Influence of dehydration on locally mediated hindlimb vasodilation in baboons

1988 ◽  
Vol 255 (2) ◽  
pp. H266-H271
Author(s):  
R. M. Thornton ◽  
D. W. Proppe
Keyword(s):  
Blood Flow ◽  
Iliac Artery ◽  
Water Deprivation ◽  
Arterial Occlusion ◽  
External Iliac Artery ◽  
Artery Blood Flow ◽  
Vascular Conductance ◽  
Similar Reduction ◽  
Arterial Blood ◽  
Cutaneous Vasodilation

Previous studies indicate that the heat stress-induced cutaneous vasodilation in baboons is attenuated during dehydration by mechanisms other than the well-known neurohumoral vasoconstrictor mechanisms. Therefore, this study sought to determine whether dehydration also attenuates locally mediated maximum hindlimb blood flow and vascular conductance in baboons. Five baboons were chronically instrumented to measure arterial blood pressure and mean external iliac artery blood flow (MIBF). Hindlimb vasodilation was induced by occlusions of the external iliac artery for 2.5, 5.0, 7.5, and 10.0 min and by close-arterial injections of acetylcholine (ACh) and sodium nitroprusside (NP) in graded doses. These vasodilatory stimuli were applied in euhydrated and dehydrated states, the latter being produced by water deprivation for 64-68 h. Maximum MIBF and iliac vascular conductance (IVC) after arterial occlusion were reduced by 67–70% during dehydration. Also, maximum MIBF and IVC produced by ACh in the dehydrated state were 46–;52% lower than in the euhydrated state. A similar reduction in the responses to NP occurred during dehydration. It is concluded that the maximum hindlimb blood flow and vascular conductance produced by local, nonneurohumoral mechanisms are attenuated in the baboon during dehydration.

The Effects of Barbiturates On External Iliac Artery Blood Flow in Macaque Monkeys

Angiology ◽  
1972 ◽  
Vol 23 (5) ◽  
pp. 305-310
Author(s):  
Elizabeth M. Cuthbertson ◽  
Rutherford S. Gilfillan
Keyword(s):  
Blood Flow ◽  
Iliac Artery ◽  
External Iliac Artery ◽  
Artery Blood Flow ◽  
Macaque Monkeys

scholarly journals EXTERNAL ILIAC ARTERY BLOOD FLOW IN PATIENTS WITH ARTERIOSCLEROSIS OBLITERANS

1975 ◽  
Vol 125 (2) ◽  
pp. 437-441 ◽  
Author(s):  
YACOV ITZCHAK ◽  
MICHAELA MODAN ◽  
RAFAEL ADAR ◽  
VICTOR DEUTSCH
Keyword(s):  
Blood Flow ◽  
Iliac Artery ◽  
External Iliac Artery ◽  
Artery Blood Flow ◽  
Arteriosclerosis Obliterans

Effects of compartmental fluid repletion on heat-induced limb vasodilation in dehydrated baboons

1990 ◽  
Vol 259 (6) ◽  
pp. R1139-R1147 ◽  
Author(s):  
K. L. Ryan ◽  
D. W. Proppe
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Water Deprivation ◽  
Interstitial Fluid ◽  
Artery Blood Flow ◽  
Intravascular Volume ◽  
Vascular Conductance ◽  
Vascular Volume ◽  
Ambient Temperatures ◽  
Dextran Solution

Dehydration attenuates the increase in hindlimb blood flow produced by environmental heating (EH) in baboons. This study explored whether intravascular volume repletion alone was sufficient to remove this dehydration-induced attenuation. In six unanesthetized, chronically instrumented baboons, the increases in hindlimb blood flow during EH were measured under these conditions: euhydrated, dehydrated (64-68 h of water deprivation) without fluid replenishment, and dehydrated with intravenous fluid replenishment by either 6% high-molecular-weight dextran solution (to replenish vascular volume) or hyperosmotic saline (to replenish vascular and interstitial fluid volumes). EH consisted of acute exposure to ambient temperatures of 38-42 degrees C until core temperature (Tc) reached 39.5 degrees C. During dehydration without fluid replenishment the increments in mean iliac artery blood flow (MIBF) and iliac vascular conductance (IVC) produced by EH (i.e., value at Tc = 39.5 degrees C - pre-EH value) were reduced by 39 and 44%, respectively. After infusion of a volume of dextran solution equal to blood volume lost during dehydration, the increment in MIBF during EH was partially restored to the euhydrated level, but the increment in IVC remained at the dehydrated level. Infusion of hyperosmotic saline during dehydration completely restored the increases in MIBF and IVC during EH to euhydrated levels. Thus restoration of normal blood volume alone in dehydrated baboons does not completely restore normal hindlimb vasodilation during EH.

