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PubMed1982

Degeneration activity of the pineal gland after sympathetic denervation.

After removal of the superior cervical ganglia the pineal gland of the rat showed a period of transient increase in activity of serotonin-N-acetyltransferase. This degeneration activity was preceded by a decline of the levels of endogenous noradrenaline and an impairment of the 3H-metaraminol uptake. Twenty-seven hours after sympathetic denervation the levels of the endogenous neurotransmitter were almost completely depleted, while either 24 h or 21 days after denervation total uptake of the tritiated amine decreased to only about 50% of the control values. Previous chronic sympathetic decentralization elicited in the pineal gland post-junctional supersensitivity, as judged by the enhanced degeneration activity observed in decentralized glands after sympathetic denervation. The present findings confirm that, in endocrine glands and similarly to other autonomically innervated organs, acute denervation induces degeneration activity.

Animals↗
PubMed1984

Changes in sensitivity to the inhibitory effects of adrenergic agonists on intestinal motor activity after chronic sympathetic denervation.

The concentration-effect relationships of adrenergic agonists in inhibiting muscular tone, carbachol-induced contraction of circular muscle strips and nerve-mediated motor activity during the peristaltic reflex have been studied in intact and sympathetically denervated preparations of isolated guinea-pig colon. The order of potencies of adrenergic agonists was different for muscular and nerve-mediated effects, being clonidine greater than noradrenaline greater than methoxamine greater than isoprenaline for the inhibition of peristalsis and isoprenaline greater than noradrenaline greater than methoxamine greater than clonidine for the relaxation of circular muscle. Denervation supersensitivity was specific for the adrenergic agonists and developed both to the muscular and nerve-mediated effects, involving both alpha and beta receptors. The degree of potentiation was similar for noradrenaline and isoprenaline when measured for the muscular effects but was significantly higher for noradrenaline than for isoprenaline or methoxamine when measured for peristalsis inhibition. No potentiation could be observed for papaverine and for the muscular effects of methoxamine and phenylephrine. The increase in potency of noradrenaline ranged from a 26-fold increase for the inhibition of propulsion velocity to a 2.5-fold increase for the inhibition of carbachol-induced contraction. A much narrower range was observed for isoprenaline. Potentiation could also be observed for the inhibitory effect of noradrenaline on acetylcholine release. Clonidine was the most potent agonist against peristaltic reflex and the weakest agonist in relaxing circular muscle. Denervated preparations became subsensitive to the inhibitory effect of clonidine on peristaltic reflex. The potency of clonidine relative to noradrenaline was 488 in intact preparations and only 3.1 in denervated organs.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Obstetric fecal incontinence. Role of pelvic floor denervation and results of delayed sphincter repair.

During the last five years, 37 patients with fecal incontinence because of childbirth have been investigated. Ages varied from 22 to 62 years and duration of symptoms from 0.3 to 26 years. Anal manometry was performed in all patients and electromyography was performed in 24 patients. Thirty patients underwent delayed sphincter repair. In all patients, a dehiscence was found anteriorly, bridged by scar tissue. Continence was restored in 25 patients (83 percent). Electromyography was performed postoperatively in patients who remained incontinent and who demonstrated severe denervation. All these patients had undergone previous sphincter repair. In seven patients, there were no signs of obstetric injury. Electromyography demonstrated severe denervation, but sphincter mapping did not demonstrate muscle discontinuity. Continence improved in four patients within one year as a result of reinnervation demonstrated by electromyography. The authors conclude that fecal incontinence after childbirth may be due to either obstetric rupture or denervation. Both disorders may coexist. Delayed sphincter repair gives excellent results provided that denervation is not present. Preoperative assessment with electromyography is mandatory.

Adult↗
PubMed2004

Teres minor denervation on routine magnetic resonance imaging of the shoulder.

