sagepub.com

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Tomoto, Tsubasa, Takashi Tarumi, Jason Chen, Evan P. Pasha, C. Munro Cullum, and Rong Zhang. "Cerebral Vasomotor Reactivity in Amnestic Mild Cognitive Impairment." Journal of Alzheimer's Disease 77, no. 1 (September 1, 2020): 191–202. http://dx.doi.org/10.3233/jad-200194.

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Background: Cerebral blood flow (CBF) is sensitive to changes in arterial CO2, referred to as cerebral vasomotor reactivity (CVMR). Whether CVMR is altered in patients with amnestic mild cognitive impairment (aMCI), a prodromal stage of Alzheimer disease (AD), is unclear. Objective: To determine whether CVMR is altered in aMCI and is associated with cognitive performance. Methods: Fifty-three aMCI patients aged 55 to 80 and 22 cognitively normal subjects (CN) of similar age, sex, and education underwent measurements of CBF velocity (CBFV) with transcranial Doppler and end-tidal CO2 (EtCO2) with capnography during hypocapnia (hyperventilation) and hypercapnia (rebreathing). Arterial pressure (BP) was measured to calculate cerebrovascular conductance (CVCi) to normalize the effect of changes in BP on CVMR assessment. Cognitive function was assessed with Mini-Mental State Examination (MMSE) and neuropsychological tests focused on memory (Logical Memory, California Verbal Learning Test) and executive function (Delis-Kaplan Executive Function Scale; DKEFS). Results: At rest, CBFV and MMSE did not differ between groups. CVMR was reduced by 13% in CBFV% and 21% in CVCi% during hypocapnia and increased by 22% in CBFV% and 20% in CVCi% during hypercapnia in aMCI when compared to CN (all p < 0.05). Logical Memory recall scores were positively correlated with hypocapnia (r = 0.283, r = 0.322, p < 0.05) and negatively correlated with hypercapnic CVMR measured in CVCi% (r = –0.347, r = –0.446, p < 0.01). Similar correlations were observed in D-KEFS Trail Making scores. Conclusion: Altered CVMR in aMCI and its associations with cognitive performance suggests the presence of cerebrovascular dysfunction in older adults who have high risks for AD.

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Gur, A. Y., D. Gücüyener, A. D. Korczyn, N. Üzüner, Y. Gilutz, G. Özdemir, and N. M. Bornstein. "Cerebral vasomotor reactivity and dementia after ischemic stroke." Acta Neurologica Scandinavica 122, no. 6 (January 19, 2010): 383–88. http://dx.doi.org/10.1111/j.1600-0404.2010.01323.x.

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Yonas, H., and S. Durham. "Technology used to assess vasomotor reactivity affects results." Stroke 23, no. 8 (August 1992): 1179–80. http://dx.doi.org/10.1161/str.23.8.1179b.

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Jansen, Gerard F. A., Anne Krins, and Buddha Basnyat. "Cerebral vasomotor reactivity at high altitude in humans." Journal of Applied Physiology 86, no. 2 (February 1, 1999): 681–86. http://dx.doi.org/10.1152/jappl.1999.86.2.681.

