Acute and chronic head-down tail suspension diminishes cerebral perfusion in rats

2002 ◽  
Vol 282 (1) ◽  
pp. H328-H334 ◽  
Author(s):  
M. Keith Wilkerson ◽  
Patrick N. Colleran ◽  
Michael D. Delp

10.1152/ajpheart.00727.2001.—The purpose of this study was to test the hypothesis that regional brain blood flow and vascular resistance are altered by acute and chronic head-down tail suspension (HDT). Regional cerebral blood flow, arterial pressure, heart rate, and vascular resistance were measured in a group of control rats during normal standing and following 10 min of HDT and in two other groups of rats after 7 and 28 days of HDT. Heart rate was not different among conditions, whereas mean arterial pressure was elevated at 10 min of HDT relative to the other conditions. Total brain blood flow was reduced from that during standing by 48, 24, and 27% following 10 min and 7 and 28 days of HDT, respectively. Regional blood flows to all cerebral tissues and the eyes were reduced with 10 min of HDT and remained lower in the eye, olfactory bulbs, left and right cerebrum, thalamic region, and the midbrain with 7 and 28 days of HDT. Total brain vascular resistance was 116, 44, and 38% greater following 10 min and 7 and 28 days of HDT, respectively, relative to that during control standing. Vascular resistance was elevated in all cerebral regions with 10 min of HDT and remained higher than control levels in most brain regions. These results demonstrate that HDT results in chronic elevations in total and regional cerebral vascular resistance, and this may be the underlying stimulus for the HDT-induced smooth muscle hypertrophy of cerebral resistance arteries.

1993 ◽  
Vol 75 (4) ◽  
pp. 1740-1747 ◽  
Author(s):  
J. Peters ◽  
B. Hecker ◽  
D. Neuser ◽  
W. Schaden

To assess the effects of continuous positive (CPAP) or negative airway pressure (CNAP) breathing (+/- 10#x2013;12 cmH2O, duration 25 min) on blood content in the body's capacitance vasculature, regional distribution of labeled red blood cells was evaluated in seven spontaneously breathing supine volunteers. Counts were acquired by whole body scans and detectors overlying the liver, intestine, left ventricle, and lower arm, and arterial pressure, heart rate, calf blood flow and vascular resistance, hematocrit, vasopressin, and atrial natriuretic peptide plasma concentrations were also obtained. With CPAP, thoracic, cardiac, and left ventricular counts diminished significantly by 7#x2013;10%, were accompanied by significant increases in counts over both the gut and liver, and remained decreased during CPAP but reversed to baseline with zero airway pressure. Calf blood flow and vascular resistance significantly decreased and increased, respectively, whereas limb counts, arterial pressure, heart rate, and hormone concentrations remained unchanged. With CNAP, in contrast, regional counts and other variables did not change. Thus, moderate levels of CPAP deplete the intrathoracic vascular bed and heart, shifting blood toward the gut and liver but not toward the limbs. No short-term compensation increasing cardiac filling during CPAP was seen. In contrast, CNAP did not alter intrathoracic or organ blood content and, therefore, does not simply mirror the effects evoked by CPAP.


1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.


1995 ◽  
Vol 7 (5) ◽  
pp. 1381 ◽  
Author(s):  
BS Stonestreet ◽  
ES Barefield ◽  
D Piva ◽  
M Goldstein

