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At least 19 recordsLinked to original sources

PubMed1986

Blood pressure of sinoaortic-denervated dogs is not increased by cardiac denervation.

Although blood pressure rises markedly after acute sinoaortic denervation, animals with chronic sinoaortic denervation have normal or only slightly elevated mean arterial pressures. The present study was performed to determine whether reflexes from cardiac receptors exert antihypertensive effects and thereby lower blood pressure in animals with chronic sinoaortic denervation. We made multiple measurements of blood pressures in dogs with chronic sinoaortic denervation before and after their hearts were denervated surgically. Mean arterial pressure after cardiac denervation (100.3 +/- 4.2 mm Hg) was not significantly different from the mean pressures recorded before cardiac denervation in these sinoaortic-denervated dogs (104.8 +/- 3.1 mm Hg). Also, mean heart rate after cardiac denervation (107.4 +/- 5.5 beats/min) did not differ significantly from the mean heart rate recorded before cardiac denervation (107.2 +/- 5.9 beats/min). Cardiac denervation did, however, appear to reduce the lability of both blood pressure and heart rate in sinoaortic-denervated dogs. We conclude that cardiac receptors are not responsible for maintaining arterial pressure within essentially normal limits in animals with chronic sinoaortic denervation.

Animals↗

PubMed2001

Effect of chronic denervation and denervation-reinnervation on cytoplasmic creatine kinase transcript accumulation.

The extensor digitorum longus (EDL) and soleus muscles of adult mice were chronically denervated or denervated and allowed to reinnervate. Muscles were evaluated 1, 5, 14, 21, and 52 days after sciaticectomy. In terms of weight loss, myofiber atrophy, degeneration, and fibrosis, the soleus muscle was more affected than the EDL by chronic denervation. Fifty-two days after chronic denervation, the number of molecules of MCK/ng total RNA in both muscles (determined with competitive PCR) decreased, with the soleus muscle being more affected. At that stage, BCK mRNA levels in the denervated soleus were unchanged, but they were increased (>50%) in the EDL. Reinnervation restored MCK transcript accumulation in the EDL, whereas, in the soleus MCK, transcripts exceeded control values by 57%, approaching levels in the reinnervated EDL. Despite restoration of MCK mRNA levels, the number of molecules of BCK mRNA/ng total RNA was four- to fivefold higher in reinnervated versus control muscles, suggesting that the genes encoding the CK mRNAs are not coordinately regulated in adult muscle. The role of denervation induced, fiber type changes in regulating CK mRNA accumulation has been evaluated. Electron microscopic analyses have established that fibrosis is not a factor that determines BCK mRNA levels in the chronically denervated or denervated-reinnervated muscles. CK isozyme analyses support the hypothesis that a greater proportion of BCK mRNA found in 52 day chronically denervated and denervated-reinnervated muscles is produced in myofibers vs. nonmuscle cells than in control muscles.

Animals↗

PubMed1990

Denervation-induced alterations of acetylcholinesterase in denervated and nondenervated muscle.

The influence of denervation on acetylcholinesterase (AchE) molecular forms in rat skeletal muscle for durations up to 30 days is examined in denervated anterior tibialis, the innervated contralateral muscle, and diaphragm. Denervated rats at a common age of 8.5 weeks are compared with age-matched, nondenervated animals. The results indicate that time-dependent losses of AchE in denervated muscle occur more rapidly than loss of muscle mass and are not uniform among the different molecular forms. Loss of the 4 S and 16 S forms is rapid and essentially complete within 3.5 days of denervation, while during this same period the 10.5 S form undergoes a transient twofold increase and its presence in denervated muscle is never abolished. Within 30 days of denervation, all forms of AchE including the 16 S species reappear. A salient finding of these studies is that the effects of denervation are evident also in anatomically remote, innervated muscle such as anterior tibialis of the contralateral limb and in diaphragm. These alterations appear as pronounced reductions in 4 S AchE and increases in 10.5 S AchE; the asymmetric collagen-tailed 16 S form is unaltered. Treatment of primary cultures of embryonic chick pectoral muscle with sera from denervated but not nondenervated rat causes reductions in AchE. These results indicate that the appearance and retention of AchE, in particular the 16 S form, occur in the absence of functional innervation. The effects of denervation on AchE metabolism in remote, innervated tissue are consistent with the action of a diffusible factor released from severed nerve or muscle, or both.