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The purpose of this study was twofold: 1) to determine whether at high altitude cerebral blood flow (CBF) as assessed during CO2 inhalation and during hyperventilation in subjects with acute mountain sickness (AMS) was different from that in subjects without AMS and 2) to compare the CBF as assessed under similar conditions in Sherpas at high altitude and in subjects at sea level. Resting control values of blood flow velocity in the middle cerebral artery ( V MCA), pulse oxygen saturation ([Formula: see text]), and transcutaneous [Formula: see text] were measured at 4,243 m in 43 subjects without AMS, 17 subjects with AMS, 20 Sherpas, and 13 subjects at sea level. Responses of CO2 inhalation and hyperventilation on V MCA,[Formula: see text], and transcutaneous[Formula: see text] were measured, and the cerebral vasomotor reactivity (VMR = Δ V MCA/[Formula: see text]) was calculated as the fractional change of V MCA per Torr change of [Formula: see text], yielding a hypercapnic VMR and a hypocapnic VMR. AMS subjects showed a significantly higher resting control V MCA than did no-AMS subjects (74 ± 22 and 56 ± 14 cm/s, respectively; P < 0.001), and[Formula: see text] was significantly lower (80 ± 8 and 88 ± 3%, respectively; P < 0.001). Resting control V MCA values in the sea-level group (60 ± 15 cm/s), in the no-AMS group, and in Sherpas (59 ± 13 cm/s) were not different. Hypercapnic VMR values in AMS subjects were 4.0 ± 4.4, in no-AMS subjects were 5.5 ± 4.3, in Sherpas were 5.6 ± 4.1, and in sea-level subjects were 5.6 ± 2.5 (not significant). Hypocapnic VMR values were significantly higher in AMS subjects (5.9 ± 1.5) compared with no-AMS subjects (4.8 ± 1.4; P < 0.005) but were not significantly different between Sherpas (3.8 ± 1.1) and the sea-level group (2.8 ± 0.7). We conclude that AMS subjects have greater cerebral hemodynamic responses to hyperventilation, higher V MCAresting control values, and lower[Formula: see text] compared with no-AMS subjects. Sherpas showed a cerebral hemodynamic pattern similar to that of normal subjects at sea level.

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Topcuoglu, Mehmet Akif, Suk-tak Chan, Gisele Sampaio Silva, Eric Edward Smith, Kenneth K. Kwong, and Aneesh Bhim Singhal. "Cerebral vasomotor reactivity in reversible cerebral vasoconstriction syndrome." Cephalalgia 37, no. 6 (May 20, 2016): 541–47. http://dx.doi.org/10.1177/0333102416650706.

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Background Altered cerebrovascular tone is implicated in reversible cerebral vasoconstriction syndrome (RCVS). We evaluated vasomotor reactivity using bedside transcranial Doppler in RCVS patients. Methods In this retrospective case-control study, middle cerebral artery (MCA) blood flow velocities were compared at rest and in response to breath-hold in RCVS ( n = 8), Migraineurs ( n = 10), and non-headache Controls ( n = 10). Hyperventilation response was measured in RCVS. Results In RCVS, Breath Holding Index (BHI) was severely reduced in seven of eight patients and 14/16 MCAs; seven of 16 MCAs showed exhausted (BHI < 0.1) or inverted (BHI < 0) vasomotor reactivity. Mean BHI in RCVS (0.23 ± 0.5) was significantly lower than Migraine (1.52 ± 0.57) and Controls (1.51 ± 0.32), p < 0.001. Triphasic velocity responses were seen in all groups. The maximum Vmean decline during the middle negative phase was −15.5 ± 9.2% in RCVS, −15.4 ± 7% in Migraine, and −10.3 ± 5% in Controls ( p = 0.04). In the late positive phase, average Vmean increase was 6.2 ± 14% in RCVS, which was significantly lower ( p < 0.001) than Migraine (30.5 ± 11%) and Controls (30.2 ± 6%). With hyperventilation, RCVS patients showed 23% decrease in Vmean. Conclusion Cerebral arterial tone is abnormal in RCVS, with proximal vasoconstriction and abnormally reduced capacity for vasodilation. Further studies are needed to determine the utility of BHI to diagnose RCVS before angiographic reversibility is established, and to estimate prognosis.

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Forteza, Alejandro, Jose G. Romano, Iszet Campo-Bustillo, Nelly Campo, Diogo C. Haussen, Jose Gutierrez, and Sebastian Koch. "High-Dose Atorvastatin Enhances Impaired Cerebral Vasomotor Reactivity." Journal of Stroke and Cerebrovascular Diseases 21, no. 6 (August 2012): 487–92. http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2010.12.002.

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Gomi, S., F. Gotoh, S. Komatsumoto, Y. Ishikawa, N. Araki, and J. Hamada. "Sweating Function and Retinal Vasomotor Reactivity in Migraine." Cephalalgia 9, no. 3 (September 1, 1989): 179–85. http://dx.doi.org/10.1046/j.1468-2982.1989.903179.x.

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Hanby, Martha F., Ronney B. Panerai, Thompson G. Robinson, and Victoria J. Haunton. "Is cerebral vasomotor reactivity impaired in Parkinson disease?" Clinical Autonomic Research 27, no. 2 (February 20, 2017): 107–11. http://dx.doi.org/10.1007/s10286-017-0406-x.

