Interstitial norepinephrine concentrations in skeletal muscle of ischemic heart failure

2007 ◽  
Vol 293 (2) ◽  
pp. H1190-H1195 ◽  
Author(s):  
Jihong Xing ◽  
Satoshi Koba ◽  
Valerie Kehoe ◽  
Zhaohui Gao ◽  
Kristen Rice ◽  
...  
Keyword(s):  
Heart Failure ◽  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Hplc Method ◽  
Arterial Blood ◽  
Hindlimb Muscle ◽  
Uptake Studies ◽  
Sympathetic Discharge ◽  
Stimulation Of

During exercise, sympathetic nerve responses are accentuated in heart failure (HF), and this enhances norepinephrine (NE) release and evokes vasoconstriction. Two key pathophysiological responses could contribute to the greater NE release: 1) increased sympathetic nerve discharge and 2) increased NE in the neurovascular junction for a given level of sympathetic discharge. In this report, we focus on the second of these two general issues and test the following hypotheses: 1) in HF for a given level of sympathetic nerve stimulation, NE concentration in the interstitium (an index of neurovascular NE) would be greater, and 2) the greater interstitial NE concentration would be linked to reduced NE uptake. Studies were performed in rats 8–10 wk after induction of myocardial infarction (MI). Interstitial NE samples were collected from microdialysis probes inserted into the hindlimb muscle. Dialysate concentration of NE was determined by the HPLC method. First, interstitial NE concentration increased during electrical stimulation of the lumbar sympathetic nerves in eight control rats. An increase in interstitial NE concentration was significantly greater in 10 rats with severe MI. Additionally, an NE uptake-1 inhibitor (desipramine, 1 μM) was injected into the arterial blood supply of the muscle in six control and eight MI rats. Desipramine increased interstitial NE concentration by 24% in control and by only 3% ( P < 0.05 vs. control) in MI rats. In conclusion, given levels of electrical stimulation of the lumbar sympathetic nerve lead to higher interstitial NE concentration in HF. This effect is due, in part, to reduced NE uptake-1 in HF.

Midbrain central gray: influence on medullary sympathoexcitatory neurons and the baroreflex in rats

1992 ◽  
Vol 263 (1) ◽  
pp. R24-R33 ◽  
Author(s):  
A. J. Verberne ◽  
P. G. Guyenet
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Pressor Responses ◽  
Central Gray ◽  
Train Stimulation ◽  
Pulse Stimulation ◽  
Site Of Stimulation ◽  
Stimulation Of

The influence of the central gray (CG) of the midbrain on the activity of 19 barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) and on the sympathetic vasomotor baroreflex was studied in halothane-anesthetized rats. Eighteen RVLM barosensitive units were readily activated by train stimulation of the CG, although twin-pulse stimulation was less effective (10 of 19 neurons responded). Inhibition of neurons within the RVLM by bilateral microinjection of the GABA-mimetic drug muscimol abolished the pressor responses to CG stimulation, while the accompanying lumbar nerve sympathoexcitation was converted to sympathoinhibition. In baroreceptor-denervated vagotomized animals, unilateral microinjection of muscimol into the RVLM ipsilateral or contralateral to the site of CG stimulation resulted in approximately equal attenuation of the CG sympathoexcitatory and pressor responses. In contrast, the sympathoexcitatory response to electrical stimulation of the sciatic nerve was reduced more effectively by inhibition of the RVLM contralateral to the site of stimulation. Electrical stimulation of the CG lateral and ventrolateral to the aqueduct produced sympathoexcitation [increased discharge of the greater splanchnic and lumbar sympathetic nerves (SSN and LSN)] with an increase in mean arterial blood pressure. Activation of the SSN by CG stimulation was greater than that observed for the LSN (n = 5 rats). This differential influence of the CG on the sympathetic outflow was not a result of a differential influence of the baroreflex. Electrical stimulation of the CG produced elevations of the gain and the cut-off pressure of the baroreflex for both the SSN and LSN.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Maintenance of contractile force of the hind limb muscles by the somato-lumbar sympathetic reflexes

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Harumi Hotta ◽  
Kaori Iimura ◽  
Nobuhiro Watanabe ◽  
Kazuhiro Shigemoto
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Sympathetic Nerve ◽  
Skeletal Muscles ◽  
Sympathetic Nerves ◽  
Contractile Force ◽  
Triceps Surae ◽  
Dorsal Roots ◽  
Before And After ◽  
Stimulation Of

AbstractThis study aimed to clarify whether the reflex excitation of muscle sympathetic nerves induced by contractions of the skeletal muscles modulates their contractility. In anesthetized rats, isometric tetanic contractions of the triceps surae muscles were induced by electrical stimulation of the intact tibial nerve before and after transection of the lumbar sympathetic trunk (LST), spinal cord, or dorsal roots. The amplitude of the tetanic force (TF) was reduced by approximately 10% at 20 min after transection of the LST, spinal cord, or dorsal roots. The recorded postganglionic sympathetic nerve activity from the lumbar gray ramus revealed that both spinal and supraspinal reflexes were induced in response to the contractions. Repetitive electrical stimulation of the cut peripheral end of the LST increased the TF amplitude. Our results indicated that the spinal and supraspinal somato-sympathetic nerve reflexes induced by contractions of the skeletal muscles contribute to the maintenance of their own contractile force.

Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat

1996 ◽  
Vol 270 (4) ◽  
pp. R713-R719 ◽  
Author(s):  
A. J. Verberne
Keyword(s):  
Blood Pressure ◽  
Electrical Stimulation ◽  
Prefrontal Cortex ◽  
Arterial Blood Pressure ◽  
Medial Prefrontal Cortex ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Stimulation Of ◽  
Nerve Discharge

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

scholarly journals Effect of Low-Level Electrical Stimulation of the Arotic Root Ventricular Ganglionated Plexi on Electrical and Structural Remodling in Dogs with Heart Failure

2016 ◽  
Vol 1 (1) ◽  
Keyword(s):  
Heart Failure ◽  
Nervous System ◽  
Electrical Stimulation ◽  
Autonomic Nervous System ◽  
Aortic Root ◽  
General Argument ◽  
Low Level ◽  
Ganglionated Plexi ◽  
Atrial Enlargement ◽  
Stimulation Of

Low-level electrical stimulation (LL-ES) of aortic root ventricular ganglionated plexi (GP) was proved to be antiarrhythmic in the initiation of AF mediated by autonomic nervous system. However,it is still uncertain whether LL-ES of the ventricular GP can reverse the structural remodeling of myocardial fibrosis and atrial enlargement following heart failure by attenuating the sympathetic tone. Therefore,this review will give an general argument on this topic.

Involvement of trigeminal spinal nucleus in parasympathetic reflex vasodilatation in cat lower lip

2002 ◽  
Vol 282 (2) ◽  
pp. R492-R500 ◽  
Author(s):  
Kentaro Mizuta ◽  
Satoshi Kuchiiwa ◽  
Takashi Saito ◽  
Hideaki Mayanagi ◽  
Keishiro Karita ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Kainic Acid ◽  
Local Anesthesia ◽  
Similar Degree ◽  
Dependent Manner ◽  
Lower Lip ◽  
Arterial Blood ◽  
Blood Flow Increase ◽  
Spinal Nucleus ◽  
Stimulation Of

We examined whether the trigeminal spinal nucleus (Vsp) forms part of the central mechanism by which electrical stimulation of the central cut end of the lingual nerve (LN) evokes parasympathetic reflex vasodilatation in the lower lip in artificially ventilated, cervically vagosympathectomized cats deeply anesthetized with α-chloralose and urethane. For this purpose, we made microinjections within the brain stem to produce nonselective, reversible local anesthesia (lidocaine) or soma-selective, irreversible neurotoxic damage (kainic acid). Local anesthesia of Vsp by microinjection of lidocaine (2%; 1 μl/site) reversibly and significantly reduced the ipsilateral-LN-evoked parasympathetic reflex vasodilatation. Unilateral microinjection of kainic acid (10 mM/site; 1 μl) into Vsp ipsilateral to the stimulated LN led to an irreversible reduction in the reflex vasodilatation but had no effect on the vasodilatation elicited by stimulation of the contralateral LN. Such microinjection of kainic acid into Vsp had no effect on the vasodilatation evoked by electrical stimulation of the ipsilateral inferior salivatory nucleus. Electrical stimulation of Vsp elicited a blood flow increase in the lower lip in an intensity- and frequency-dependent manner, regardless of whether systemic arterial blood pressure rose or fell. Hexamethonium (1.0 mg/kg iv) significantly reduced the vasodilator responses elicited by electrical stimulation of the central cut end of LN or of Vsp, each to a similar degree. After hexamethonium, both vasodilator responses showed time-dependent recovery. These results strongly suggest that Vsp is an important bulbar relay for LN-evoked parasympathetic reflex vasodilatation in the cat lower lip.

