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PubMed1990

Potentiation of the halothane-cooling contractures of mammalian muscles by denervation.

Denervation potentiated the cooling-induced contractures and the halothane-cooling contractures of isolated extensor digitorum longus and soleus muscles of the mouse. These effects were more striking in extensor digitorum longus than in soleus muscles. Significant increases in the peak amplitudes of the halothane-cooling contractures of both muscles and of the cooling contractures of soleus muscle were observed within 2 and 7 days of denervation. The potentiation of the contractures persisted for 90 days, the period of this study. Denervation (greater than 2 days) endowed extensor digitorum longus with the ability to generate cooling contractures in the absence of halothane. The rate of tension development of cooling-induced contractures in the absence or presence of halothane was significantly greater in denervated (2-90 days) than in innervated muscles. Denervation also reduced the effectiveness of procaine in inhibiting the halothane-cooling contractures. It is proposed that the potentiation of cooling-induced contractures in denervated muscles results primarily from an increase in the rate of efflux and in the quantity of Ca2+ released from the sarcoplasmic reticulum, upon cooling and (or) when challenged with halothane.

Animals↗
PubMed1991

Effects of postnatal growth and denervation on characteristics of the saphenous artery in SHR and WKY rats between 3 and 6 weeks of age: an in vitro study.

Thigh vessels of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were unilaterally surgically denervated at 10 days of age by femoral nerve section. Denervated and contralateral control segments of saphenous arteries from 3- and 6-week-old rats were mounted in a small vessel myograph for study. Both strains showed growth changes in blood pressure, but there was no significant difference between WKY and SHR. Both strains also had significant growth changes in vessel dimensions and the in vitro measurements suggested that SHR vessels had a thicker wall. Denervation did not affect vessel size. Transmural nerve stimulation indicated loss of innervation due to the surgical procedure. In the denervated vessels, both norepinephrine (NE) and 5-hydroxytryptamine (5-HT) dose response curves were shifted to the left, indicating a postjunctional increase in sensitivity. Maximum tension developed was in the order K+ greater than 5-HT greater than NE. In comparing the two strains, vessels from 6-week-old SHR were less sensitive to 5-HT. Relaxation to acetylcholine was significantly decreased in denervated arteries from WKY, whereas in SHR the significant decrease occurred only at 3 weeks. Denervated vessels from both rat strains at 3 weeks showed greater relaxation to beta-receptor activation, but not at 6 weeks of age. Therefore, the absence of functional innervation resulted in altered function of the saphenous artery wall.

Aging↗
PubMed1992

Recovery of rat tibialis anterior motor unit properties following partial denervation.

The recovery of selected mechanical, morphological, and metabolic properties of rat tibialis anterior fast motor units was determined following partial denervation (n = 7) or partial denervation and hemispinal cord transection (n = 5) and compared with age-matched control units (n = 7). Following 1-12 months of recovery, the mechanical properties of each unit were measured and the fibres depleted of glycogen by using standard ventral root filament stimulation techniques. Quantitative histochemical techniques were used to determine cross-sectional area and the activities of succinate dehydrogenase and alpha-glycerolphosphate dehydrogenase in individual unit fibres. Partial denervation increased the mean fibre area but decreased alpha-glycerolphosphate dehydrogenase activity. Succinate dehydrogenase was unchanged in the denervated groups. The variability in area and enzymatic activities among the unit fibres was unchanged. However, the interrelationship between the enzymes was altered by both denervation procedures. Succinate dehydrogenase activity was directly related to fatigue resistance and inversely related to tetanic tension across the units. These findings suggest that a motor unit reestablishes many of its properties despite marked changes to the composition of the unit brought about by partial denervation. In addition, a reduction in the neuromuscular activity of units during reorganization had a limited effect on recovery.

Animals↗
PubMed2007

Atrophy, but not necrosis, in rabbit skeletal muscle denervated for periods up to one year.

Our understanding of the effects of long-term denervation on skeletal muscle is heavily influenced by an extensive literature based on the rat. We have studied physiological and morphological changes in an alternative model, the rabbit. In adult rabbits, tibialis anterior muscles were denervated unilaterally by selective section of motor branches of the common peroneal nerve and examined after 10, 36, or 51 wk. Denervation reduced muscle mass and cross-sectional area by 50-60% and tetanic force by 75%, with no apparent reduction in specific force (force per cross-sectional area of muscle fibers). The loss of mass was associated with atrophy of fast fibers and an increase in fibrous and adipose connective tissue; the diameter of slow fibers was preserved. Within fibers, electron microscopy revealed signs of ultrastructural disorganization of sarcomeres and tubular systems. This, rather than the observed transformation of fiber type from IIx to IIa, was probably responsible for the slow contractile speed of the muscles. The muscle groups denervated for 10, 36, or 51 wk showed no significant differences. At no stage was there any evidence of necrosis or regeneration, and the total number of fibers remained constant. These changes are in marked contrast to the necrotic degeneration and progressive decline in mass and force that have previously been found in long-term denervated rat muscles. The rabbit may be a better choice for a model of the effects of denervation in humans, at least up to 1 yr after lesion.

