Synchronous changes in ear and tail blood flow following salient and noxious stimuli in rabbits

1999 ◽  
Vol 847 (2) ◽  
pp. 343-346 ◽  
Author(s):  
Eugene Nalivaiko ◽  
William W. Blessing
Keyword(s):  
Blood Flow ◽  
Noxious Stimuli ◽  
Tail Blood

Heat acclimation and hypohydration: involvement of central angiotensin II receptors in thermoregulation

1999 ◽  
Vol 277 (1) ◽  
pp. R47-R55 ◽  
Author(s):  
Michal Horowitz ◽  
Pavel Kaspler ◽  
Eckhart Simon ◽  
Ruediger Gerstberger
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Angiotensin Ii ◽  
Heat Acclimation ◽  
Angiotensin Ii Receptors ◽  
Ang Ii ◽  
Biphasic Response ◽  
Temperature Thresholds ◽  
Before And After ◽  
Tail Blood

This investigation attempted to confirm the involvement of central ANG II-ergic signals in thermoregulation. Experiments were conducted on rats undergoing short (STHA)- and long (LTHA)-term heat acclimation, with and without superimposed hypohydration. Vasodilatation (VTsh) and salivation (STsh) temperature thresholds, tail blood flow, and heat endurance were measured in conscious rats during heat stress (40°C) before and after losartan (Los), an ANG II AT1-selective receptor antagonist, administration either to the lateral ventricle or intravenously. Heat acclimation alone resulted in decreased VTsh. STsh decreased during STHA and resumed the preacclimation value, together with markedly increased heat endurance on LTHA. Hypohydration did not affect this biphasic response, although STsh was elevated in all groups. The enhanced heat endurance attained by LTHA was blunted. Neither Los treatment affected the nonacclimated rats. In the heat-acclimated, euhydrated rats, intracerebroventricular Los resulted in decreased VTsh, whereas intravenous Los resulted in elevated STsh. Both intracerebroventricular and intravenous Los led to markedly enhanced heat endurance of the LTHA hypohydrated rats. It is concluded that the LTHA group showed a loss of the benefits acquired by acclimation on hypohydration, whereas the STHA rats, which show an accelerated autonomic excitability in that phase, gained some benefit. It is suggested that ANG II modulates thermoregulation in conditions of chronic adjustments. Central ANG II signals may lead to VTsh upshift, whereas circumventricular structures, activated via circulating ANG II, decrease STsh. On hypohydration these responses seem to be desensitized.

Body temperature control of rat tail blood flow

1983 ◽  
Vol 245 (3) ◽  
pp. R426-R432 ◽  
Author(s):  
E. R. Raman ◽  
M. F. Roberts ◽  
V. J. Vanhuyse
Keyword(s):  
Blood Flow ◽  
Heat Exchange ◽  
Body Temperature ◽  
Heat Flow ◽  
Thermal Conductance ◽  
Venous Occlusion ◽  
Albino Rats ◽  
Blood Flows ◽  
Rat Tail ◽  
Tail Blood

Tail blood flow (BF) and heat flow (HF) were measured in five albino rats during transients in rectal temperature (Tre) caused by body heating at rest. During heating, tail temperature (Tt) was kept at 15, 20, 25, 30, 35, or 42 degrees C by enclosing the tail in a water-perfused tube. Thermal conductance (K) was computed as HF/(Tre-Tt). BF was measured by venous occlusion plethysmography. Heating caused a rise in Tre that was accompanied by proportional increases in both K and BF. The ratio R = K/BF represents conductance per unit BF and reflects the amount of heat exchange for a given BF. R can thus be used to estimate the distribution of BF within the tail. R was independent of Tre at all Tt, indicating that BF distribution is controlled by the tail. R was low at low Tt and rose at higher Tt. This suggests that at low Tt, blood flows primarily in central veins of the tail and at higher Tt blood flows in peripheral tail veins.