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Assenza, G., P. Maggio, F. Tibuzzi, F. Zappasodi, M. Corbetto, L. Trotta, C. Altamura, et al. "P2-27 Cortical neuromodulation modifies cerebral vasomotor reactivity." Clinical Neurophysiology 121 (October 2010): S114. http://dx.doi.org/10.1016/s1388-2457(10)60468-3.

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Milosevic, Dusanka, Ljiljana Janosevic, and Slobodanka Janosevic. "Intradermal tests with vasomotor agents in chronic non(infectious rhinitis." Vojnosanitetski pregled 59, no. 1 (2002): 37–41. http://dx.doi.org/10.2298/vsp0201037m.

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The aim of this prospective study was to examine the skin reactivity to four vasomotor agents in chronic, non-infectious rhinitis patients, and to determine whether non-allergic rhinitis (NAR) patients differ from allergic rhinitis (AR) patients. Seventy four patients with NAR and 44 with AR were subjected to intradermal testing with papaverin (5 mg/ml), metacholine (0.02, 0.2 and 2.0 mg/ml), histamine (0.01, 0.1, 1.0 and 10.0 ?g/ml) compound 48/80 (0.01, 0.1, 1.0 and 10.0 ?g/ml) and saline. It was found that the frequency of pathological skin reactivity to papaverin in the patients with NAR (25/74) was significantly greater (p=5.0?10-3) then in the patients with AR (4/44). No significant inter-group difference in skin reactivity to metacholine, histamine, compound 48/80 and saline was observed. The frequency of the total pathological skin reactivity to vasomotor agents, singly and in combinations, in patients with NAR (80%) was significantly greater (p=0.03) than in patients with AR (61%). These findings suggested that the pathological skin reactivity to papaverin, metacholine, histamine and compound 48/80 was a feature of chronic, non-infectious rhinitis patients and it was more frequently associated with non-allergic than with the allergic etiology of rhinitis.

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39

Hu, Han-Hwa, Terry Bo-Jau Kuo, Wen-Jang Wong, Yun-On Luk, Chang-Ming Chern, Li-Chi Hsu, and Wen-Yung Sheng. "Transfer Function Analysis of Cerebral Hemodynamics in Patients with Carotid Stenosis." Journal of Cerebral Blood Flow & Metabolism 19, no. 4 (April 1999): 460–65. http://dx.doi.org/10.1097/00004647-199904000-00012.

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This study evaluates the validity of the transfer function analysis of spontaneous fluctuations of arterial blood pressure (ABP) and blood flow velocity of the middle cerebral artery (MCAFV) as a simple, convenient method to assess human cerebral autoregulation in patients with carotid stenosis. Eighty-three consecutive patients with various degrees of carotid stenosis and 37 healthy controls were enrolled. The carotid stenosis was graded based on the diagnostic criteria of duplex ultrasound. Instantaneous bilateral MCAFV and ABP of all participants were assessed noninvasively using transcranial Doppler sonography and the servocontrolled infrared finger plethysmography, respectively. Spectral analyses of ABP and MCAFV were performed by fast Fourier transform. The fluctuations in ABP as well as in MCAFV were diffracted into three components at specific frequency ranges designated as high-frequency (HF; 0.15 to 0.4 Hz), low-frequency (LF; 0.04 to 0.15 Hz), and very low-frequency (VLF; 0.016 to 0.04 Hz). Cross-spectral analysis was applied to quantify the coherence, transfer phase, and magnitude in individual HF, LF, and VLF components. Transcranial Doppler CO2 vasomotor reactivity was measured with 5% CO2 inhalation. The LF phase angle (r = −0.53, P < 0.001); magnitude of VLF (r = −0.29, P = 0.002), LF (r = −0.35, P < 0.001), and HF (r = −0.47, P < 0.001); and CO2 vasomotor reactivity (r = −0.66, P < 0.001) were negatively correlated with the severity of stenosis. Patients with unilateral high-grade (greater than 90% stenosis) carotid stenosis demonstrated significant reduction in LF phase angle ( P < 0.001) and HF magnitude ( P = 0.018) on the ipsilateral side of the affected vessel compared with their contralateral side. The study also revealed a high sensitivity, specificity, and accuracy using LF phase angle and HF magnitude to detect a high-grade carotid stenosis. A strong correlation existed between the LF phase angle and the CO2 vasomotor reactivity test (r = 0.62, P < 0.001), and the correlation between the HF magnitude and the CO2 vasomotor reactivity (r = 0.44, P < 0.001) was statistically significant as well. We conclude that transfer function analysis of spontaneous fluctuations of MCAFV and ABP could be used to identify hemodynamically significant high-grade carotid stenosis with impaired cerebral autoregulation or vasomotor reserve.

