Forearm skin and muscle vasoconstriction during lower body negative pressure

1986 ◽  
Vol 60 (5) ◽  
pp. 1535-1541 ◽  
Author(s):  
A. Tripathi ◽  
E. R. Nadel

In view of conflicting reports of skeletal muscle and skin blood flow participation in baroreceptor-mediated reflexes, we studied the effects of graded lower body negative pressure (LBNP) on cutaneous and muscular components of forearm blood flow (FBF) in seven male subjects at 28 degrees C. FBF was measured by venous occlusion plethysmography and cutaneous flow by laser-Doppler velocimetry, the difference being the muscular flow. Mean FBF decreased by 39 and 56% from control at LBNP of 20 and 50 Torr, respectively. Skin flow decreased linearly with graded LBNP contributing 32% of the decrease of total blood flow at 20 Torr and then 50% of total decrease of blood flow at 50 Torr. Conversely, the decrease in muscle flow represented 68% of the total decrease at LBNP of 20 Torr and then 50% of the total decrease at LBNP of 50 Torr. We concluded that both skin and muscle circulations participate in sustained peripheral vasoconstriction during LBNP, with muscle flow achieving near maximum vasoconstriction by 20 Torr and skin showing a graded vasoconstriction to decreases in LBNP.

1990 ◽  
Vol 78 (4) ◽  
pp. 399-401 ◽  
Author(s):  
M. J. Cullen ◽  
J. R. Cockcroft ◽  
D. J. Webb

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.


1990 ◽  
Vol 68 (3) ◽  
pp. 1004-1009 ◽  
Author(s):  
M. J. Joyner ◽  
J. T. Shepherd ◽  
D. R. Seals

The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)


2018 ◽  
Vol 6 (4) ◽  
pp. e13594 ◽  
Author(s):  
Noud van Helmond ◽  
Blair D. Johnson ◽  
Walter W. Holbein ◽  
Humphrey G. Petersen-Jones ◽  
Ronée E. Harvey ◽  
...  

2007 ◽  
Vol 102 (5) ◽  
pp. 1839-1843 ◽  
Author(s):  
David A. Low ◽  
Manabu Shibasaki ◽  
Scott L. Davis ◽  
David M. Keller ◽  
Craig G. Crandall

We tested the hypothesis that local heating-induced nitric oxide (NO) production attenuates cutaneous vasoconstrictor responsiveness. Eleven subjects (6 men, 5 women) had four microdialysis membranes placed in forearm skin. Two membranes were perfused with 10 mM of NG-nitro-l-arginine (l-NAME) and two with Ringer solution (control), and all sites were locally heated to 34°C. Subjects then underwent 5 min of 60-mmHg lower body negative pressure (LBNP). Two sites (a control and an l-NAME site) were then heated to 39°C, while the other two sites were heated to 42°C. At the l-NAME sites, skin blood flow was elevated using 0.75–2 mg/ml of adenosine in the perfusate solution (Adn + l-NAME) to a similar level relative to control sites. Subjects then underwent another 5 min of 60-mmHg LBNP. At 34°C, cutaneous vascular conductance (CVC) decreased (Δ) similarly at both control and l-NAME sites during LBNP (Δ7.9 ± 3.0 and Δ3.4 ± 0.8% maximum, respectively; P > 0.05). The reduction in CVC to LBNP was also similar between control and Adn + l-NAME sites at 39°C (control Δ11.4 ± 2.5 vs. Adn + l-NAME Δ7.9 ± 2.0% maximum; P > 0.05) and 42°C (control Δ1.9 ± 2.7 vs. Adn + l-NAME Δ 4.2 ± 2.7% maximum; P > 0.05). However, the decrease in CVC at 42°C, regardless of site, was smaller than at 39°C ( P < 0.05). These results do not support the hypothesis that local heating-induced NO production attenuates cutaneous vasoconstrictor responsiveness during high levels of LBNP. However, elevated local temperature, per se, attenuates cutaneous vasoconstrictor responsiveness to LBNP, presumably through non-nitric oxide mechanisms.


2000 ◽  
Vol 99 (5) ◽  
pp. 363-369 ◽  
Author(s):  
Gerard A. RONGEN ◽  
Jacques W. M. LENDERS ◽  
Paul SMITS ◽  
John S. FLORAS