Central command, but not muscle reflex, stimulates cutaneous sympathetic efferents of cats

1998 ◽  
Vol 274 (5) ◽  
pp. H1552-H1559 ◽  
Author(s):  
Janeen M. Hill ◽  
Marc P. Kaufman
Keyword(s):  
Electrical Stimulation ◽  
Blocking Agent ◽  
Muscle Afferents ◽  
Group Iii ◽  
Hairy Skin ◽  
Sympathetic Efferents ◽  
Muscle Reflex ◽  
Decerebrate Cats ◽  
Sympathetic Discharge ◽  
Stimulation Of

We determined the effects of stimulation of the mesencephalic locomotor region (MLR) and the muscle reflex, each evoked separately, on the discharge of cutaneous sympathetic fibers innervating the hairy skin of decerebrate cats. Electrical stimulation of the MLR was performed while the cats were paralyzed with vecuronium bromide. The muscle reflex was evoked while the cats were not paralyzed by electrical stimulation of the tibial nerve at current intensities that did not activate directly group III and IV muscle afferents. MLR stimulation increased, on average, the discharge of the 23 cutaneous sympathetic fibers tested ( P < 0.05). The muscle reflex, in contrast, had no overall effect on the discharge of 21 sympathetic fibers tested ( P > 0.05). Both maneuvers markedly increased mean arterial pressure and heart rate ( P < 0.05). Prevention of the baroreceptor reflex with the α-adrenergic blocking agent phentolamine did not reveal a stimulatory effect of the muscle reflex on cutaneous sympathetic discharge. We conclude that the MLR is a more important mechanism than is the muscle reflex in controlling sympathetic discharge to hairy skin during dynamic exercise.

Different effects of halothane on diaphragm and hindlimb muscle in rats

1987 ◽  
Vol 63 (5) ◽  
pp. 1757-1762 ◽  
Author(s):  
B. Dureuil ◽  
N. Viires ◽  
Y. Nivoche ◽  
M. Fiks ◽  
R. Pariente ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Phrenic Nerve ◽  
Muscle Function ◽  
Negative Inotropic Effect ◽  
Abdominal Pressure ◽  
Mechanically Ventilated ◽  
Diaphragmatic Muscle ◽  
Hindlimb Muscle ◽  
Supramaximal Stimulation ◽  
Stimulation Of

The effects of halothane administration on diaphragm and tibialis anterior (TA) muscle were investigated in 30 anesthetized mechanically ventilated rats. Diaphragmatic strength was assessed in 17 rats by measuring the abdominal pressure (Pab) generated during supramaximal stimulation of the intramuscular phrenic nerve endings at frequencies of 0.5, 30, and 100 Hz. Halothane was administered during 30 min at a constant minimum alveolar concentration (MAC): 0.5, 1, and 1.5 MAC in three groups of five rats. For each MAC, Pab was significantly reduced for all frequencies of stimulation except at 100 Hz during 0.5 MAC halothane exposure. The effects of halothane (0.5, 1, and 1.5 MAC) on diaphragmatic neuromuscular transmission were assessed in five other rats by measuring the integrated electrical activity of the diaphragm (Edi) during electrical stimulation of the phrenic nerve. No change in Edi was observed during halothane exposure. In five other rats TA contraction was studied by measuring the strength of isometric contraction of the muscle during electrical stimulation of its nerve supply at different frequencies (0.5, 30, and 100 Hz). Muscle function was unchanged during administration of halothane in a cumulative fashion from 0.5 to 1.5 MAC. These results demonstrate that halothane does not affect hindlimb muscle function, whereas it had a direct negative inotropic effect on rat diaphragmatic muscle.

Norepinephrine uptake as an indicator of cardiac reinnervation in dogs

1978 ◽  
Vol 235 (3) ◽  
pp. H289-H294 ◽  
Author(s):  
M. P. Kaye ◽  
G. M. Tyce
Keyword(s):  
Electrical Stimulation ◽  
Sympathetic Nerves ◽  
Progressive Increase ◽  
Canine Heart ◽  
Storage Mechanism ◽  
Specific Membrane ◽  
Heart Uptake ◽  
Membrane Mechanism ◽  
Stimulation Of

To study the possible role of uptake of [3H]norepinephrine ([3H]NE) as an indicator of sympathetic reinnervation of the surgically denervated canine heart, uptake was determined from multiple areas of hearts at various stages of reinnervation (1--6 mo), and these data were correlated with myocardial catecholamine content and functional response of the heart to electrical stimulation of the sympathetic nerves. Our experiments confirm that NE content correlates poorly with the degree of reinnervation of the previously denervated canine heart. There is, however, a progressive increase of [3H]NE uptake from 1 mo to 6 mo, at which time uptake has returned to approximately 57% of control values in the left atrium. The development of the storage mechanism lags far behind the specific-membrane mechanism for uptake in the reinnervating surgically denervated canine heart.

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation

1977 ◽  
Vol 233 (6) ◽  
pp. H647-H654 ◽  
Author(s):  
P. D. Richardson ◽  
P. G. Withrington
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Blood ◽  
Vascular Bed ◽  
Arterial Responses ◽  
Sympathetic Discharge ◽  
Glucagon Concentration

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

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