OBJECTIVE: To try to define an association between clinical history and the finding of isolated teres minor denervation on routine magnetic resonance (MR) examination of the shoulder. DESIGN: A retrospective review of all shoulder MR examinations performed at our institution over a 2-year period ( n=2,563) PATIENTS: All patients and MR examinations demonstrating isolated denervation of the teres minor muscle as determined by review of this subset of patients ( n=61) RESULTS: A 3% incidence of isolated teres minor denervation was found. No patient had a clinical history concerning the classic quadrilateral space syndrome, and no patient had a structural lesion in the quadrilateral space. CONCLUSIONS: Isolated teres minor denervation is not an uncommon finding on routine shoulder MR imaging and may be associated with pathology other than a structural lesion in and about the axillary neurovascular structures, such as rotator cuff injuries and traction injury on the axillary nerve sustained during a glenohumeral joint translational event.

Axilla↗
PubMed1999

Denervation syndromes of the shoulder girdle: MR imaging with electrophysiologic correlation.

OBJECTIVE: To investigate the use of MR imaging in the characterization of denervated muscle of the shoulder correlated with electrophysiologic studies. DESIGN AND PATIENTS: We studied with MR imaging five patients who presented with shoulder weakness and pain and who underwent electrophysiologic studies. On MR imaging the distribution of muscle edema and fatty infiltration was recorded, as was the presence of masses impinging on a regional nerve. RESULTS: Acute/subacute denervation was best seen on T2-weighted fast spin-echo images with fat saturation, showing increased SI related to neurogenic edema. Chronic denervation was best seen on T1-weighted spin-echo images, demonstrating loss of muscle bulk and diffuse areas of increased signal intensity within the muscle. Three patients showed MR imaging and electrophysiologic findings of Parsonage Turner syndrome. One patient demonstrated an arteriovenous malformation within the spinoglenoid notch, impinging on the suprascapular nerve with associated atrophy of the infraspinatus muscle. The fifth patient demonstrated fatty atrophy of the teres minor muscle caused by compression by a cyst of the axillary nerve and electrophysiologic findings of an incomplete axillary nerve block. CONCLUSION: MR imaging is useful in detecting and characterizing denervation atrophy and neurogenic edema in shoulder muscles. MR imaging can provide additional information to electrophysiologic studies by estimating the age (acute/chronic) and identifying morphologic causes for shoulder pain and atrophy.

Adult↗
PubMed2000

Cardiac adrenergic denervation in patients with non-Q-wave versus Q-wave myocardial infarction.

In spite of smaller infarct size and better preserved left ventricular function the long-term prognosis after a non-Q-wave infarction is not better than after a Q-wave infarction. In fact, the risk of sudden cardiac death is higher in patients with a non-Q-wave infarction than in patients with a Q-wave infarction. One possible reason for postinfarction arrhythmias is cardiac adrenergic denervation resulting from myocardial infarction. In this study we compared cardiac adrenergic innervation after non-Q-wave and Q-wave infarctions. Single-photon emission tomography using iodine-123 metaiodobentzylguanidine (MIBG) and technetium-99m sestamibi (MIBI) tracers were conducted in order to compare cardiac adrenergic denervation and myocardial perfusion in 12 patients with a non-Q-wave infarction and 15 patients with a Q-wave infarction. MIBG and MIBI defects were determined as regional uptake < or = 30% of maximal myocardial activity. The size of MIBI defects calculated as a percentage of left ventricular mass was significantly smaller in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (4%+/-3% vs 9%+/-7%, P<0.05, respectively). According to the maximal serum creatine kinase activity, less myocardium was damaged in patients with a non-Q-wave infarction than in patients with a Q-wave infarction (502+/-436 IU/l vs 1878+/-1265 IU/l, P<0.001). In spite of this, the extent of MIBG defects was similar in patients with a non-Q-wave and patients with a Q-wave infarction (21%+/-18% vs 23%+/-12%, respectively). In addition, the size of MIBG defect correlated with the infarct size (maximal creatine kinase activity) (r=0.52, P<0.05) after a Q-wave infarction but not after a non-Q-wave infarction. In conclusion, despite a smaller infarct size in non-Q-wave infarct patients, the extent of cardiac adrenergic denervation was similar in patients with a non-Q-wave and patients with a Q-wave infarction. In addition, the extent of cardiac adrenergic denervation was related to the infarct size in patients with a Q-wave infarction but not in patients with a non-Q-wave infarction.

