Blockade of the pressor response to muscle ischemia by sensory nerve block in man

1979 ◽  
Vol 237 (4) ◽  
pp. H433-H439 ◽  
Author(s):  
P. R. Freund ◽  
L. B. Rowell ◽  
T. M. Murphy ◽  
S. F. Hobbs ◽  
S. H. Butler
Keyword(s):  
Nerve Block ◽  
Pressor Response ◽  
Sensory Nerve ◽  
Sensory Block ◽  
Nerve Fibers ◽  
Dynamic Exercise ◽  
Sensory Blockade ◽  
Muscle Ischemia ◽  
Respiratory Responses ◽  
Stimulation Of

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.

Relationships between permeable vessels, nerves, and mast cells in rat cutaneous neurogenic inflammation

1990 ◽  
Vol 68 (6) ◽  
pp. 2305-2311 ◽  
Author(s):  
J. N. Baraniuk ◽  
M. L. Kowalski ◽  
M. A. Kaliner
Keyword(s):  
Electrical Stimulation ◽  
Mast Cells ◽  
Neurogenic Inflammation ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Sensory Nerves ◽  
Neurokinin A ◽  
Rat Skin ◽  
Protein Extravasation ◽  
Stimulation Of

Electrical stimulation of rat sensory nerves produces cutaneous vasodilation and plasma protein extravasation, a phenomenon termed “neurogenic inflammation”. Rat skin on the dorsum of the paw developed neurogenic inflammation after electrical stimulation of the saphenous nerve. In tissue sections, the extravasation of the supravital dye monastral blue B identified permeable vessels. Mast cells were identified by toluidine blue stain. Permeable vessels were significantly more dense in the superficial 120 microns of the dermis than in the deeper dermis, whereas mast cells were significantly more frequent in the deeper dermis. The relationships between nociceptive sensory nerve fibers, permeable vessels, and mast cells were examined by indirect immunohistochemistry for calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and substance P (SP). CGRP-, NKA-, and SP-containing nerves densely innervated the superficial dermis and appeared to innervate the vessels that became permeable during neurogenic inflammation. In contrast, mast cells were not associated with either permeable vessels or nerve fibers. These data suggest that electrical stimulation of rat sensory nerves produces vascular permeability by inducing the release of neuropeptides that may directly stimulate the superficial vascular bed. Mast cells may not be involved in this stage of cutaneous neurogenic inflammation in rat skin.

Effect of indomethacin on the pressor responses to sustained isometric contraction in humans

1993 ◽  
Vol 75 (1) ◽  
pp. 273-278 ◽  
Author(s):  
K. P. Davy ◽  
W. G. Herbert ◽  
J. H. Williams
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Voluntary Contraction ◽  
Plasma Norepinephrine ◽  
Isometric Handgrip ◽  
Double Blind ◽  
Muscle Ischemia ◽  
Stimulation Of

The purpose of this study was to test the hypothesis that prostaglandins participate in metaboreceptor stimulation of the pressor response to sustained isometric handgrip contraction in humans. To accomplish this, mean arterial pressure, heart rate (n = 10), and plasma norepinephrine levels (n = 8) were measured in healthy male subjects during sustained isometric handgrip at 40% of maximal voluntary contraction force to exhaustion and during a period of postcontraction muscle ischemia. The subjects were given a double-blind and counterbalanced administration of placebo or a single 100-mg dose of indomethacin. A period of 1 wk was allowed for systemic clearance of the drug. Mean arterial pressure increased 25 +/- 5 vs. 22 +/- 4 mmHg during the final minute of isometric handgrip contraction and 26 +/- 2 vs. 21 +/- 5 during the last minute of postcontraction muscle ischemia in the placebo vs. the indomethacin trial (P > 0.05), respectively. Heart rate was increased 21 +/- 4 vs. 17 +/- 3 beats/min during the final minute of isometric handgrip contraction in the placebo vs. the indomethacin trial (P > 0.05), respectively, and returned to control values during postcontraction muscle ischemia. Plasma norepinephrine levels increased 343 +/- 89 vs. 289 +/- 89 pg/ml after isometric handgrip contraction and 675 +/- 132 vs. 632 +/- 132 pg/ml after postcontraction muscle ischemia (P > 0.05) in the placebo vs. the indomethacin trial, respectively. These results suggest that prostaglandin inhibition does not significantly modulate muscle contraction-induced stimulation of mean arterial pressure, heart rate, or plasma norepinephrine levels.