Acetylcholinesterase↗

PubMed2005

Comparison of gene expression of 2-mo denervated, 2-mo stimulated-denervated, and control rat skeletal muscles.

Loss of innervation in skeletal muscles leads to degeneration, atrophy, and loss of force. These dramatic changes are reflected in modifications of the mRNA expression of a large number of genes. Our goal was to clarify the broad spectrum of molecular events associated with long-term denervation of skeletal muscles. A microarray study compared gene expression profiles of 2-mo denervated and control extensor digitorum longus (EDL) muscles from 6-mo-old rats. The study identified 121 genes with increased and 7 genes with decreased mRNA expression. The expression of 107 of these genes had not been identified previously as changed after denervation. Many of the genes identified were genes that are highly expressed in skeletal muscles during embryonic development, downregulated in adults, and upregulated after denervation of muscle fibers. Electrical stimulation of denervated muscles preserved muscle mass and maximal force at levels similar to those in the control muscles. To understand the processes underlying the effect of electrical stimulation on denervated skeletal muscles, mRNA and protein expression of a number of genes, identified by the microarray study, was compared. The hypothesis was that loss of nerve action potentials and muscle contractions after denervation play the major roles in upregulation of gene expression in skeletal muscles. With electrical stimulation of denervated muscles, the expression levels for these genes were significantly downregulated, consistent with the hypothesis that loss of action potentials and/or contractions contribute to the alterations in gene expression in denervated skeletal muscles.

Animals↗

PubMed1993

Mechanisms of denervation supersensitivity in regionally denervated canine hearts.

Mechanisms responsible for "denervation supersensitivity" in regionally denervated canine hearts were examined by measuring beta-adrenergic receptor density and affinity and the density of the alpha-subunit of the stimulatory G protein (Gs alpha). Sympathetic denervation was produced by applying an epicardial strip of phenol midway between the left ventricular (LV) base and apex. Six to eight days after denervation, dogs were anesthetized and then underwent functional studies (n = 4) or hearts were excised for biochemical analyses (n = 6). Biochemical studies were also done on 3 nondenervated hearts. Effective refractory periods (ERPs) were measured in innervated (base) and denervated (apex) LV myocardium. During sympathetic stimulation (2 and 4 Hz), the ERP shortened more (P < 0.05) at basal than at apical sites, whereas during norepinephrine infusion (0.05 to 0.5 mg.kg-1 x min-1), the ERP shortened more (P < 0.001) at apical than at basal sites. In regionally denervated hearts, however, the density and affinity of beta-adrenergic receptors did not differ significantly (P > 0.2) in nondenervated basal compared with denervated apical myocardium. Quantitative immunoblotting of the Gs alpha demonstrated that the density of the 47- and 52-kDa subunits was also similar (P > 0.6) in basal compared with apical myocardium from regionally denervated hearts. In addition, beta-adrenergic receptor density and affinity and Gs alpha density did not differ significantly (P > 0.5) in basal compared with apical myocardium from nondenervated control hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Dorsal root ganglia grafts stimulate regeneration of denervated urodele forelimbs: timing of graft implantation with respect to denervation.

Amphibian forelimb regeneration is a nerve-dependent process; nerves presumably release one or more neurotrophic factors that stimulate blastema cell division. To date several candidate molecules/factors have been shown to stimulate macromolecular synthesis and/or mitosis but sustained cell cycle activity and blastema development have not been achieved. Because dorsal root ganglia (DRG) implants are capable of promoting regeneration of denervated adult newt limbs (Kamrin & Singer, 1959), we have evaluated the DRG stimulation of regeneration in denervated limbs of adult newts and larval axolotls; two alternative timing strategies were tested as a step toward defining bioassay parameters that best reflect neurotrophic activity. The frequency of regeneration in denervated adult newt limbs was compared after providing DRG before or at the time of denervation (to maintain neurotrophic and cell cycle activity) versus DRG implantation at various postdenervation times (to resupply neurotrophic activity and restimulate suppressed cell cycle activity). The results show that denervated adult newt limbs regenerated most frequently using the maintenance strategy, but as the denervation interval was extended in the restimulation strategy, the frequency of regeneration declined. Larval axolotl limbs responded positively in both maintenance and restimulation DRG-grafting protocols. These results suggest that the efficacy of DRG stimulation of regeneration in adult newts was related to the relative number of blastema cells present at the time of denervation and the proliferative status of the blastema cells; bioassays with denervated adult newt limbs should be designed with these constraints in mind. Because such constraints are not as problematic with the larval axolotl, this species may provide the best opportunity for further defining bioassay parameters related to the neurotrophic stimulation of regeneration.