Animals↗
PubMed1991

Mitochondrial adaptations in denervated muscle: relationship to muscle performance.

We have studied mitochondrial adaptations in muscle subject to chronic denervation, and their relationship to muscle performance, using a model of unilateral sciatic nerve denervation in rats over periods of 2, 5, 8, 14, 21, 28, 35, and 42 days (n = 5-9 rats/day). Time to peak tension (TPT), one-half relaxation time (1/2RT), and endurance performance were evaluated during in situ stimulation of denervated and contralateral gastrocnemius-plantaris muscles. Denervation led to a 70% decline in muscle mass after 42 days. TPT and 1/2RT increased 17 and 30%, respectively, indicating a transformation toward slower muscle. The activities of the enzymes cytochrome-c oxidase (CYTOX), succinate dehydrogenase, and citrate synthase were decreased by 8-14 days, and by 42 days these were 34-58% of control. The mitochondrial phospholipid cardiolipin was reduced earlier, by 5 days, and gradually decreased to 37% of control. Thus phospholipid removal appears to precede the loss of enzyme activity during decreases in mitochondrial content. Endurance performance was reduced in parallel with decreases in enzyme activity and cardiolipin. Cytochrome c mRNA levels decreased to 52% of control by 5 days. Denervation resulted in coordinated changes in mRNA levels encoding the nuclear-derived CYTOX subunit VIc and the mitochondrially derived CYTOX subunit III. However, changes in CYTOX activity did not always parallel alterations in subunit mRNA levels. Thus transcriptional and translational mechanisms operate in regulating mitochondrial gene expression during denervation.

Animals↗
PubMed1991

Effects of insulin and phospholipase C in control and denervated rat skeletal muscle.

Phospholipase C (PLC), an enzyme that increases endogenous 1,2-diacylglycerol (DAG), caused dose-dependent stimulation of 2-deoxy-D-glucose (2-DG) uptake in rat soleus muscles; the maximal effect was less than that of insulin. In denervated muscles the effect of insulin on 2-DG uptake was markedly reduced, whereas the response to PLC was identical to that of control muscles. Both PLC and insulin stimulated glucose incorporation into glycogen in control but not in denervated solei. Amino acid transport was unaffected by PLC; however, the enzyme completely inhibited the stimulation of amino acid transport by insulin. PLC did not activate the insulin receptor tyrosine kinase but decreased activation of the receptor by insulin in vivo. Basal muscle DAG content increased after denervation. Incubation with PLC markedly increased DAG in control and in denervated muscle. Insulin increased total DAG mass less than PLC in control muscles and did not affect DAG in denervated muscles. In media without added Ca2+, PLC stimulation of DAG production was impaired, and 2-DG uptake was unresponsive to PLC. The data are consistent with, but do not prove, that a subpopulation of DAGs may participate in insulin-mediated stimulation of glucose transport. They also suggest that the denervation-induced insulin resistance of glucose transport may reflect impaired generation of certain DAGs involved in the signaling cascade.

Animals↗
PubMed1995

Lactate transport studied in sarcolemmal giant vesicles from rat skeletal muscles: effect of denervation.

The effect of denervation on lactate transport capacity was studied in giant sarcolemmal vesicles obtained from rat muscle. The rate of lactate transport was determined in soleus and red (RG) and white gastrocnemius (WG) after 1, 3, and 21 days of denervation and in the corresponding contralateral muscles. In addition, muscle lactate dehydrogenase (LDH) and succinate dehydrogenase (SDH) activities were determined. After 1, 3, and 21 days of denervation the rate of lactate transport was lower (P < 0.05) in WG (9, 11, and 36%), RG (15, 21, and 41%), and soleus (12, 24, and 50%) compared with the contralateral muscles. After 21 days of denervation LDH activity was 26, 25, and 34% and SDH activity 33, 25, and 27% lower (P < 0.05) in WG, RG, and soleus, respectively, compared with the contralateral muscles. In the control muscles the lactate transport capacity was 20 and 32% lower (P < 0.05) in WG than in RG and soleus, respectively. The present findings provide support that the sarcolemmal lactate carrier is a plastic system; the transport capacity in soleus, RG, and WG already declines after 1 day of denervation and is further reduced after 21 days of denervation. In addition, the data suggest that the lactate transport capacity in fast-twitch glycolytic fibers < fast-twitch oxidative-glycolytic fibers < slow-twitch oxidative fibers.

