Middle cerebral artery blood velocity during a Valsalva maneuver in the standing position

2000 ◽  
Vol 88 (5) ◽  
pp. 1545-1550 ◽  
Author(s):  
Frank Pott ◽  
Johannes J. van Lieshout ◽  
Kojiro Ide ◽  
Per Madsen ◽  
Niels H. Secher
Keyword(s):  
Cardiac Output ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Valsalva Maneuver ◽  
Venous Pressure ◽  
Standing Position ◽  
Blood Velocity ◽  
Central Venous ◽  
Mouth Pressure ◽  
The Brain

Occasionally, lifting of a heavy weight leads to dizziness and even to fainting, suggesting that, especially in the standing position, expiratory straining compromises cerebral perfusion. In 10 subjects, the middle cerebral artery mean blood velocity ( V mean) was evaluated during a Valsalva maneuver (mouth pressure 40 mmHg for 15 s) both in the supine and in the standing position. During standing, cardiac output decreased by 16 ± 4 (SE) % ( P < 0.05), and at the level of the brain mean arterial pressure (MAP) decreased from 89 ± 2 to 78 ± 3 mmHg ( P < 0.05), as did V mean from 73 ± 4 to 62 ± 5 cm/s ( P < 0.05). In both postures, the Valsalva maneuver increased central venous pressure by ∼40 mmHg with a nadir in MAP and cardiac output that was most pronounced during standing (MAP: 65 ± 6 vs. 87 ± 3 mmHg; cardiac output: 37 ± 3 vs. 57 ± 4% of the resting value; P < 0.05). Also, V mean was lowest during the standing Valsalva maneuver (39 ± 5 vs. 47 ± 4 cm/s; P < 0.05). In healthy individuals, orthostasis induces an ∼15% reduction in middle cerebral artery V mean that is exaggerated by a Valsalva maneuver performed with 40-mmHg mouth pressure to ∼50% of supine rest.

Middle cerebral artery blood velocity during intense static exercise is dominated by a Valsalva maneuver

2003 ◽  
Vol 94 (4) ◽  
pp. 1335-1344 ◽  
Author(s):  
Frank Pott ◽  
Johannes J. Van Lieshout ◽  
Kojiro Ide ◽  
Per Madsen ◽  
Niels H. Secher
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Valsalva Maneuver ◽  
Venous Pressure ◽  
Blood Velocity ◽  
Static Exercise ◽  
Central Venous

Lifting of a heavy weight may lead to “blackout” and occasionally also to cerebral hemorrhage, indicating pronounced consequences for the blood flow through the brain. We hypothesized that especially strenuous respiratory straining (a Valsalva-like maneuver) associated with intense static exercise would lead to a precipitous rise in mean arterial and central venous pressures and, in turn, influence the middle cerebral artery blood velocity (MCA V mean) as a noninvasive indicator of changes in cerebral blood flow. In 10 healthy subjects, MCA V mean was evaluated in response to maximal static two-legged exercise performed either with a concomitantly performed Valsalva maneuver or with continued ventilation and also during a Valsalva maneuver without associated exercise ( n = 6). During static two-legged exercise, the largest rise for mean arterial pressure and MCA V meanwas established at the onset of exercise performed with a Valsalva-like maneuver (by 42 ± 5 mmHg and 31 ± 3% vs. 22 ± 6 mmHg and 25 ± 6% with continued ventilation; P < 0.05). Profound reductions in MCA V mean were observed both after exercise with continued ventilation (−29 ± 4% together with a reduction in the arterial CO2 tension by −5 ± 1 Torr) and during the maintained Valsalva maneuver (−21 ± 3% together with an elevation in central venous pressure to 40 ± 7 mmHg). Responses to performance of the Valsalva maneuver with and without exercise were similar, reflecting the deterministic importance of the Valsalva maneuver for the central and cerebral hemodynamic response to intense static exercise. Continued ventilation during intense static exercise may limit the initial rise in arterial pressure and may in turn reduce the risk of hemorrhage. On the other hand, blackout during and after intense static exercise may reflect a reduction in cerebral blood flow due to expiratory straining and/or hyperventilation.

scholarly journals The effect of changes in cardiac output on middle cerebral artery mean blood velocity at rest and during exercise

2005 ◽  
Vol 569 (2) ◽  
pp. 697-704 ◽  
Author(s):  
Shigehiko Ogoh ◽  
R. Matthew Brothers ◽  
Quinton Barnes ◽  
Wendy L. Eubank ◽  
Megan N. Hawkins ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Blood Velocity

Cerebral hypoxia-ischemia and middle cerebral artery occlusion induce expression of the cannabinoid CB2 receptor in the brain

2007 ◽  
Vol 412 (2) ◽  
pp. 114-117 ◽  
Author(s):  
John C. Ashton ◽  
Rosanna M.A. Rahman ◽  
Shiva M. Nair ◽  
Brad A. Sutherland ◽  
Michelle Glass ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Cerebral Hypoxia ◽  
Cb2 Receptor ◽  
Hypoxia Ischemia ◽  
Cerebral Artery Occlusion ◽  
The Brain