3-Iodobenzylguanidine↗
PubMed1997

The effect of selective sympathetic denervation on pancreatic exocrine secretion.

The purpose of this study was to investigate the influence of selective sympathetic denervation of the rat pancreas on exocrine secretion and to study whether the observed effects were due to pancreatic trophism. Sprague-Dawley rats were divided into two groups. One group underwent selective sympathetic denervation by skeletonizing the superior and inferior pancreaticoduodenal and splenic arteries. The other group underwent simple laparotomy and served as controls. One week after the operation a catheter was introduced into the bile-pancreatic duct and pancreatic juice was collected at 30-min intervals for 4 h. The output of bicarbonate, total protein, amylase, trypsin, chymotrypsin, lipase, colipase and carboxyesterlipase were determined. Following denervation secretion of pancreatic enzymes was significantly enhanced compared with sham-operated animals. We did not find any signs of pancreatic trophism 1 week after denervation.

Amylases↗
PubMed1977

Lack of acquisition in dopamine denervated animals tested in an underwater Y-maze.

There are a number of conflicting reports in the literature on the ability of dopamine (DA) denervated animals to acquire various instrumental tasks, mostly conditioned avoidance responding. The interpretational difficulties stem partly from the difficulties to test an animal that is deficient in initiating voluntary movements and partly from the difficulties to produce complete DA denervations. We have tried to solve these problems by testing DA denervated animals in an underwater swim maze where even severely denervated animals will overcome their akinesia and swim the maze. 6-Hydroxydopamine was injected into the bundle of ascending DA axons in order to produce the best possible DA degeneration and the animals were tested as soon as the degeneration was complete (48 h) in order to avoid compensatory processes. We found that such animals were unable to acquire a brightness as well as a spatial discrimination task even when the experimental situation was such that they were able to overcome their difficulties to initiate voluntary movements. Possible explanations to the discrepancies between our studies and others are discussed.

Animals↗
PubMed1980

Synapse formation after injury in the adult rat brain: preferential reinnervation of denervated fimbrial sites by axons of the contralateral fimbria.

The dorsolateral quadrant of the lateral septal nucleus receives projections from both the ipsilateral and the contralateral fimbria. In the adult rat the effect of fimbrial lesions on synapse formation has been studied by a quantitative electron microscopic analysis of the various types of synapses present, using electron-dense degeneration to identify fimbrial fibre terminals. In this area, the fimbrial axons from both sides together account for about 30% of the total number of synapses and they terminate mainly on dendritic spines. The ipsilateral fimbria forms twice as many synapses as the contralateral fimbria. When one fimbria is cut and time left for the degeneration to be removed, the numbers of synapses are restored to normal levels and the remaining fimbria acquires, on both sides of the septum, a number of synapses equal to the sum of the two individual fimbria, This suggests that the axons of the surviving fimbria have completely reinnervated the denervated postsynaptic sites formerly occupied by the cut fimbria of the other side, effectively excluding non-fimbrial axon terminals, even though the latter constitute the majority (70%) of the synaptic terminals in the region. When both fimbria are cut the numbers of synapses are once again restored to normal levels. However, since there are now no fimbrial axons left, the denervated fimbrial postsynaptic sites must this time have been reinnervated by non-fimbrial axons. Reinnervation by non-fimbrial axons is numerically equally effective in reclaiming the denervated sites, although when compared to the reinnervation by fimbrial axons, the removal of degenerating terminals is somewhat slower, and among the reinnervating terminals there is a much higher incidence of axon terminals making more than one synaptic contact in the plane of section. Thus, fimbrial axons, when present, have the ability to exclude the reinnervation of denervated fimbrial sites by non-fimbrial axons, despite the fact that the latter are both more numerous and also clearly capable of reinnervating those sites when no fimbrial axons are present. Two possible mechanisms are discussed: a spatial preference based on the geometrical arrangements in the neuropil, and a temporal preference based on the relative rates of response of the fimbrial vs the non-fimbrial axons.