Animals↗
PubMed1982

Denervation of arterial chemoreceptors and baroreceptors in fetal lambs in utero.

Arterial baroreceptors and chemoreceptors were denervated in eight fetal lambs in utero. Carotid sinus and carotid body denervation was accomplished by stripping the carotid artery rostral and caudal to the origin of the occipital and lingual arteries. Aortic bodies were denervated by section of the superior laryngeal nerve and aortic nerve in the neck. The anatomy relevant to the technique is presented. The effectiveness of the denervation was tested by injection of 20 micrograms phenylephrine. The slowing of the fetal heart rate normally present in the intact lambs was abolished in the denervated fetuses. Denervation of the carotid and aortic chemoreceptors abolished the reflex bradycardia following injection of 200 micrograms cyanide or following acute hypoxemia produced by uterine blood flow reduction for 20 s. These results indicate that the baroreflex and chemoreflex can be elicited in utero and eliminated by the method we described. The preparation we present allows the study of the role of the arterial chemoreceptors and baroreceptors in normal fetal cardiovascular regulation and in fetal responses to stress.

Animals↗
PubMed1984

Renal effects of volume expansion in the renal-denervated nonhuman primate.

Experiments were performed to determine the role of renal nerves in mediating the renal excretory effects of volume expansion in the nonhuman primate. Male Macaca fascicularis monkeys underwent chronic bilateral renal denervation or sham surgery. After a 1- to 2-wk recovery period, each animal was anesthetized with pentobarbital sodium and volume expanded 20% of estimated blood volume. Two types of volume expansion were used, a hemodilutional expansion using 6% dextran in isotonic saline and an isohemic expansion using each monkey's own blood that had previously been withdrawn in exchange for dextran. Renal denervation did not attenuate the excretory responses to volume expansion in that similar increases in urine flow, sodium excretion, filtered load of sodium excreted, osmolar and free water clearances occurred in both the renal-denervated and sham-operated groups. The onset of the responses was not delayed by renal denervation. Furthermore, the results were the same with both volume expansions. These results suggest that, in the monkey, decreases in renal nerve activity that occur with volume expansion are not necessary for eliciting the excretory responses to this hypervolemic stimulus or that other factors compensate if the kidneys are chronically denervated. In addition, the failure of renal denervation to attenuate the excretory effects of a cell-free volume expansion is not related to any dilutional characteristics of the expansion.

Animals↗
PubMed1985

Effect of chronic surgical denervation of dog heart on myocardial Na+-K+ pump.

The effect of chronic denervation of the myocardium on myocardial Na+-K+ pump activity and numbers of pump sites was studied in dogs. Right ventricular biopsies were taken immediately before and 4 wk after chronic surgical denervation, when depletion of norepinephrine is complete. Na+-K+ pump activity was assayed by ouabain-sensitive 86Rb uptake into ventricular tissue slices. The number of pump sites was measured by [3H]ouabain binding in ventricular tissue slices. Ouabain-sensitive Rb uptake was increased after denervation by an average of 147%. [3H]-ouabain binding at a concentration of 1.25 X 10(-6) M increased by an average of 27.6% after denervation. Acutely applied norepinephrine (2 X 10(-7) M) stimulated ouabain-sensitive Rb uptake both before and after denervation. The stimulation was greater after denervation, indicating supersensitivity. The cause of these changes is not known.

Animals↗
PubMed1988

Arterial pressure control after chronic carotid sinus denervation.

This study examines the control of arterial blood pressure in conscious, instrumented dogs with atrioventricular block before and greater than or equal to 9 days after carotid sinus baroreceptor denervation. Strength of reflex control of blood pressure was quantitated by measuring the changes in peripheral resistance and atrial rate after square wave changes in cardiac output. Surprisingly, nine or more days after carotid denervation, the strength of baroreflex control of peripheral resistance and atrial rate were not different (P greater than 0.05) from the values before denervation. This was not due to a change in the base-line levels of arterial pressure, atrial rate, cardiac output, or peripheral resistance. Bilateral vagal block after carotid denervation removed reflex effects from remaining baroreceptors and virtually eliminated changes in peripheral resistance in response to changes in arterial pressure. Therefore, the compensatory responses observed after carotid denervation were mediated by the remaining baroreceptors. Thus, after chronic carotid sinus denervation, there is no decrease in the strength of baroreflex control of peripheral resistance or heart rate.