Animals↗

PubMed1992

[The effect of prostacyclin (PGI) on denervated tissues--especially, about denervation supersensitivity].

It is well known that contractive agents of smooth muscle have denervation supersensitivity. But, the existence of denervation supersensitivity in relaxed ones does not become so clear. We investigated these supersensitivity, especially prostacyclin (PGI2). We made the denervated artery by lumbar sympathetic ganglionectomy in mongrel dogs. Namely, saphenous and dorsal pedal arteries were denervated by this ganglionectomy. And we studied the changes of these arterial tensions by magnus apparatus. Dose-response (D-R) curves of denervated arteries for KCl and noradrenaline (NE) shifted to left against control arteries. Next, we studied effects of PGI2. At first, we measured ED50 of KCl and NE contraction. And, we produced the half contraction on each artery by using ED50 of KCl and NE. Lastly, PGI2 was added on the half contractive arteries to study relaxed changes. D-R curves of denervated arteries for PGI2 shifted to left, too. These denervated arteries acquired the supersensitivity for PGI2. Clinically, if we use relaxants after organ transplantation, these drugs may be very effective for the perfusion of the grafts.

Animals↗

PubMed1988

Insulin resistance in denervated skeletal muscle. Inability of insulin to stimulate dephosphorylation of glycogen synthase in denervated rat epitrochlearis muscles.

We have investigated the effects of insulin and motor denervation on the phosphorylation of glycogen synthase in skeletal muscle. Rat epitrochlearis muscles were denervated in vivo 3 days before the contralateral and denervated muscles were incubated in vitro with 32Pi to label sites in glycogen synthase. The 32P-labeled synthase was rapidly immunoprecipitated from extracts under conditions which prevented changes in the phosphorylation state of the enzyme. When 32P-labeled synthase from contralateral muscles was cleaved with CNBr, essentially all of the 32P was recovered in two fragments, denoted CB-1 and CB-2. Incubating these muscles with insulin decreased the 32P content of each fragment by approximately 25%, indicating that the hormone stimulated dephosphorylation of at least two sites. Peptide mapping by reverse phase high performance liquid chromatography was performed to resolve phosphorylation sites more completely. The results suggest that the enzyme was phosphorylated in sites 1a, 1b, 2, 3(a+b+c), and 5. Insulin stimulated dephosphorylation of sites in peptides presumed to contain sites 1b, 2, and 3(a+b+c). Synthase from denervated muscles appeared to contain the same amount of phosphate as enzyme from contralateral muscles, and denervation did not detectably affect the distribution of 32P within the subunit. However, denervation abolished the effect of insulin on decreasing the 32P content of synthase. The results indicate that the insulin resistance induced by denervation involves a loss in the ability of insulin to stimulate dephosphorylation of glycogen synthase.

Animals↗

PubMed1980

Sensitization of the rat parotid gland to secretagogues following either parasympathetic denervation or sympathetic denervation or decentralization.

The sensitivity of the rat parotid gland to chemical agents was examined 2--3 weeks after either parasympathetic denervation or sympathetic denervation or decentralization. The parasympathetically denervated gland was markedly sensitized towards methacholine; a nonspecific supersensitivity mainly mediated via alpha-adrenoceptors was also demonstrated. The sympathetically denervated gland had developed a supersensitivity which was both of the pre- and the postjunctional type; it was predominantly of the former type to noradrenaline and adrenaline, and entirely so to phenylephrine; it was of the latter type to isoprenaline, and also to methacholine. The sympathetically decentralized gland was mainly sensitized towards noradrenaline, adrenaline and isoprenaline. The postjunctional supersensitivity developed towards the sympathomimetic drugs after sympathetic decentralization was of about the same magnitude as that observed after sympathetic denervation; this type of supersensitivity was mainly mediated via beta-adrenoceptors.

