Hypohydration effect on finger skin temperature and blood flow during cold-water finger immersion.

This study was conducted to determine whether hypohydration (Hy) alters blood flow, skin temperature, or cold-induced vasodilation (CIVD) during peripheral cooling. Fourteen subjects sat in a thermoneutral environment (27 degrees C) during 15-min warm-water (42 degrees C) and 30-min cold-water (4 degrees C) finger immersion (FI) while euhydrated (Eu) and, again, during Hy. Hy (-4% body weight) was induced before FI by exercise-heat exposure (38 degrees C, 30% relative humidity) with no fluid replacement, whereas during Eu, fluid intake maintained body weight. Finger pad blood flow [as measured by laser-Doppler flux (LDF)] and nail bed (T(nb)), pad (T(pad)), and core (T(c)) temperatures were measured. LDF decreased similarly during Eu and Hy (32 +/- 10 and 33 +/- 13% of peak during warm-water immersion). Mean T(nb) and T(pad) were similar between Eu (7.1 +/- 1.0 and 11.5 +/- 1.6 degrees C) and Hy (7.4 +/- 1.3 and 12.6 +/- 2.1 degrees C). CIVD parameters (e.g., nadir, onset time, apex) were similar between trials, except T(pad) nadir was higher during Hy (10.4 +/- 3.8 degrees C) than during Eu (7.9 +/- 1.6 degrees C), which was attributed to higher T(c) in six subjects during Hy (37.5 +/- 0.2 degrees C), compared with during Eu (37.1 +/- 0.1 degrees C). The results of this study provide no evidence that Hy alters finger blood flow, skin temperature, or CIVD during peripheral cooling.     

Gill blood flow control

The arrangement of the fish gill vasculature is quite complex, and varies between the different fish groups. The use of vascular casting techniques has greatly enhanced our knowledge of the anatomy of the branchial microcirculation, not least through the contributions of Pierre Laurent and co-workers at Strasbourg. At different physiological situations, the contact surface between water and blood (functional surface area) varies to balance oxygen uptake against osmotic water flow ("respiratory-osmoregulatory compromise"). This is controlled by nerves and by blood-borne or locally released substances that affect blood flow patterns in the gill. Histochemical techniques have been used to demonstrate neurotransmitter substances in the branchial innervation. In combination with physioly-osmoregulatory compromise" at different physiological situations.     

Thermoregulatory reaction in the rabbit fetuses developing under the reduced utero-placental blood flow

Rectal temperature, temperature of the brown adipose tissue, and the heart rate were studied in the rabbit foetus under intact and reduced utero-placenta blood flow in the end of the intrauterine development. With the reduced utero-placenta blood flow, bradycardia and a drop in the brown fat metabolism due, probably, to an insufficient development and functional immaturity of this tissue, were revealed.     

Local control of blood flow

Organ blood flow is determined by perfusion pressure and vasomotor tone in the resistance vessels of the organ. Local factors that regulate vasomotor tone include myogenic and metabolic autoregulation, flow-mediated and conducted responses, and vasoactive substances released from red blood cells. The relative importance of each of these factors varies over time, from tissue to tissue, and among vessel generations.     

Neural control of muscle blood flow during exercise.

Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.     

Parasympathetic control of coronary blood flow

Active parasympathetic coronary vasodilation in excess of any changes in myocardial metabolism has been observed in a number of circumstances. Electrical stimulation of the cardiac end of the cut vagus nerve produces a cholinergic coronary vasodilation that is blocked by atropine. Activation of carotid body chemoreceptors, carotid sinus baroreceptors, or left ventricular receptors elicits reflex parasympathetic coronary vasodilation. The coronary vasodilation produced by these reflexes can be prevented by vagotomy or atropine. The relative importance of parasympathetic coronary control in relation to sympathetic and local metabolic coronary control awaits further research.     

Differential neural control of intrarenal blood flow

To test whether renal sympathetic nerve activity (RSNA) can differentially regulate blood flow in the renal medulla (MBF) and cortex (CBF) of pentobarbital sodium-anesthetized rabbits, we electrically stimulated the renal nerves while recording total renal blood flow (RBF), CBF, and MBF. Three stimulation sequences were applied 1) varying amplitude (0.5-8 V), 2) varying frequency (0.5-8 Hz), and 3) a modulated sinusoidal pattern of varying frequency (0. 04-0.72 Hz). Increasing amplitude or frequency of stimulation progressively decreased all flow variables. RBF and CBF responded similarly, but MBF responded less. For example, 0.5-V stimulation decreased CBF by 20 +/- 9%, but MBF fell by only 4 +/- 6%. The amplitude of oscillations in all flow variables was progressively reduced as the frequency of sinusoidal stimulation was increased. An increased amplitude of oscillation was observed at 0.12 and 0.32 Hz in MBF and to a lesser extent RBF, but not CBF. MBF therefore appears to be less sensitive than CBF to the magnitude of RSNA, but it is more able to respond to these higher frequencies of neural stimulation.     