Animals↗
PubMed1990

Time course of recovery of arterial pressure control after carotid denervation.

We examined the recovery of arterial pressure control after carotid sinus baroreceptor denervation in conscious dogs with atrioventricular block. Strength of control was assessed by measuring changes in peripheral resistance and atrial rate after step changes in cardiac output. One day after carotid denervation, arterial pressure was significantly elevated (+13.7 mmHg), and the strength of control of peripheral resistance and atrial rate were significantly decreased to 46.1 and 36.6% of control, respectively. Over 4-7 days, the strength of control of both peripheral resistance and atrial rate and the mean arterial pressure returned to the levels observed before denervation. After carotid denervation, the pressor response to bilateral carotid artery occlusion was abolished, and thus the recovery of arterial pressure control was not caused by inadequate carotid denervation or regeneration of carotid baroreceptors. The recovery of arterial pressure control after carotid denervation is probably caused by an increase in the reflex responses to pressure changes at the aortic baroreceptors and may reflect plasticity within the baroreflex pathway.

Animals↗
PubMed1998

Renal denervation alters cardiovascular and endocrine responses to hemorrhage in conscious newborn lambs.

To investigate the role of renal sympathetic nerves in modulating cardiovascular and endocrine responses to hemorrhage early in life, we carried out three experiments in conscious, chronically instrumented lambs with intact renal nerves (intact; n = 8) and with bilateral renal denervation (denervated; n = 5). Measurements were made 1 h before and 1 h after 0, 10, and 20% hemorrhage. Blood pressure decreased transiently after 20% hemorrhage in intact lambs and returned to control levels. In denervated lambs, however, blood pressure remained decreased after 60 min. After 20% hemorrhage, heart rate increased from 170 +/- 16 to 207 +/- 18 beats/min in intact lambs but not in denervated lambs, in which basal heart rates were already elevated to 202 +/- 21 beats/min. Despite an elevated plasma renin activity (PRA) measured in denervated (12.0 +/- 6.4 ng ANG I . ml-1 . h-1) compared with intact lambs (4.0 +/- 1.1 ng ANG I . ml-1 . h-1), the increase in PRA in response to 20% hemorrhage was similar in both groups. Plasma levels of arginine vasopressin increased from 11 +/- 8 to 197 +/- 246 pg/ml after 20% hemorrhage in intact lambs but remained unaltered in denervated lambs from baseline levels of 15 +/- 10 pg/ml. These observations provide evidence that in the newborn, renal sympathetic nerves modulate cardiovascular and endocrine responses to hemorrhage.

Angiotensin I↗
PubMed1976

Erythropoietin production after renal denervation or beta-adrenergic blockade.

The ability of either beta-adrenergic blockade or bilateral renal denervation to alter erythropoietin (ESF) production in rabbits exposed to hypobaric hypoxia was studied. ESF elaboration during 5 h of exposure to hypoxia was not affected by beta-blockade, but was markedly reduced by prior surgical denervation of both kidneys. After 18 h of hypoxia plasma ESF levels in renal denervated rabbits did not differ significantly from those of sham-operated controls. Previous studies have shown that ESF production during this more prolonged exposure to hypoxia was significantly inhibited by some beta-adrenergic blocking agents. Combined renal denervation and beta-blockade were more effective than renal denervation alone in attenuating ESF production during 5 h of exposure to hypoxia. However, ESF elaboration during 18 h of hypoxia was significantly greater in animals with combined denervation and beta-blockade than in control rabbits. These results suggest the existence of two distinct mechanisms for ESF production in rabbits exposed to hypobaric hypoxia.

Adrenergic beta-Antagonists↗
PubMed2005

Brain stem control of arterial pressure in chronic arterial baroreceptor-denervated rats.