Neural Mechanisms of Antinociceptive Effects of Hypnosis

2000 ◽  
Vol 92 (5) ◽  
pp. 1257-1267 ◽  
Author(s):  
Marie Elisabeth Faymonville ◽  
Steven Laureys ◽  
Christian Degueldre ◽  
Guy DelFiore ◽  
André Luxen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pain Perception ◽  
Cingulate Cortex ◽  
Neural Mechanisms ◽  
Anterior Cingulate ◽  
Noxious Stimulation ◽  
Pain Sensation ◽  
Brain Areas ◽  
Noxious Stimuli

Background The neural mechanisms underlying the modulation of pain perception by hypnosis remain obscure. In this study, we used positron emission tomography in 11 healthy volunteers to identify the brain areas in which hypnosis modulates cerebral responses to a noxious stimulus. Methods The protocol used a factorial design with two factors: state (hypnotic state, resting state, mental imagery) and stimulation (warm non-noxious vs. hot noxious stimuli applied to right thenar eminence). Two cerebral blood flow scans were obtained with the 15O-water technique during each condition. After each scan, the subject was asked to rate pain sensation and unpleasantness. Statistical parametric mapping was used to determine the main effects of noxious stimulation and hypnotic state as well as state-by-stimulation interactions (i.e., brain areas that would be more or less activated in hypnosis than in control conditions, under noxious stimulation). Results Hypnosis decreased both pain sensation and the unpleasantness of noxious stimuli. Noxious stimulation caused an increase in regional cerebral blood flow in the thalamic nuclei and anterior cingulate and insular cortices. The hypnotic state induced a significant activation of a right-sided extrastriate area and the anterior cingulate cortex. The interaction analysis showed that the activity in the anterior (mid-)cingulate cortex was related to pain perception and unpleasantness differently in the hypnotic state than in control situations. Conclusions Both intensity and unpleasantness of the noxious stimuli are reduced during the hypnotic state. In addition, hypnotic modulation of pain is mediated by the anterior cingulate cortex.

scholarly journals Locus coeruleus noradrenergic innervation of the amygdala facilitates alerting-induced constriction of the rat tail artery

2016 ◽  
Vol 310 (11) ◽  
pp. R1109-R1119 ◽  
Author(s):  
Mazher Mohammed ◽  
Keerthi Kulasekara ◽  
Youichirou Ootsuka ◽  
William W. Blessing
Keyword(s):  
Blood Flow ◽  
Locus Coeruleus ◽  
Sympathetic Outflow ◽  
Sprague Dawley ◽  
Release Of Noradrenaline ◽  
Tail Artery ◽  
Sprague Dawley Rats ◽  
Noradrenergic Innervation ◽  
Environmental Events ◽  
Tail Blood

The amygdala, innervated by the noradrenergic locus coeruleus, processes salient environmental events. α2-adrenoceptor-stimulating drugs (clonidine-like agents) suppress the behavioral and physiological components of the response to salient events. Activation of sympathetic outflow to the cutaneous vascular bed is part of the physiological response to salience-mediated activation of the amygdala. We have determined whether acute systemic and intra-amygdala administration of clonidine, and chronic immunotoxin-mediated destruction of the noradrenergic innervation of the amygdala, impairs salience-related vasoconstrictor episodes in the tail artery of conscious freely moving Sprague-Dawley rats. After acute intraperitoneal injection of clonidine (10, 50, and 100 μg/kg), there was a dose-related decrease in the reduction in tail blood flow elicited by alerting stimuli, an effect prevented by prior administration of the α2-adrenergic blocking drug idazoxan (1 mg/kg ip or 75 nmol bilateral intra-amygdala). A dose-related decrease in alerting-induced tail artery vasoconstriction was also observed after bilateral intra-amygdala injection of clonidine (5, 10, and 20 nmol in 200 nl), an effect substantially prevented by prior bilateral intra-amygdala injection of idazoxan. Intra-amygdala injection of idazoxan by itself did not alter tail artery vasoconstriction elicited by alerting stimuli. Intra-amygdala injection of saporin coupled to antibodies to dopamine-β-hydroxylase (immunotoxin) destroyed the noradrenergic innervation of the amygdala and the parent noradrenergic neurons in the locus coeruleus. The reduction in tail blood flow elicited by standardized alerting stimuli was substantially reduced in immunotoxin-treated rats. Thus, inhibiting the release of noradrenaline within the amygdala reduces activation of the sympathetic outflow to the vascular beds elicited by salient events.

scholarly journals Systemic application of the TRPV4 antagonist GSK2193874 induces tail vasodilation in a mouse model of thermoregulation

2021 ◽  
Author(s):  
Fiona O'Brien ◽  
Caroline Staunton ◽  
Richard Barrett-Jolley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Blood Vessels ◽  
Intraperitoneal Administration ◽  
Ambient Temperatures ◽  
Body Cooling ◽  
A Site ◽  
Systemic Application ◽  
Tail Blood