Animals↗

PubMed1981

Effects of reserpinization, surgical denervation and in vitro chemical denervation with 6-hydroxydopamine on the contractile response of isolated rabbit ear artery to propranolol.

The contractile effect of propranolol in isolated rabbit ear artery was assessed in reserpinized and in surgically and chemically denervated blood vessels. Reserpinization and surgical denervation either had no effect on or enhanced the ear artery contractile response to 10(-6) to 10(-4) M propranolol. In contrast, the contractile response to propranolol was nearly abolished after denervation of the ear artery in vitro with 6-hydroxydopamine (6-OHDA). Dose-response curves to norepinephrine were shifted to the left by factors of 4.9 in 6-OHDA denervated ear arteries and 15.6 in untreated arteries in the presence of 10(-7) M desipramine. The diluent for 6-OHDA shifted both the norepinephrine and propranolol dose-response curves to the right. It is proposed that propranolol caused a contractile response in ear artery by an action on the postsynaptic tissues of this vessel. 6-OHDA denervation caused nonspecific desensitization in rabbit ear artery leading to the loss of response of this vessel to propranolol.

Animals↗

PubMed1980

[Variations in the resting membrane potential of denervated and tenotomized-denervated rat skeletal muscles].

Resting membrane potential (RMP) was studied in denervated (D), tenotomized (T) and tenotomized-denervated (TD) Soleus (S) and Tibialis Anterior (TA) muscles of the rat. In TD muscles, denervation was performed 1 week after tenotomy. The measurements were performed "in vitro" at 20 degrees C, 1-7 days after denervation in D and TD muscles, and 7 days after tenotomy in T muscles. In T muscles there were not differences in comparison with the controls. In D muscles RMP decreased earlier in S than in TA. The time course of membrane depolarization was similar in TD and D muscles until the 2nd day after denervation. At the 3rd day, RMP showed a further, significant reduction in TD muscles, both in S and TA, but not in D muscles. In D muscles, the depolarization increased very slowly up to the 7th day.

Animals↗

PubMed2001

Do denervated peripheral nerve trunks become ischemic? The impact of chronic denervation on vasa nervorum.

The long-term relationship between the peripheral nerve trunk and its vascular supply, the vasa nervorum, has not been considered in the context of denervation and regeneration. While the microvessels of peripheral nerve are not thought to influence Wallerian degeneration itself, in this work we explored how vasa nervorum respond to denervation of the nerve trunk. Our hypotheses were that the presence of axons had a significant impact on the vasa nervorum and that the absence of reinnervation might eventually lead to an unfavorable ischemic regenerative microenvironment. We studied rat sciatic nerve trunks for up to 6 months following transection and either prevented regeneration or allowed it to proceed. Vasa nervorum were studied in several ways: (i) measurements of local endoneurial blood flow using microelectrode hydrogen clearance polarography; (ii) measurements of erythrocyte flux (flow) in the extrinsic nerve plexus using laser Doppler flowmetry; (iii) India ink perfusion of microvessels in unfixed nerve; (iv) mRNA expression of vascular endothelial growth factor (VEGF) using reverse transcription polymerase chain reaction. Early after injury, there were rises in endoneurial and extrinsic flow, microvessel numbers, and VEGF mRNA expression. Angiogenesis was apparently confined to the epineurial and perineurial compartments. Later, however, there were substantial declines in flow observed in long-term (6-month) denervated sciatic nerve trunks associated with declines in the caliber of new microvessels. Reinnervated sciatic nerves had restored endoneurial blood flow. The findings confirm important relationships between axon presence and local blood flow. Angiogenesis is a feature of the injured peripheral nerve, but long term denervated nerve trunks have declines of flow despite retaining new microvessels.

Animals↗

PubMed1980

Partial denervation in inactive muscle effects innervated and denervated fibres equally.

Possible causal factors of denervation-induced changes in muscle include inactivity, products of nerve degeneration and lack of a nerve-borne trophic agent. We now show that if the innervated fibres in a partially denervated rat muscle are rendered inactive, they undergo a reaction as intense as that of the denervated fibres. This provides further support for the view that the effects of denervation on the extrajunctional muscle membrane result from a combination of muscle inactivity and of nerve breakdown products acting diffusely throughout the muscle.