Animals↗
PubMed1991

Regional changes of striatal dopamine receptors following denervation by 6-hydroxydopamine and fetal mesencephalic grafts in the rat.

Young adult female rats received a 6-hydroxydopamine lesion in the left substantia nigra and, 3 weeks later, some of them were grafted with a cell suspension from the ventral mesencephalon of rat embryos (14-15 days old). Six months after transplantation, some grafted rats, following injection of amphetamine, had switched to turning only toward the intact side (type 1), whereas others turned toward the intact side only during the first half of the test (type 2). Levels of dopamine, dihydroxyphenylacetic acid and homovanillic acid were, respectively, 2%, 15% and 35% of the intact side in the denervated striatum of 6-hydroxydopamine rats. Dopamine concentrations were restored to 13% and 10% of the intact side in the grafted striatum of type 1 and type 2 animals, respectively. Levels of homovanillic acid were unchanged following grafts whereas those of dihydroxyphenylacetic acid increased by 209% and 247% in the grafted striatum of type 1 and type 2 animals, respectively. The ratios of dihydroxyphenylacetic acid/dopamine as well as homovanillic acid/dopamine were low in the intact striatum whereas they increased in the denervated striatum with or without graft. The tyrosine hydroxylase immunoreactivity decreased by about 80% in the denervated striatum of 6-hydroxydopamine rats. In type 1 rats, tyrosine hydroxylase immunoreactivity revealed that the graft was localized in the dorsomedial part of the denervated striatum, whereas in type 2 animals, it was also in the medial striatum but it overlapped the dorsal and ventral parts of it equally. D1 as well as D2 dopamine receptors were measured throughout the striatum (9.0-7.6 rostral-caudal coordinates), by autoradiography, using [3H]SCH 23390 (D1 antagonist) and [3H]spiperone (D2 antagonist) binding. Supersensitive D2 receptors were normalized in the dorso- and ventromedial parts of the grafted striatum. D2 receptor density was higher in type 2 than in type 1 rats, more specifically at 8.6-8.2 rostral-caudal coordinates, where the graft was. D1 receptor supersensitivity was modest compared to D2 receptors in the striatum of 6-hydroxydopamine rats and decreased following grafts. DA receptors changes in the striatum, following fetal mesencephalic grafts, may explain the behavioral recovery seen in grafted rats.

Amphetamine↗
PubMed1996

Coronary denervation attenuates coronary constriction induced by muscarinic receptor stimulation in pigs.

OBJECTIVES: We tested the hypothesis that coronary denervation attenuates the reactivity of the coronary vessel to cholinergic stimulation. METHODS: Heart rate, left ventricular (LV) pressure, LV dP/dt, coronary blood flow at the left anterior descending (LAD) coronary artery, and epicardial ECG mapping were measured before and after topical application of 1% methacholine to the LAD in 10 pigs anesthetized with alpha-chloralose (100 mg/kg, i.v.); these were compared with 10 other pigs submitted 2 weeks previously to a denervation of the LAD with phenol. Coronary denervation was confirmed in all cases by adrenergic histofluorescence and by acetyl-cholinesterase staining. Isolated LAD rings from 10 additional pigs (5 controls and 5 treated with phenol) were stimulated with endothelin-1 to verify whether phenol affected coronary reactivity to noncholinergic stimulation. RESULTS: Methacholine induced a fall in coronary blood flow (10.3 +/- 5.3 ml/min vs 4.8 +/- 6.2 ml/min, ANOVA: P < 0.001), a drop in systolic LV pressure (113 +/- 19 mmHg vs 93 +/- 19 mmHg, P < 0.001) and LV dP/dt (1608 +/- 363 mmHg/s vs 1203 +/- 302 mmHg/s, P = 0.02) and elevation of the ST segment (1.4 +/- 0.9 vs 11.1 +/- 4.7 mV, P < 0.001) in controls. These changes were not preceded by heart rate variations and were inhibited by atropine. As compared to controls, phenol-treated pigs showed a smaller decline in coronary blood flow (13.1 +/- 4.5 ml/min to 10.4 +/- 5.4 ml/min, P < 0.001), a lower drop in LV pressure (107 +/- 20 mmHg to 100 +/- 19.7 mmHg, P < 0.001) and lesser ST segment elevation (2.2 +/- 1.7 mV to 5.6 +/- 4.2 mV, P < 0.001). Isolated LAD rings contracted after exposure to endothelin-1 in both controls and phenol-treated pigs (3.5 +/- 0.7 g vs 2.4 +/- 1.0 g, P = 0.06). CONCLUSIONS: Coronary denervation attenuates coronary constriction induced selectively by direct muscarinic receptor stimulation in the in situ pig heart.