We tested the hypothesis that, in newborn piglets, hypercarbia impairs autoregulation of total and regional brain blood flow at the lower limb of the autoregulatory curve. Cerebral oxygen metabolism was measured in the same piglets to relate changes in metabolism to blood flow. Instrumented hypercarbic (n = 9) and normocarbic (n = 8) newborn piglets exposed to phlebotomy were studied during normotension and graded hypotension with mean arterial blood pressures of 55-41, 40-31 and < 30 mmHg. In the hypercarbic piglets, total brain blood flow decreased (P < 0.01) from the hypercarbic-normotensive value of 187 +/- 15 mliter min-1 100 g-1 to 139 +/- 18, 66 +/- 11 and 34 +/- 6 at mean arterial blood pressures of 55-41, 40-31 and < 30 mmHg, respectively; in the normocarbic piglets, total brain blood flow did not change from the normotensive value (70 +/- 11 mliter min-1 100 g-1) until the mean arterial blood pressure was < 30 mmHg, when brain blood flow had decreased (P < 0.01) to 49 +/- 8 mliter min-1 100 g-1. In the hypercarbic piglets, all brain regions (cerebrum, caudate nucleus, cerebellum, brainstem and medulla) demonstrated similar response patterns to that of total brain blood flow during hypotension. Thus, during hypercarbia, none of the brain regions demonstrated autoregulation. In the normocarbic piglets, cerebral blood flow decreased (P < 0.01) from the normocarbic-normotensive value of 74 +/- 6 mloter min-1 100 g-1 to 51 +/- 8 and 37 +/- 7 at mean arterial blood pressures of 40-31 and < 30 mmHg, respectively, and blood flow to the caudate nucleus, cerebellum and brainstem did not decrease significantly, and in fact increased (P < 0.01) to the medulla during hypotension. Although cerebral oxygen metabolism was compromised in the hypercarbic and normocarbic piglets, the relationship between metabolism and blood flow was altered such that the cerebral metabolic rate of oxygen per unit of blood flow was lower in the hypercarbic than the normocarbic piglets. We conclude that hypercarbia impairs total and regional brain blood flow autoregulation in newborn piglets.


2007 ◽  
Vol 22 (4) ◽  
pp. 291-298 ◽  
Author(s):  
Marco Aurelio Marangoni ◽  
Alex Hausch ◽  
Pedro Thadeu Galvão Vianna ◽  
José Reinaldo Cerqueira Braz ◽  
Rosa Marlene Viero ◽  
...  

PURPOSE: About 50 % of indications for dialysis in acute renal failure are related to problems originated during the perioperative period. Intraoperative hemodynamic changes lead to renal vasoconstriction and hypoperfusion. Previous studies have not defined the dexmedetomidine renal role in hemorrhage situations. This study evaluated the effect of dexmedetomidine on renal function and histology after acute hemorrhage in rats. METHODS: Covered study with 20 Wistars rats, anesthetized with sodium pentobarbital, 50 mg. kg-1, intraperitoneal, randomized into 2 groups submitted to 30% volemia bleeding: DG - iv dexmedetomidine, 3 µg. kg-1 (10 min) and continuous infusion - 3 µg. kg-1. h-1; CG - pentobarbital. For renal clearance estimative, sodium p-aminohippurate and iothalamate were administered. Studied attributes: heart rate, mean arterial pressure, rectal temperature, hematocrit, iothalamate and p-aminohippurate clearance, filtration fraction, renal blood flow, renal vascular resistance, and histological evaluations of the kidneys. RESULTS: DG showed smaller values of heart rate, mean arterial pressure, and renal vascular resistance, but iothalamate clearance and filtration fraction values were higher. There was similarity in p-aminohippurate clearance and renal blood flow. Both groups had histological changes ischemia-like, but dexmedetomidine determined higher tubular dilatation scores. CONCLUSION: In rats, after acute hemorrhage, dexmedetomidine determined better renal function, but higher tubular dilation scores.


1990 ◽  
Vol 78 (2) ◽  
pp. 193-197 ◽  
Author(s):  
Abraham Koshy ◽  
Tatsuya Sekiyama ◽  
Jean-Michel Cereda ◽  
Antoine Hadengue ◽  
Catherine Girod ◽  
...  