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Wolf, ME, T. Jäger, H. Bäzner, and M. Hennerici. "Changes in Functional Vasomotor Reactivity in Migraine With Aura." Cephalalgia 29, no. 11 (November 2009): 1156–64. http://dx.doi.org/10.1111/j.1468-2982.2009.01843.x.

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Migraine with aura (MA) is associated with cerebral hyper- and hypoperfusion during and after the attacks. Several attempts to estimate individual perfusion changes and asymmetries in patients with MA using transcranial Doppler (TCD) have not been consistent. In 70 patients with MA and 40 controls with migraine without aura (MoA) or without any history of migraine, interictally recorded TCD sequences were prospectively analysed. Formal curve analysis of the visually evoked flow response (VEFR) was performed semiautomatically. As a main parameter for functional vasomotor reactivity (fVMR), the visually evoked flow rate (VEFR%) was calculated. The VEFR% showed a significantly higher mean difference of 14.7 ± 12% in MA patients vs. 5.8 ± 4.4% ( P < 0.001) in controls. The significant asymmetry of fVMR in MA patients is suggested to reflect interattack persisting vasomotor changes which are of pathophysiological interest and may be used as a monitoring tool under prophylactic medication.

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Gurtner, G. H., and T. Burke-Wolin. "Interactions of oxidant stress and vascular reactivity." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (April 1, 1991): L207—L211. http://dx.doi.org/10.1152/ajplung.1991.260.4.l207.

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Oxidants have complex effects on pulmonary vascular reactivity. They can stimulate production of vasoconstrictor arachidonate mediators and can also cause vasodilation through activation of guanylate cyclase. Oxidants can also inactivate vasomotor phenomenon by interfering with mechanisms of signal transduction or smooth muscle contraction. The final physiological response depends on the balance of these complex actions.

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42

Ringelstein, Erich Bernd, Sabine Van Eyck, and Irene Mertens. "Evaluation of Cerebral Vasomotor Reactivity by Various Vasodilating Stimuli: Comparison of CO2 to Acetazolamide." Journal of Cerebral Blood Flow & Metabolism 12, no. 1 (January 1992): 162–68. http://dx.doi.org/10.1038/jcbfm.1992.20.

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To evaluate the role of different vasomotor stimuli for the measurement of cerebrovascular vasomotor reactivity (VMR), 47 patients (i.e., 93 hemispheres) with various degrees of internal carotid artery (ICA) occlusive disease were studied. Patients were divided into clinical [asymptomatic, transient ischemic attack (TIA) or completed stroke] as well as angiological subgroups. Low-grade or high-grade unilateral ICA lesions were compared to bilateral ICA occlusive disease. Relative flow velocity changes within the middle cerebral artery were measured by means of transcranial Doppler during hyper- and hypocapnia (VMRTOT), during hypercapnia alone, and after injection of 1 g acetazolamide (VMRACE). VMR was expressed as the percentage change in flow velocity after stimulus application as compared with flow velocity at rest. There was a close and statistically highly significant correlation of CO2-induced with acetazolamide-induced VMR ( r = 0.69 in VMRTOT versus VMRACE and 0.79 in versus VMRACE; p < 0.0001; linear regression), indicating a strong similarity of the vasodilatative effects of CO2 and acetazolamide on cerebral arteries. Both stimulation techniques highly significantly differentiated between asymptomatic patients and those with TIA or completed stroke. Angiological subgroups were separated best by the acetazolamide test. Reclassification of patients into angiological subgroups by linear discriminant analysis was equally good with all three methods. We conclude that both acetazolamide- and CO2-induced stimulation of the cerebral vasomotors are valid techniques to measure reduction in perfusion reserve due to extracranial cerebrovascular occlusive disease. Acetazolamide has the advantage of being independent of the patient's cooperation. However, it has the disadvantage of increasing the intracranial pressure and not permitting evaluation of the vasoconstrictor capabilities of the cerebral vasculature.