scholarly journals Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

2015 ◽  
Vol 308 (7) ◽  
pp. R650-R658 ◽  
Author(s):  
Marty D. Spranger ◽  
Jasdeep Kaur ◽  
Javier A. Sala-Mercado ◽  
Tiago M. Machado ◽  
Abhinav C. Krishnan ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Hindlimb Ischemia ◽  
Muscle Metaboreflex ◽  
Muscle Ischemia ◽  
Normal Individuals ◽  
Before And After ◽  
Exercise Muscle ◽  
Sustained Increase

During dynamic exercise, muscle metaboreflex activation (MMA; induced via partial hindlimb ischemia) markedly increases mean arterial pressure (MAP), and MAP is sustained when the ischemia is maintained following the cessation of exercise (postexercise muscle ischemia, PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 km/h), MMA, and PEMI in the same animals before and after the induction of HTN [Goldblatt two kidney, one clip (2K1C)]. In controls, MAP, CO and HR increased with MMA (+52 ± 6 mmHg, +2.1 ± 0.3 l/min, and +37 ± 7 beats per minute). After induction of HTN, MAP at rest increased from 97 ± 3 to 130 ± 4 mmHg, and the metaboreflex responses were markedly attenuated (+32 ± 5 mmHg, +0.6 ± 0.2 l/min, and +11 ± 3 bpm). During PEMI in HTN, HR and CO were not sustained, and MAP fell to normal recovery levels. We conclude that the attenuated metaboreflex-induced HR, CO, and MAP responses are not sustained during PEMI in HTN.

Activation of EP4 receptors contributes to prostaglandin E2-mediated stimulation of renal sensory nerves

2004 ◽  
Vol 287 (6) ◽  
pp. F1269-F1282 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Kazuhiro Nakamura ◽  
Rolf M. Nüsing ◽  
Lori A. Smith ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Prostaglandin E ◽  
Ep4 Receptor ◽  
Pelvic Wall ◽  
Ep4 Receptor Antagonist ◽  
Cox 2 ◽  
Ep3 Receptor ◽  
Stimulation Of

Induction of cyclooxygenase-2 (COX-2) in the renal pelvic wall increases prostaglandin E2 (PGE2) leading to stimulation of cAMP production, which results in substance P (SP) release and activation of renal mechanosensory nerves. The subtype of PGE receptors involved, EP2 and/or EP4, was studied by immunohistochemistry and renal pelvic administration of agonists and antagonists of EP2 and EP4 receptors. EP4 receptor-like immunoreactivity (LI) was colocalized with calcitonin gene-related peptide (CGRP)-LI in dorsal root ganglia (DRGs) at Th9-L1 and in nerve terminals in the renal pelvic wall. Th9-L1 DRG neurons also contained EP3 receptor-LI and COX-2-LI, each of which was colocalized with CGRP-LI in some neurons. No renal pelvic nerves contained EP3 receptor-LI and only very few nerves COX-2-LI. The EP1/EP2 receptor antagonist AH-6809 (20 μM) had no effect on SP release produced by PGE2 (0.14 μM) from an isolated rat renal pelvic wall preparation. However, the EP4 receptor antagonist L-161,982 (10 μM) blocked the SP release produced by the EP2/EP4 receptor agonist butaprost (10 μM) 12 ± 2 vs. 2 ± 1 and PGE2, 9 ± 1 vs. 1 ± 0 pg/min. The SP release by butaprost and PGE2 was similarly blocked by the EP4 receptor antagonist AH-23848 (30 μM). In anesthetized rats, the afferent renal nerve activity (ARNA) responses to butaprost 700 ± 100 and PGE2·780 ± 100%·s (area under the curve of ARNA vs. time) were unaffected by renal pelvic perfusion with AH-6809. However, 1 μM L-161,982 and 10 μM AH-23848 blocked the ARNA responses to butaprost by 94 ± 5 and 78 ± 10%, respectively, and to PGE2 by 74 ± 16 and 74 ± 11%, respectively. L-161,982 also blocked the ARNA response to increasing renal pelvic pressure 10 mmHg, 85 ± 5%. In conclusion, PGE2 increases renal pelvic release of SP and ARNA by activating EP4 receptors on renal sensory nerve fibers.