Animals↗
PubMed1980

Effects of sympathetic denervation or chronic reserpine on potassium (42K) and chloride (36Cl) efflux from guinea-pig vas deferens.

Potassium (42K) or chloride (36Cl) efflux curves were determined in guinea-pig vas deferens from control, reserpine-treated animals (1 mg/kg/day i.p. for 5 days), and from animals whose vas deferens had been sympathetically denervated 1 week before. Steady-state 42K turnover in control tissues was 0.0052 +/- 0.0002 min-1; neither reserpine treatment nor sympathetic denervation changed this parameter signicantly. Control 36Cl turnover was 0.058 +/- 0.002 min-1 and it was unaffected by either procedure. Methoxamine (3 x 10(-6) to 10(-4) M) induced dose-related increases in the fractional exchange of 42K and 36Cl. These were of greater magnitude after sympathetic denervation or reserpine treatment. Furtrethonium also produced dose-dependent increases in 42K efflux; its dose-response curve was shifted 2.6-fold to the left of the control curve by reserpine treatment. These results indicate that interruption of adrenergic transmission to the guinea-pig vas deferens is associated with increased changes in membrane permeability to Cl and possibly K in response to drug activation of alpha-adrenergic and cholinegic receptors. It is suggested that the supersensitivity phenomenon observed in the guinea-pig vas deferens after reserpine or sympathetic denervation is, in part, related to improved transduction of drug-receptor interaction into ionic permeability changes.

Animals↗
PubMed1989

Effects of imipramine and serotonin-2 agonists and antagonists on serotonin-2 and beta-adrenergic receptors following noradrenergic or serotonergic denervation.

The effects of chronic (14 day) administration of the tricyclic antidepressant imipramine, the serotonin-2 (5-HT2) antagonist ketanserin, and the serotonin agonist quipazine on 5-HT2 receptor binding parameters and 5-HT2-mediated behavior were examined in rats with or without prior serotonergic denervation [via 5,7-dihydroxytryptamine (5,7-DHT)] or noradrenergic denervation [via N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4)]. Chronic administration of imipramine, ketanserin, or quipazine produced a marked reduction in the number of 5-HT2 binding sites which was accompanied by reductions in the 5-HT2-mediated quipazine-induced head shake response. In animals receiving DSP4 or 5,7-DHT lesions and continuous vehicle treatment, beta-adrenergic receptor binding sites were significantly up-regulated while 5-HT2 receptor binding sites did not change. Imipramine normalized the lesion-induced increases in beta-adrenergic binding observed in DSP4 and 5,7-DHT-lesioned rats but failed to down-regulate beta-adrenergic binding sites below non-lesioned control levels. Chronic imipramine, ketanserin, and quipazine reduced quipazine-induced head shakes and down-regulated 5-HT2 binding sites in rats with noradrenergic denervation. While imipramine, ketanserin, and quipazine all down-regulated 5-HT2 binding sites in animals with serotonergic denervation, only imipramine's ability to reduce quipazine-induced head shakes was attenuated in 5,7-DHT-lesioned rats. The present results suggest that imipramine-induced down-regulation of 5-HT2 receptors may not involve presynaptic 5-HT mechanisms, and imipramine-induced alterations in 5-HT2 sensitivity as reflected in the quipazine-induced head shake may, in part, be influenced by beta-adrenergic receptors.