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43

Nandadeva, Damsara, Jordan C. Patik, Zachary T. Martin, Paul J. Fadel, and R. Matthew Brothers. "Repeatability of Cerebral Vasomotor Reactivity to Hypercapnia in Humans." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.04751.

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44

Giannopoulos, S., J. H. Choi, and R. S. Marshall. "Metabolic syndrome and cerebral vasomotor reactivity in atherosclerotic disease." European Journal of Neurology 17, no. 12 (August 16, 2010): e109-e109. http://dx.doi.org/10.1111/j.1468-1331.2010.03181.x.

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Bove, A. A., and J. D. Dewey. "Proximal coronary vasomotor reactivity after exercise training in dogs." Circulation 71, no. 3 (March 1985): 620–25. http://dx.doi.org/10.1161/01.cir.71.3.620.

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Edvinsson, L., and R. Uddman. "The Feline Carotid Rete: Vasomotor Reactivity of Isolated Arteries." Acta Pharmacologica et Toxicologica 52, no. 2 (March 13, 2009): 128–34. http://dx.doi.org/10.1111/j.1600-0773.1983.tb03414.x.

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47

Hamann, G. F., and G. J. del Zoppo. "Leukocyte involvement in vasomotor reactivity of the cerebral vasculature." Stroke 25, no. 11 (November 1994): 2117–19. http://dx.doi.org/10.1161/01.str.25.11.2117.

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48

Karnik, Ronald, Andreas Valentin, Walther-Benedikt Winkler, Nadja Khaffaf, Peter Donath, and Jörg Slany. "Sex-Related Differences in Acetazolamide-Induced Cerebral Vasomotor Reactivity." Stroke 27, no. 1 (January 1996): 56–58. http://dx.doi.org/10.1161/01.str.27.1.56.

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49

Forteza, A., Y. Echeverria, D. C. Haussen, J. Gutierrez, E. Wiley, and C. De Gusmao. "Cerebral vasomotor reactivity monitoring in posterior reversible encephalopathy syndrome." Case Reports 2010, may11 1 (May 11, 2010): bcr1020092345. http://dx.doi.org/10.1136/bcr.10.2009.2345.

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50

Volynsky, Margaryants, Mamontov, and Kamshilin. "Contactless Monitoring of Microcirculation Reaction on Local Temperature Changes." Applied Sciences 9, no. 22 (November 17, 2019): 4947. http://dx.doi.org/10.3390/app9224947.

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Assessment of skin blood flow is an important clinical task which is required to study mechanisms of microcirculation regulation including thermoregulation. Contactless assessment of vasomotor reactivity in response to thermal exposure is currently not available. The aim of this study is to show the applicability of the imaging photoplethysmography (IPPG) method to measure quantitatively the vasomotor response to local thermal exposure. Seventeen healthy subjects aged 23 ± 7 years participated in the study. A warm transparent compress applied to subject’s forehead served as a thermal impact. A custom-made IPPG system operating at green polarized light was used to monitor the subject’s face continuously and simultaneously with skin temperature and electrocardiogram (ECG) recordings. We found that the thermal impact leads to an increase in the amplitude of blood pulsations (BPA) simultaneously with the skin temperature increase. However, a multiple increase in BPA remained after the compress was removed, whereas the skin temperature returned to the baseline. Moreover, the BPA increase and duration of the vasomotor response was associated with the degree of external heating. Therefore, the IPPG method allows us to quantify the parameters of capillary blood flow during local thermal exposure to the skin. This proposed technique of assessing the thermal reactivity of microcirculation can be applied for both clinical use and for biomedical research.

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Journal articles on the topic 'Vasomotor reactivity'

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