scholarly journals Role of cardiac output versus peripheral vasoconstriction in mediating muscle metaboreflex pressor responses: dynamic exercise versus postexercise muscle ischemia

2013 ◽  
Vol 304 (8) ◽  
pp. R657-R663 ◽  
Author(s):  
Marty D. Spranger ◽  
Javier A. Sala-Mercado ◽  
Matthew Coutsos ◽  
Jasdeep Kaur ◽  
Doug Stayer ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Pressor Response ◽  
Dynamic Exercise ◽  
Muscle Metaboreflex ◽  
Peripheral Vasoconstriction ◽  
Muscle Ischemia ◽  
Normal Individuals ◽  
Pressor Responses ◽  
Sustained Increase

Muscle metaboreflex activation (MMA) during submaximal dynamic exercise in normal individuals increases mean arterial pressure (MAP) via increases in cardiac output (CO) with little peripheral vasoconstriction. The rise in CO occurs primarily via increases in heart rate (HR) with maintained or slightly increased stroke volume. When the reflex is sustained during recovery (postexercise muscle ischemia, PEMI), HR declines yet MAP remains elevated. The role of CO in mediating the pressor response during PEMI is controversial. In seven chronically instrumented canines, steady-state values with MMA during mild exercise (3.2 km/h) were observed by reducing hindlimb blood flow by ∼60% for 3–5 min. MMA during exercise was followed by 60 s of PEMI. Control experiments consisted of normal exercise and recovery. MMA during exercise increased MAP, HR, and CO by 55.3 ± 4.9 mmHg, 42.5 ± 6.9 beats/min, and 2.5 ± 0.4 l/min, respectively. During sustained MMA via PEMI, MAP remained elevated and CO remained well above the normal recovery levels. Neither MMA during dynamic exercise nor during PEMI significantly affected peripheral vascular conductance. We conclude that the sustained increase in MAP during PEMI is driven by a sustained increase in CO not peripheral vasoconstriction.

scholarly journals Mechanisms of blood flow regulation of in the skin during stimulation of the spinal cord in humans

2019 ◽  
Vol 485 (1) ◽  
pp. 114-116
Author(s):  
G. I. Lobov ◽  
Yu. P. Gerasimenko ◽  
T. R. Moshonkina
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Motor Threshold ◽  
Doppler Flowmetry ◽  
Important Mediator ◽  
Antidromic Stimulation ◽  
Cutaneous Blood ◽  
Stimulation Of

Changes of the blood flow in the shin skin in the case of 12 healthy subjects by laser doppler flowmetry were observed under transcutaneous electrical spinal cord stimulation (TSCS) by subthreshold bipolar pulses with a frequency of 30 Hz were detected. It was found that the TSCS in the area of the vertebrae T11 and L1 leads to a significant increase in skin blood flow. With a stimulus intensity of 90% of the motor threshold, the microcirculation rate increased by more than 85% relative to baseline.The results of the study show that the stimulation of blood flow in the skin by TSCS is realized mainly due to the antidromic stimulation of sensory nerve fibers. An important mediator that contributes to vasodilation and increase of cutaneous blood flow in PSCS is nitric oxide (NO), which is predominantly endothelial in origin.