Fibro-vascular coupling in the control of cochlear blood flow

Background

Transduction of sound in the cochlea is metabolically demanding. The lateral wall and hair cells are critically vulnerable to hypoxia, especially at high sound levels, and tight control over cochlear blood flow (CBF) is a physiological necessity. Yet despite the importance of CBF for hearing, consensus on what mechanisms are involved has not been obtained.

Methodology/Principal Findings

We report on a local control mechanism for regulating inner ear blood flow involving fibrocyte signaling. Fibrocytes in the super-strial region are spatially distributed near pre-capillaries of the spiral ligament of the albino guinea pig cochlear lateral wall, as demonstrably shown in transmission electron microscope and confocal images. Immunohistochemical techniques reveal the inter-connected fibrocytes to be positive for Na+/K+ ATPase β1 and S100. The connected fibrocytes display more Ca²⁺ signaling than other cells in the cochlear lateral wall as indicated by fluorescence of a Ca²⁺ sensor, fluo-4. Elevation of Ca²⁺ in fibrocytes, induced by photolytic uncaging of the divalent ion chelator o-nitrophenyl EGTA, results in propagation of a Ca²⁺ signal to neighboring vascular cells and vasodilation in capillaries. Of more physiological significance, fibrocyte to vascular cell coupled signaling was found to mediate the sound stimulated increase in cochlear blood flow (CBF). Cyclooxygenase-1 (COX-1) was required for capillary dilation.

Conclusions/Significance

The findings provide the first evidence that signaling between fibrocytes and vascular cells modulates CBF and is a key mechanism for meeting the cellular metabolic demand of increased sound activity.     

Thermoregulatory model of sleep control: losing the heat memory

Thermoregulatory mechanisms were hypothesized to provide primary control of non-rapid-eye-movement sleep (NREM). On the basis of this hypothesis, we incorporated the thermoregulatory feedback loops mediated by the "heat memory," heat load, and loss processes associated with sleep-wake cycles, which were modulated by two circadian oscillators. In addition, hypnogenic warm-sensitive neurons (HWSNs) were assumed to integrate thermoregulation and NREM control. The heat memory described above could be mediated by some sleep-promoting substances. In this paper, considering the possible carrier of the heat memory, its losing process is newly included in the model. The newly developed model can generate the appropriate features of human sleep-wake patterns. One of the special features of the model is to generate the bimodal distribution of the sleepiness. This bimodality becomes distinct, as the losing rate of the heat memory decreases or the amplitude of the Y oscillator increases. The theoretical analysis shows the losing rate of the heat memory control's rapidity of model response to a thermal perturbation, which is confirmed by simulating the responses with various losing rates to transient heat loads ("heat load pulse"). The sleepiness exhibits large responses to the heat load pulses applied in the early and late phases of wake period, while the response is significantly reduced to the pulse applied in the supposed wake-maintenance zone. This bimodality of the response appears to reflect the sensitivity of the HWSNs. In addition, the early pulse raises the immediate sleepiness rather than the nocturnal sleepiness, while the heat load pulse applied in the later phase of waking period significantly raises the sleepiness during a nocturnal sleep. In simulations of sleep deprivation, the discontinuous relationship between recovery sleep length and deprivation time is reproduced, where the critical sleep deprivation time at which the recovery sleep length jumps is extended as the losing rate increases. This is possibly due to the dissipation of the heat memory accumulated by the sleep deprivation. The simulation results here qualitatively reproduce the experimental observations or predict the intriguing phenomena of human circadian rhythms. Therefore, our model could provide a novel framework for investigating the relationship between thermoregulation and sleep control processes.     