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 ± 4 to 92 ± 4 mmHg (mean ± sem), cardiac output from 56 ± 4 to 24 ± 2 ml min−1 100 g−1 body weight, portal pressure from 15.1 ± 1.5 to 10.0 ± 1.4 mmHg and portal tributary blood flow from 19.9 ± 2.3 to 8.3 ± 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 ± 0.9 × 103 to 11.1 ± 2.0 × 103 kPal−1 s. 3. Volume expansion reduced arterial pressure from 98 ± 3 to 90 ± 3 mmHg, and significantly increased cardiac output from 43 ± 3 to 55 ± 3 ml min−1 100 g−1 body weight, portal pressure from 13.9 ± 0.7 to 16.5 ± 0.8 mmHg and portal tributary blood flow from 16.4 ± 1.3 to 28.2 ± 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 ± 0. 5 × 103 to 4.9 ± 0.4 × 103 kPa l−1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.


2001 ◽  
Vol 90 (4) ◽  
pp. 1516-1522 ◽  
Author(s):  
Urs A. Leuenberger ◽  
J. Cullen Hardy ◽  
Michael D. Herr ◽  
Kristen S. Gray ◽  
Lawrence I. Sinoway

Obstructive apnea and voluntary breath holding are associated with transient increases in muscle sympathetic nerve activity (MSNA) and arterial pressure. The contribution of changes in blood flow relative to the contribution of changes in vascular resistance to the apnea-induced transient rise in arterial pressure is unclear. We measured heart rate, mean arterial blood pressure (MAP), MSNA (peroneal microneurography), and femoral artery blood velocity ( V FA, Doppler) in humans during voluntary end-expiratory apnea while they were exposed to room air, hypoxia (10.5% inspiratory fraction of O2), and hyperoxia (100% inspiratory fraction of O2). Changes from baseline of leg blood flow (Q˙) and vascular resistance (R) were estimated from the following relationships: Q˙ ∝ V FA, corrected for the heart rate, and R ∝ MAP/Q˙. During apnea, MSNA rose; this rise in MSNA was followed by a rise in MAP, which peaked a few seconds after resumption of breathing. Responses of MSNA and MAP to apnea were greatest during hypoxia and smallest during hyperoxia ( P < 0.05 for both compared with room air breathing). Similarly, apnea was associated with a decrease in Q˙ and an increase in R. The decrease in Q˙ was greatest during hypoxia and smallest during hyperoxia (−25 ± 3 vs. −6 ± 4%, P < 0.05), and the increase in R was the greatest during hypoxia and the least during hyperoxia (60 ± 8 vs. 21 ± 6%, P < 0.05). Thus voluntary apnea is associated with vasoconstriction, which is in part mediated by the sympathetic nervous system. Because apnea-induced vasoconstriction is most intense during hypoxia and attenuated during hyperoxia, it appears to depend at least in part on stimulation of arterial chemoreceptors.


1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.


1963 ◽  
Vol 18 (5) ◽  
pp. 987-990 ◽  
Author(s):  
Shanker Rao

Reports of cardiovascular responses to head-stand posture are lacking in literature. The results of the various responses, respectively, to the supine, erect, and head-stand posture, are as follows: heart rate/min 67, 84, and 69; brachial arterial pressure mm Hg 92, 90, and 108; posterior tibial arterial pressure mm Hg 98, 196, and 10; finger blood flow ml/100 ml min 4.5, 4.4, and 5.2; toe blood flow ml/100 ml min 7.1, 8.1, and 3.4; forehead skin temperature C 34.4, 34.0 and 34.3; dorsum foot skin temperature C 28.6, 28.2, and 28.2. It is inferred that the high-pressure-capacity vessels between the heart level and posterior tibial artery have little nervous control. The high-pressure baroreceptors take active part in postural adjustments of circulation. The blood pressure equating mechanism is not as efficient when vital tissues are pooled with blood as when blood supply to them is reduced. man; heart rate; blood flow; skin temperature Submitted on January 3, 1963


2002 ◽  
Vol 93 (6) ◽  
pp. 1966-1972 ◽  
Author(s):  
Maria T. E. Hopman ◽  
Jan T. Groothuis ◽  
Marcel Flendrie ◽  
Karin H. L. Gerrits ◽  
Sibrand Houtman

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.


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