Although there is as yet no method which measures directly the neuronal release of noradrenaline in humans in vivo, the isotope dilution technique with [3H]noradrenaline has been applied to estimate forearm neuronal noradrenaline release into plasma. Two different equations have been developed for this purpose: one to estimate the spillover of noradrenaline into the venous effluent, and a modified formula (often referred to as the appearance rate) which may reflect more closely changes in the neuronal release of noradrenaline into the synaptic cleft, particularly during interventions that alter forearm blood flow. The present study was performed to compare the effects of two interventions known to exert contrasting actions on neuronal forearm noradrenaline release and forearm blood flow. Intra-arterial infusion of sodium nitroprusside at doses without systemic effect increases forearm blood flow, but not neuronal noradrenaline release. In contrast, lower-body negative pressure at -25 mmHg causes forearm vasoconstriction by stimulating neuronal noradrenaline release. During sodium nitroprusside infusion, forearm noradrenaline spillover increased from 1.1±0.3 to 2.2±1.0 pmol·min-1·100 ml-1 (P < 0.05), whereas the forearm noradrenaline appearance rate was unchanged. Lower-body negative pressure did not affect the forearm noradrenaline spillover rate, but increased the forearm noradrenaline appearance rate from 3.4±0.4 pmol·min-1·100 ml-1 at baseline to 5.0±0.9 pmol·min-1·100 ml-1 (P < 0.05). These results indicate that the noradrenaline appearance rate provides the better approximation of changes in forearm neuronal noradrenaline release in response to stimuli which alter local blood flow.


1987 ◽  
Vol 65 (6) ◽  
pp. 1329-1332 ◽  
Author(s):  
Tetsuo Nagasaka ◽  
Kozo Hirata ◽  
Tadahiro Nunomura ◽  
Michel Cabanac

Blood flow of the finger and the forearm were measured in five male subjects by venous occlusion plethysmography using mercury-in-Silastic strain gauges in either a cool–dry (COOL: 25 °C, 40% relative humidity), a hot–dry (WARM: 35 °C, 40% relative humidity), or a hot–wet (HOT: 35 °C, 80% relative humidity) environment. One hand or forearm was immersed in a water bath, the temperature (Tw) of which was raised every 10 min by steps of 2 °C until it reached 41° or 43 °C. While the other hand or forearm was kept immersed in a water bath (Tw, 35 °C), blood flow in the heated side (BFw) was compared with the corresponding blood flow in the control side (BFc). Under WARM or HOT conditions, linger BFw was significantly lower than finger BFc at a Tw of 39–41 °C in the majority of subjects. When Tw was raised to 43 °C, however, finger BFw became higher than BFc in nearly half of the subjects. In the COOL state, finger BFw did not decrease but increased steadily when Tw increased from 37° to 43 °C. In the forearm, BFw increased steadily with increasing Tw even in WARM–HOT environments. No such heat-induced vasoconstriction was observed in the forearm. From these results we conclude that in hyperthermic subjects, the rise in local temperature to above the core temperature produces vasoconstriction in the fingers, an area where no thermal sweating takes place.


1986 ◽  
Vol 61 (3) ◽  
pp. 994-998 ◽  
Author(s):  
L. K. Essandoh ◽  
D. S. Houston ◽  
P. M. Vanhoutte ◽  
J. T. Shepherd

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.


2014 ◽  
Vol 307 (7) ◽  
pp. R908-R913 ◽  
Author(s):  
Daniel Gagnon ◽  
R. Matthew Brothers ◽  
Matthew S. Ganio ◽  
Jeffrey L. Hastings ◽  
Craig G. Crandall

Facial pallor is commonly observed at presyncope in humans, suggestive of reductions in facial skin blood flow (SkBF). Yet, cutaneous vasoconstriction is usually minimal at presyncope when measured at the forearm. We tested the hypothesis that reductions in forehead SkBF at presyncope are greater than in the forearm. Forehead and forearm SkBF (laser-Doppler) and blood pressure (Finometer or radial artery catheterization) were measured during lower body negative pressure (LBNP) to presyncope in 11 normothermic and 13 heat-stressed subjects (intestinal temperature increased ∼1.4°C). LBNP reduced mean arterial pressure from 91 ± 5 to 57 ± 7 mmHg during normothermia ( P ≤ 0.001) and from 82 ± 5 to 57 ± 7 mmHg during heat stress ( P ≤ 0.001). During normothermia, LBNP decreased forehead SkBF 55 ± 14% compared with 24 ± 11% at the forearm ( P = 0.002), while during heat stress LBNP decreased forehead SkBF 39 ± 11% compared with 28 ± 8% in the forearm ( P = 0.007). In both conditions, most (≥68%) of the decreases in SkBF were due to decreases in blood pressure. However, a greater contribution of actively mediated reductions in SkBF was observed at the forehead, relative to the forearm during normothermia (32 ± 13% vs. 11 ± 11%, P = 0.031) and heat stress (30 ± 13% vs. 10 ± 13%, P = 0.004). These data suggest that facial pallor at presyncope is due to a combination of passive decreases in forehead SkBF secondary to reductions in blood pressure and to active decreases in SkBF, the latter of which are relatively greater than in the forearm.


2021 ◽  
Vol 53 (8S) ◽  
pp. 93-93
Author(s):  
Ai Hirasawa ◽  
Kazukuni Hirabuki ◽  
Noritaka Hata ◽  
Tomoya Suda ◽  
Yuki Sano ◽  
...  

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