Maximal vascular leg conductance in trained and untrained men

1987 ◽  
Vol 62 (2) ◽  
pp. 606-610 ◽  
Author(s):  
P. G. Snell ◽  
W. H. Martin ◽  
J. C. Buckey ◽  
C. G. Blomqvist
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Vascular Conductance ◽  
Blood Flows ◽  
Arterial Blood ◽  
Sedentary Subjects

Lower leg blood flow and vascular conductance were studied and related to maximal oxygen uptake in 15 sedentary men (28.5 +/- 1.2 yr, mean +/- SE) and 11 endurance-trained men (30.5 +/- 2.0 yr). Blood flows were obtained at rest and during reactive hyperemia produced by ischemic exercise to fatigue. Vascular conductance was computed from blood flow measured by venous occlusion plethysmography, and mean arterial blood pressure was determined by auscultation of the brachial artery. Resting blood flow and mean arterial pressure were similar in both groups (combined mean, 3.0 ml X min-1 X 100 ml-1 and 88.2 mmHg). After ischemic exercise, blood flows were 29- and 19-fold higher (P less than 0.001) than rest in trained (83.3 +/- 3.8 ml X min-1 X 100 ml-1) and sedentary subjects (61.5 +/- 2.3 ml X min-1 X 100 ml-1), respectively. Blood pressure and heart rate were only slightly elevated in both groups. Maximal vascular conductance was significantly higher (P less than 0.001) in the trained compared with the sedentary subjects. The correlation coefficients for maximal oxygen uptake vs. vascular conductance were 0.81 (trained) and 0.45 (sedentary). These data suggest that physical training increases the capacity for vasodilation in active limbs and also enables the trained individual to utilize a larger fraction of maximal vascular conductance than the sedentary subject.

Effects of Sufentanil on Cerebral Hemodynamics and Intracranial Pressure in Patients with Brain Injury

1995 ◽  
Vol 83 (4) ◽  
pp. 721-726. ◽  
Author(s):  
Christian Werner ◽  
Eberhard Kochs ◽  
Hanswerner Bause ◽  
William E. Hoffman ◽  
Jochen Schulte am Esch
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Artery Blood Flow ◽  
Arterial Blood ◽  
Norepinephrine Infusion ◽  
Group 2 ◽  
Group 1

Background The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). Methods Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. Results Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. Conclusions The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.

Effect of active muscle mass during ischemic exercise on peak lower leg vascular conductance

2005 ◽  
Vol 98 (3) ◽  
pp. 765-771 ◽  
Author(s):  
Aaron J. Polichnowski ◽  
Ellen K. Heyer ◽  
Alexander V. Ng
Keyword(s):  
Blood Flow ◽  
Muscle Mass ◽  
Plantar Flexion ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Lower Leg ◽  
Isokinetic Dynamometer ◽  
Active Muscle ◽  
Vascular Conductance ◽  
The Right

Uncertainty exists as to whether a period of passive arterial occlusion (PAO) or ischemic exercise (IE) results in peak lower leg vascular conductance (LVC). This uncertainty is due to the different body positions, active muscle mass, and occlusion times used for PAO or IE. The purpose of this study was to examine whether 10 min of PAO elicits a similar LVC compared with ischemic dorsiflexion (IDF), ischemic plantar flexion (IPF), and ischemic plantar-dorsiflexion (IPDF). Ten subjects (5 women, 27 ± 9 yr, 68 ± 3 kg) were studied on 3 days over 1 wk in a semireclined position with the right foot attached to an isokinetic dynamometer. Mean arterial pressure (Finapres) and lower leg blood flow (LBF, venous occlusion plethysmography) were measured at rest and after PAO and IE. PAO was administered randomly on 1 of the 3 days and before IE. IE protocols consisted of maximal isokinetic dorsiflexion and/or plantar flexion at 120 and 60°/s, respectively. In a second experiment, an additional eight subjects (4 women, 29 ± 12 yr, 77 ± 12 kg) were studied to examine the effect of isokinetic speed during IDF on peak LBF and LVC. Peak LVC (ml·min−1·100 ml−1·mmHg−1) was similar among IPF (0.590 ± 0.16), IPDF (0.532 ± 0.17), and PAO (0.511 ± 0.18), and significantly lower after IDF (0.334 ± 0.15). No differences in peak LBF and LVC were observed after IDF using different isokinetic speeds. We conclude that 10 min of PAO, IPF, and IPDF performed in a similar posture are adequate stimuli to elicit peak LVC.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

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