Abstract 166: Endothelial Overexpression of LOX-1 Increases Stroke Size in vivo

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Alexander Akhmedov ◽  
Remo D Spescha ◽  
Francesco Paneni ◽  
Giovani G Camici ◽  
Thomas F Luescher
Keyword(s):  
Endothelial Cells ◽  
Ischemic Stroke ◽  
Endothelial Dysfunction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Oxidized Ldl ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
The Brain

Background— Stroke is one of the most common causes of death and long term disability worldwide primarily affecting the elderly population. Lectin-like oxidized LDL receptor 1 (LOX-1) is the receptor for oxidized LDL identified in endothelial cells. Binding of OxLDL to LOX-1 induces several cellular events in endothelial cells, such as activation of transcription factor NF-kB, upregulation of MCP-1, and reduction in intracellular NO. Accumulating evidence suggests that LOX-1 is involved in endothelial dysfunction, inflammation, atherogenesis, myocardial infarction, and intimal thickening after balloon catheter injury. Interestingly, a recent study demonstrated that acetylsalicylic acid (aspirin), which could prevent ischemic stroke, inhibited Ox-LDL-mediated LOX-1 expression in human coronary endothelial cells. The expression of LOX-1 was increased at a transient ischemic core site in the rat middle cerebral artery occlusion model. These data suggest that LOX-1 expression induces atherosclerosis in the brain and is the precipitating cause of ischemic stroke. Therefore, the goal of the present study was to investigate the role of endothelial LOX-1 in stroke using experimental mouse model. Methods and Results— 12-week-old male LOX-1TG generated recently in our group and wild-type (WT) mice were applied for a transient middle cerebral artery occlusion (MCAO) model to induce ischemia/reperfusion (I/R) brain injury. LOX-1TG mice developed 24h post-MCAO significantly larger infarcts in the brain compared to WT (81.51±8.84 vs. 46.41±10.13, n=7, p < 0.05) as assessed morphologically using Triphenyltetrazolium chloride (TTC) staining. Moreover, LOX-1TG showed higher neurological deficit in RotaRod (35.57±8.92 vs. 66.14±10.63, n=7, p < 0.05) and Bederson tests (2.22±0.14 vs. 1.25±0.30, n=9-12, p < 0.05) - two experimental physiological tests for neurological function. Conclusions— Thus, our data suggest that LOX-1 plays a critical role in the ischemic stroke when expressed at unphysiological levels. Such LOX-1 -associated phenotype could be due to the endothelial dysfunction. Therefore, LOX-1 may represent novel therapeutic targets for preventing ischemic stroke.

scholarly journals Middle cerebral artery blood velocity during running: interactions of heart and stride impact rates

2012 ◽  
Vol 26 (S1) ◽  
Author(s):  
Elisa Wasson ◽  
Cody Harper ◽  
Andrew Subudhi ◽  
Sue Schneider ◽  
Nico Maestas ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Blood Velocity

Acute Middle Cerebral Artery Occlusion: Experience with Volume Expansion Therapy

Neurosurgery ◽  
1986 ◽  
Vol 18 (4) ◽  
pp. 397-401 ◽  
Author(s):  
Bruce I. Tranmer ◽  
Cordell E. Gross ◽  
Ted S. Keller ◽  
Glenn W. Kindt
Keyword(s):  
Cardiac Output ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Volume Expansion ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Life Styles ◽  
Arterial Blood ◽  
Mca Occlusion ◽  
The Mean

Abstract Five consecutive patients with acute neurological deficits after middle cerebral artery (MCA) occlusion were given emergency treatment with colloidal volume expansion. In each case, the diagnosis was confirmed promptly by computed tomography and cerebral angiography. Aggressive volume expansion therapy was started 2 to 18 hours (mean, 11 hr) after the onset of the neurological deficit. The mean colloidal volume used was 920 ml/day for an average of 4 days. During volume expansion, the mean cardiac output increased 57% from 4.6 + 0.6 to 7.2 + 1.9 litres/min (P &lt; 0.05). The mean hematocrit decreased 19% from 46 + 3% to 37 + 4% (P &lt; 0.01). The mean arterial blood pressure remained stable, and the pulmonary artery wedge pressure was maintained at &lt; 15 mm Hg. Three patients improved dramatically with volume expansion therapy and have returned to their previous life-styles. Two patients made partial recoveries and manage at home with nursing care. The three patients who improved dramatically were young (aged &lt;34) and, when compared to the older patients, they had greater increases in cardiac output (67% vs. 19%). No major complications or deaths were attributed to the volume expansion therapy. We propose that intravascular volume expansion and its concomitant augmentation of the cardiovascular dynamics may be effective in the treatment of acute neurological deficits after acute MCA occlusion.

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