Assessment of cerebrovascular and cardiovascular responses to lower body negative pressure as a test of cerebral autoregulation

2003 ◽  
Vol 208 (1-2) ◽  
pp. 71-78 ◽  
Author(s):  
Clive M. Brown ◽  
Matthias Dütsch ◽  
Martin J. Hecht ◽  
Bernhard Neundörfer ◽  
Max J. Hilz
1997 ◽  
Vol 29 (Supplement) ◽  
pp. 36
Author(s):  
S. M.C. Lee ◽  
L. Steinmann ◽  
M. Wood ◽  
L. Dussack ◽  
S. M. Fortney

1990 ◽  
Vol 68 (1) ◽  
pp. 355-362 ◽  
Author(s):  
J. M. Overton ◽  
C. M. Tipton

To determine whether hindlimb suspension is associated with the development of cardiovascular deconditioning, male rats were studied before and after undergoing one of three treatment conditions for 9 days: 1) cage control (n = 15, CON), 2) horizontal suspension (n = 15, HOZ), and 3) head-down suspension (n = 18, HDS). Testing included lower body negative pressure administered during chloralose-urethan anesthesia and graded doses of sympathomimetic agents (norepinephrine, phenylephrine, and tyramine) administered to conscious unrestrained animals. Both HDS and HOZ were associated with a small decrease in the hypotensive response to lower body negative pressure. The HOZ group, but not the HDS group, exhibited augmented reflex tachycardia. Furthermore, both HDS and HOZ groups manifested reduced pressor responses to phenylephrine after treatment. These reductions were associated with significantly attenuated increases in mesenteric vascular resistance. However, baroreflex control of heart rate was not altered by the treatment conditions. Collectively, these results indicate that 9 days of HDS in rats does not elicit hemodynamic response patterns generally associated with cardiovascular deconditioning induced by hypogravic conditions.


1987 ◽  
Vol 63 (2) ◽  
pp. 719-725 ◽  
Author(s):  
C. M. Tomaselli ◽  
M. A. Frey ◽  
R. A. Kenney ◽  
G. W. Hoffler

We have investigated the pattern of fluid redistribution and cardiovascular responses during graduated orthostatic stress. Twelve men, age 30–39 yr, underwent a 25-min lower-body negative pressure (LBNP) test protocol that involved sequential stages of LBNP at -8 mmHg (1 min), -16 mmHg (1 min), -30 mmHg (3 min), -40 mmHg (5 min), -50 mmHg (5 min), -40 mmHg (5 min), -30 mmHg (3 min), -16 mmHg (1 min), and -8 mmHg (1 min). Data were recorded at the end of each stage. For many measured variables values during the descending phase of LBNP (-8 to -40 mmHg) were significantly different from values during the ascending phase of (-40 to -8 mmHg). These differences appear to be due to a component of fluid translocation that occurs during LBNP and cannot be reversed within the duration of the procedure. We hypothesize that this slowly reversed component is sequestration of fluid in the interstitial and lymphatic compartments. In contrast, venous pooling is a rapidly reversible component of fluid movement during LBNP. A scheme describing fluid and cardiovascular responses to LBNP based on these data and the data of other investigators is presented.


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