Action Potentials↗

PubMed1977

Partial denervation affects both denervated and innervated fibers in the mammalian skeletal muscle.

Partial denervation of the rat extensor digitorum longus muscle was performed by sectioning only one of the sciatic nerve roots. Measurements of spike resistance to tetrodotoxin in individual muscle fibers revealed denervation changes not only in the denervated fibers but also in the adjacent innervated ones. The results support the concept that products of nerve degeneration play a role in the origin of muscle changes induced by denervation.

Action Potentials↗

PubMed1983

Some observations on muscle biopsies before and after denervation. Histological and biochemical changes in human extensor hallucis and digitorum brevis muscles two weeks after denervation.

In 7 patients biopsies of the extensor hallucis or digitorum brevis muscles were obtained before and 2 weeks after surgical denervation. Ultrastructural morphology showed convincing phenomena of denervation, but not of incipient regeneration. No increase (or decrease) of single or 'twin' myonuclei could be demonstrated in light microscopic examination of semithin sections. Histochemical examination did not show significant changes, but revealed type grouping in all biopsies, presumably due to previous denervation-reinnervation processes. Biochemical studies revealed decreased cytochrome c oxidase activities in the biopsies after denervation. Clinical and electromyographic examinations at later dates showed that the muscle transplantations had been successful.

Adolescent↗

PubMed1992

Unilateral vagal denervation suppresses omeprazole-induced trophic effects on the denervated side of the rat stomach.

In several experimental animals treatment with large doses of the proton pump inhibitor omeprazole leads to hypergastrinemia and with time to trophic effects in the acid-producing part of the stomach, most notably an increased density of the histamine-producing enterochromaffin-like (ECL) cells. The trophic effects are thought to reflect the increase in circulating gastrin. In the present study unilateral vagal denervation in the rat partly suppressed the tropic effects seen in the denervated side of the stomach but not those in the intact side after treatment with omeprazole for 10 weeks. Unilateral vagal denervation significantly reduced the proliferative stimulus of omeprazole on the ECL cells in the denervated part of the stomach. Thus, an intact vagal innervation appears to be essential for the capacity of the oxyntic mucosa, including the ECL cells, to respond to elevations in serum gastrin. We suggest that gastrin and the vagus interact to maintain trophic control of the oxyntic glands.

Animals↗

PubMed2006

Beta-adrenoceptor agonist treatment reverses denervation atrophy with augmentation of collagen proliferation in denervated mice gastrocnemius muscle.

Daily oral administration of isoproterenol hydrochloride (60 mg/kg body weight; for 30 days) a beta-receptor agonist to normal innervated and denervated adult male Swiss albino mice confirmed its ability to induce skeletal muscle hypertrophy and reverse denervation atrophy respectively. Measurement of total tissue proteins and dry muscle mass showed 15-17% increase with 6% rise of hypertrophy index in gastrocnemius muscle. Hydroxyproline assay employed to measure the total tissue collagen exhibited 45% increase in collagen in normal innervated gastrocnemius muscle in response to beta agonist treatment. beta-adrenoceptor agonist ameliorated denervation atrophy along with further increase in collagen content of denervated gastrocnemius muscle.

Adrenergic beta-Agonists↗

PubMed1983

Experimental study of denervated rat muscle. Part I: Histochemical and electrophysiological observations of denervated rat muscle.

Histochemical and electrophysiological observations were carried out on denervated rat muscles, mainly extensor digitorum longus muscle. The myofibrillar ATPase reaction was employed to classify the type of muscle fibers. Type 1 fiber, low ATPase activity, and type 2 fiber, high ATPase activity, were recognized. It is generally believed that denervation causes a preferential atrophy of type 2 fibers and these fibers may be more dependant on neural influence than type 1 fibers. But the result of this investigation revealed that the atrophy of type 1 fiber and the enlargement of type 2 fiber will be caused by denervation. The term of enlargement is not equivalent to hypertrophy. Enlargement means the increasing of diameter of muscle fiber reacting to the denervation in this experiment. It is deduced that type 1 fiber is affected more by neural control than type 2 fiber.

Adenosine Triphosphatases↗