Clonidine Prolongation of Lidocaine Analgesia after Sciatic Nerve Block in Rats Is Mediated via the Hyperpolarization-activated Cation Current, Not by α-Adrenoreceptors

2004 ◽  
Vol 101 (2) ◽  
pp. 488-494 ◽  
Author(s):  
Jeffrey S. Kroin ◽  
Asokumar Buvanendran ◽  
Daniel R. Beck ◽  
Julie E. Topic ◽  
Daniel E. Watts ◽  
...  
Keyword(s):  
Nerve Block ◽  
Sensory Block ◽  
Sprague Dawley ◽  
Sensory Blockade ◽  
Alpha Adrenergic Receptors ◽  
Cation Current ◽  
Adrenergic Antagonist ◽  
Zd 7288

Background Although clonidine is commonly combined with local anesthetics to extend duration of peripheral nerve block, the mechanism by which clonidine potentiates local anesthetic action in vivo is unclear. Methods Male Sprague-Dawley rats received percutaneous injections of 1% lidocaine with/without clonidine or epinephrine into the sciatic notch and duration of sensory blockade was quantified by inhibition of pinprick foot withdrawal. The antagonists prazosin or yohimbine were injected before lidocaine with clonidine or epinephrine to determine the role of alpha-adrenergic receptors. The role of the hyperpolarization-activated cation current (Ih) was evaluated by injecting the current blocker ZD 7288 as well as the current enhancers forskolin and 8-Br-cAMP before lidocaine alone or with 15 micrograms/ml clonidine. Results Mean duration of sensory block for lidocaine alone was 69 +/- 2 min. Sensory block duration increased monotonically with increasing doses of added clonidine or epinephrine. Preinjection of prazosin but not yohimbine prevented the increase in block duration seen with epinephrine. Neither alpha-adrenergic antagonist attenuated the extended duration of block with clonidine. ZD 7288 extended sensory blockade equivalent to the prolongation observed with clonidine. There was no additive effect when ZD 7288 and clonidine were combined, and a decreased duration of nerve block when either forskolin or 8-Br-cAMP preceded injection of lidocaine with clonidine. Conclusions The findings indicate that prolongation of duration of in vivo lidocaine nerve blockade by clonidine is not mediated by an alpha-adrenergic mechanism but likely involves the Ih current.

Pearls and pitfalls in experimental in vivo models of migraine: Dural trigeminovascular nociception

Cephalalgia ◽  
2013 ◽  
Vol 33 (8) ◽  
pp. 577-592 ◽  
Author(s):  
Simon Akerman ◽  
Philip R Holland ◽  
Jan Hoffmann
Keyword(s):  
Dura Mater ◽  
Sensory Nerve ◽  
Nerve Fibers ◽  
Trigeminal Nucleus ◽  
Neuronal Activation ◽  
Trigeminovascular System ◽  
In Vivo Models ◽  
Doppler Flowmetry ◽  
Trigeminal Nucleus Caudalis ◽  
Stimulation Of

Background Migraine is a disorder of the brain and is thought to involve activation of the trigeminovascular system, which includes the peripheral afferent projection to the nociceptive specific dura mater, as well as the central afferent projection to the trigeminal nucleus caudalis. Stimulation of the blood vessels of the dura mater produces pain in patients that is referred to the head similar to headache. Headache mechanisms The likely reason for the pain is because the vascular structures of the dura mater, including the superior sagittal sinus and middle meningeal artery, are richly innervated by a plexus of largely unmyelinated sensory nerve fibers from the ophthalmic division of the trigeminal ganglion. Methodology Stimulation of these nociceptive specific nerve fibers is painful and produces neuronal activation in the trigeminal nucleus caudalis. Preclinical models of headache have taken advantage of this primarily nociceptive pathway, and various animal models use dural trigeminovascular nociception to assay aspects of head pain. These assays measure responses at the level of the dural vasculature and the central trigeminal nucleus caudalis as a correlate of trigeminovascular activation thought to be involved in headache. Summary This review will summarize the history of the development of models of dural trigeminovascular nociception, including intravital microscopy and laser Doppler flowmetry at the level of the vasculature, and electrophysiology and Fos techniques used to observe neuronal activation at the trigeminal nucleus caudalis. It will also describe some of pitfalls of these assays and developments for the future.

Sign in / Sign up

Export Citation Format

Share Document