Interruption of the baroreceptor reflex by transection of afferent nerves (sinoaortic denervation; SAD) or lesions of nucleus tractus solitarius (NTS) elevates sympathetic nerve activity (SNA) and arterial pressure (AP). However, within 1 wk, mean AP returns to normal despite the absence of baroreflexes. In this study, we examine central mechanisms that control AP in chronic baroreceptor-denervated rats. In urethane-anesthetized rats (1.5 g/kg i.v.) after autonomic ganglionic blockade (5 mg/kg i.v. chlorisondamine), alpha1-adrenergic-mediated pressor responses (1-100 microg/kg i.v. phenylephrine) were not altered by chronic lesions of NTS, indicating vascular reactivity to sympathetic stimulation is normal. Transection of the spinal cord at T1 profoundly decreased AP and was not further reduced by chlorisondamine in control or denervated rats. Inhibition of the rostral ventrolateral medulla (RVLM) by microinjections of muscimol (100 pmol/side) decreased AP to levels not further reduced by chlorisondamine in control rats, rats with SAD, and rats with NTS lesions. Blockade of GABA(A) receptors in the RVLM (50 pmol/side bicuculline) increased AP similarly in control rats and denervated rats. In agreement, inhibition of the caudal ventrolateral medulla (CVLM) by microinjections of muscimol or blockade of glutamatergic inputs (2.7 nmol/side kynurenate) produced comparable increases in AP in control and denervated rats. These data suggest the RVLM continues to drive the SNA that regulates AP in the chronic absence of baroreceptor inputs. In addition, despite the absence of a tonic excitatory input from NTS, in chronic baroreceptor-denervated rats glutamatergic inputs drive the CVLM to tonically inhibit the RVLM. Baroreceptor-independent regulation of the ventrolateral medulla may underlie central mechanisms contributing to the long-term control of AP.

Animals↗
PubMed2002

Acute sympathoexcitatory action of angiotensin II in conscious baroreceptor-denervated rats.

Angiotensin II (ANG II) has complex actions on the cardiovascular system. ANG II may act to increase sympathetic vasomotor outflow, but acutely the sympathoexcitatory actions of exogenous ANG II may be opposed by ANG II-induced increases in arterial pressure (AP), evoking baroreceptor-mediated decreases in sympathetic nerve activity (SNA). To examine this hypothesis, the effect of ANG II infusion on lumbar SNA was measured in unanesthetized chronic sinoaortic-denervated rats. Chronic sinoaortic-denervated rats had no reflex heart rate (HR) responses to pharmacologically evoked increases or decreases in AP. Similarly, in these denervated rats, nitroprusside-induced hypotension had no effect on lumbar SNA; however, phenylephrine-induced increases in AP were still associated with transient decreases in SNA. In control rats, infusion of ANG II (100 ng x kg(-1) x min(-1) iv) increased AP and decreased HR and SNA. In contrast, ANG II infusion increased lumbar SNA and HR in sinoaortic-denervated rats. In rats that underwent sinoaortic denervation surgery but still had residual baroreceptor reflex-evoked changes in HR, the effect of ANG II on HR and SNA was variable and correlated to the extent of baroreceptor reflex impairment. The present data suggest that pressor concentrations of ANG II in rats act rapidly to increase lumbar SNA and HR, although baroreceptor reflexes normally mask these effects of ANG II. Furthermore, these studies highlight the importance of fully characterizing sinoaortic-denervated rats used in experiments examining the role of baroreceptor reflexes.

Angiotensin II↗
PubMed1987

Adrenal gland denervation and diving in ducks.

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.

Adrenal Glands↗
PubMed1989

Cardiovascular responses to denervation of pulmocutaneous baroreceptors in toads.

Toad pulmocutaneous arterial baroreceptors are connected to afferent fibers carried in the recurrent laryngeal nerves (rLNs). Bilateral rLN denervation in conscious toads (Bufo marinus) caused 34 and 78% increases in heart rate (Fh) and systemic arterial blood pressure (Pa) within 10-15 min, respectively. The variance of Pa was significantly increased 2 days after denervation, but Pa and Fh were not. In additional chronic experiments, 5 of 17 baroreceptor-denervated toads died within the 2-wk recovery period. No deaths occurred in sham-operated toads. The mean Pa, Fh, and cardiac interval (Ic), the mean variance of Pa, Fh, and Ic, and Pa and Fh responses to stress, plasma composition, and the dry-to-wet weight ratio of skeletal muscle and lung were not statistically different in denervated and sham-operated toads. However, the sensitivity of Ic to changes in Pa, exposed by intra-arterial injections of phenylephrine and nitroprusside, was attenuated in denervated toads. Postmortem examination revealed occasional pulmonary lesions, the incidence of which appeared correlated with causes of pulmonary hypertension: baroreceptor denervation and phenylephrine injections. We conclude that pulmocutaneous arterial baroreflex is tonically active but is not essential for the long-term maintenance of Pa in conscious undisturbed toads.

Animals↗