Partitional measurement of capillary and arteriovenous anastomotic blood flow in the human finger by laser-Doppler-flowmeter

This study was made to see whether changes in blood flow through the capillaries and arteriovenous anastomoses (AVA's) of the human finger can be measured by noninvasive flowmetry. Total finger blood flow (FBF) was measured by venous occlusion plethysmography; blood flow was measured by a laser-Doppler flowmeter (ADVANCE, ALF-2100, Tokyo, Japan) using probes with optic fiber separations of 0.3 mm (LDF-0.3) and 0.7 mm (LDF-0.7). The maximum sensitivities for LDF-0.3 and LDF-0.7 were at depths of 0.8 and 1.2 mm from the tissue surface respectively. Two series of experiments were performed on separate days. In the first series the test hand was immersed in a water bath whose temperature (Tw) was 25 degrees C at an ambient temperature (Ta) of 25 degrees C. Tw was raised to 35 degrees C (local hand warming), which was then followed by an increase in Ta to 35 degrees C (whole body warming). FBF, LDF-0.3, and LDF-0.7 increased during these thermal stimulations. However, the relationship of FBF to LDF-0.3 showed two different regression lines. In contrast, the relationship of FBF to LDF-0.7 showed a single regression line. In the second series, with Ta at 35 degrees C, the test hand was immersed in a water bath at Tw 35 degrees C. Tw was then raised every 10 min by 2 degrees C steps from 35 to 41 degrees C. At Tw 39-41 degrees C, FBF and LDF-0.7 in the test hand were significantly decreased compared with those at Tw 35 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of local heating on blood flow in the finger and the forearm skin

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 degrees C, 40% relative humidity), a hot-dry (WARM: 35 degrees C, 40% relative humidity), or a hot-wet (HOT: 35 degrees 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 degrees C until it reached 41 degrees or 43 degrees C. While the other hand or forearm was kept immersed in a water bath (Tw, 35 degrees 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, finger BFw was significantly lower than finger BFc at a Tw of 39-41 degrees C in the majority of subjects. When Tw was raised to 43 degrees 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 degrees to 43 degrees 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 core temperature produces vasoconstriction in the fingers, an area where no thermal sweating takes place.     

Tissue blood flow in control and cold-adapted hyperthyroid rats

Chronic injections (once daily for 10-14 days) of triiodothyronine (T3) stimulated oxygen consumption by 50 and 15% in anaesthetized, control (24 degrees C), and cold-adapted (5 degrees C) rats, respectively, compared with euthyroid controls. Tissue blood flow, determined from the distribution of radioactive microspheres, was unaffected by T3 treatment in skeletal muscle, scrotum, brain, bone, skin, diaphragm, and brown adipose tissue (BAT) of rats housed at 24 degrees C, but was decreased in spleen (53% of control) and significantly increased in three white adipose tissue depots (average 267% increase) and liver (56%). Blood flow to epididymal fat and leg muscle of cold-adapted rats was increased by T3 treatment (100 and 138% increases, respectively), but other tissues were unaffected. Blood oxygen extraction and oxygen consumption in vivo by interscapular BAT was increased in hyperthyroid rats compared with euthyroid controls, but was reduced by T3 treatment in cold-adapted animals. These data show that BAT makes only a minor contribution (7%) to thyroid thermogenesis, but suggest that kidney, liver, gut, and particularly white adipose tissue may be involved.     

The nervous control of blood flow to the pineal body

The minimum nutritional flow of blood to the pineal body was measured in intact rats and in those in which the superior cervical ganglia have been bilaterally removed or decentralized. In addition, blood flow was determined during infusions of high physiologic doses of epinephrine, norepinephrine or vasopressin. Either surgical procedure reduced the flow to the pineal by one-third without a loss in organ weight. In addition, the ability of the pineal to make a compensatory vasomotor response to pressor quantities of norepinephrine or vasopressin was lost. There was no evidence of denervation sensitization for vasomotor responses. The high flow of blood to the denervated pineal body suggests a continued high level of metabolic activity.     

The effect of direct and indirect hand heating on finger blood flow and dexterity during cold exposure

1. The aim of this study was to investigate if finger temperature or finger blood flow is the critical factor for maintenance of finger dexterity during cold exposure.

2. Subjects were exposed twice to −25°C air for 3 h by using a Torso Heating Test (THT) where the torso was maintained to 42°C with a heating vest while the hands were bare, and a Hand Heating Test (HHT) where the hands were heated with heated gloves.

3. Despite similar finger temperatures, finger blood flow was eight times lower and finger dexterity was decreased in HHT as compared to THT.

4. It is concluded that finger blood flow is the critical factor to maintain finger dexterity in the cold.