In humans the skin is a primary thermoregulatory organ, with vasodilation leading to rapid body cooling, whereas in rodents the tail performs an analogous function. TRPV4 is a widely distributed ion channel with both mechanical and thermosensitive properties. Previous studies have shown that TRPV4 can act as vasodilator by local action in blood vessels, and in this study we investigated whether there was a constitutive role for TRPV4 in mouse tail vascular tone and thermoregulation. We measured tail blood flow by pressure plethysmography in lightly sedated mice at a range of ambient temperatures, with and without intraperitoneal administration of the blood brain barrier crossing TRPV4 antagonist GSK2193874. We also measured heart rate and blood pressure with and without GSK2193874. As predicted, we found that tail blood flow increased with temperature. However, unexpectedly we found that the TRPV4 antagonist GSK2193874 increased tail blood flow at all temperatures. There were few detectable differences in heart rate, blood pressure or short-range heart rate variability. Since arterial TRPV4 activation is known to cause vasodilation that would increase tail blood flow, these data suggest that increases in tail blood flow resulting from the TRPV4 antagonist must arise from a site other than the blood vessels themselves, perhaps in central cardiovascular control centres such as the paraventricular nucleus of the hypothalamus.

scholarly journals Contribution of Brain Processes to Tissue Loss After Spinal Cord Injury: Does a Pain-Induced Rise in Blood Pressure Fuel Hemorrhage?

2021 ◽  
Vol 15 ◽  
Author(s):  
Gizelle N. K. Fauss ◽  
Misty M. Strain ◽  
Yung-Jen Huang ◽  
Joshua A. Reynolds ◽  
Jacob A. Davis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Blood Flow ◽  
Tissue Loss ◽  
Acute Hemorrhage ◽  
Cord Injury ◽  
Nociceptive Input ◽  
The Brain ◽  
Tail Blood

Pain (nociceptive) input soon after spinal cord injury (SCI) expands the area of tissue loss (secondary injury) and impairs long-term recovery. Evidence suggests that nociceptive stimulation has this effect because it promotes acute hemorrhage. Disrupting communication with the brain blocks this effect. The current study examined whether rostral systems exacerbate tissue loss because pain input drives an increase in systolic blood pressure (BP) and flow that fuels blood infiltration. Rats received a moderate contusion injury to the lower thoracic (T12) spinal cord. Communication with rostral processes was disrupted by cutting the spinal cord 18 h later at T2. Noxious electrical stimulation (shock) applied to the tail (Experiment 1), or application of the irritant capsaicin to one hind paw (Experiment 2), increased hemorrhage at the site of injury. Shock, but not capsaicin, increased systolic BP and tail blood flow in sham-operated rats. Cutting communication with the brain blocked the shock-induced increase in systolic BP and tail blood flow. Experiment 3 examined the effect of artificially driving a rise in BP with norepinephrine (NE) in animals that received shock. Spinal transection attenuated hemorrhage in vehicle-treated rats. Treatment with NE drove a robust increase in BP and tail blood flow but did not increase the extent of hemorrhage. The results suggest pain input after SCI can engage rostral processes that fuel hemorrhage and drive sustained cardiovascular output. An increase in BP was not, however, necessary or sufficient to drive hemorrhage, implicating other brain-dependent processes.

Innervation of endoneurial microvessels in human sural nerve

1992 ◽  
Vol 50 (1) ◽  
pp. 920-921
Author(s):  
John L. Beggs ◽  
Peter C. Johnson ◽  
Astrid G. Olafsen ◽  
C. Jane Watkins
Keyword(s):  
Blood Flow ◽  
Blood Vessels ◽  
Blood Supply ◽  
Peripheral Nerves ◽  
Sural Nerve ◽  
Nerve Fibers ◽  
Arterial Supply ◽  
Autonomic Nerve ◽  
Vasa Nervorum ◽  
Endoneurial Blood Flow

The blood supply (vasa nervorum) to peripheral nerves is composed of an interconnected dual circulation. The endoneurium of nerve fascicles is maintained by the intrinsic circulation which is composed of microvessels primarily of capillary caliber. Transperineurial arterioles link the intrinsic circulation with the extrinsic arterial supply located in the epineurium. Blood flow in the vasa nervorum is neurogenically influenced (1,2). Although a recent hypothesis proposes that endoneurial blood flow is controlled by the action of autonomic nerve fibers associated with epineurial arterioles (2), our recent studies (3) show that in addition to epineurial arterioles other segments of the vasa nervorum are also innervated. In this study, we examine blood vessels of the endoneurium for possible innervation.

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