5,7-Dihydroxytryptamine↗
PubMed1983

Does contralateral circling involve action of drugs on hyposensitive striatal dopamine receptors in the hemisphere contralateral to denervation?

Rats receiving unilateral intrastriatal injections of 6-hydroxydopamine (6-OHDA) (3 x 16 micrograms, in the presence of tranylcypromine and desmethylimipramine (DMI), resulting in 84% dopamine depletion) exhibited contralateral asymmetry and circling behaviour on peripheral challenge with apomorphine or on unilateral intrastriatal injection of dopamine (into the denervated striatum) (resulting in a stable response after 8 days). The denervated striatum was markedly more sensitive to the effects of dopamine than the normal striatum, although dopamine failed to elicit a response from an intact striatum opposite to a denervation by 6-OHDA. Following unilateral striatal electrolytic lesions (resulting in a stable response after 6-8 days) the rats exhibited ipsilateral asymmetry and circling after the apomorphine challenge. Again, the striata opposite to the lesion failed to mediate a response to dopamine. The contralateral responses to apomorphine observed in animals lesioned with 6-OHDA were not enhanced when an electrolytic lesion was subsequently placed in the intact striatum, nor were the ipsilateral responses of lesioned rats to apomorphine enhanced when 6-OHDA was subsequently injected into the opposite striatum. All asymmetric and circling responses were sensitive to neuroleptics. Thus, it is concluded that a unilateral striatal lesion produced by 6-OHDA or electrolytic lesion can cause reduced functional dopaminergic activity in the opposing striatum. This dopaminergic hyposensitivity would facilitate a contralateral response initiated by hypersensitive mechanisms in the denervated striatum.

Animals↗
PubMed1984

Time-course in binding of [3H]dihydroergokryptine to total alpha and alpha1 adrenoceptors of cerebral cortex of rat after denervation by 6-hydroxydopamine.

In control rats and in rats after intraventricular injection of 6-hydroxydopamine, the total specific binding of [3H]dihydroergokryptine to membranes of the cerebral cortex was studied. The time course of the catecholaminergic denervation in its influence on total alpha-adrenoceptors, and on the binding to alpha 1-receptors was followed, after blocking the alpha 2, with yohimbine. Using displacement curves, 5 X 10(-7) M was determined as the concentration of yohimbine needed to differentiate alpha 1 from alpha 2-adrenoceptors. In control rats, the total binding showed a Bmax of 300 pmol/g protein and a KD of 1.9 nM with a single type of binding site. The binding of [3H]dihydroergokryptine that was not displaced by yohimbine represented about 70% of the total. Denervation by 6-hydroxydopamine produced, after two days, a decrease in total binding (P less than 0.01), followed by a progressive increase, that reached 41% above the control after 22 days (P less than 0.1). The alpha 1-sites were reduced after two days and later increased to reach 63% above the control (P less than 0.01) at 22 days. These results suggest that after catecholaminergic denervation there is an increase in total alpha-adrenoceptors and in alpha 1-receptors in membranes of the cerebral cortex. These changes could be correlated with a possible post-synaptic supersensitivity after denervation.

Animals↗
PubMed1994

Glossopharyngeal denervation alters responses to nutrients and toxic substances.

Functional roles of the glossopharyngeal (GL) nerve on food and fluid intake were studied by examining effects of the GL denervation on two biologically different activities induced by specific diets using mice and rats. First, we examined whether GL section alters the acceptability of a bitter tasting essential amino acid, L-lysine (Lys), by Lys-deficiency in mice. The aversion threshold for Lys, normally about 3 uM in mice, increased to about 300 uM when mice were fed the Lys-deficient diet for 10 days. This increase of the Lys aversion threshold (increase of acceptability for Lys) by Lys-deficiency was also evident in mice with the chorda tympani denervation but was not observed in mice with the GL denervation. Next, we examined whether GL section alters the induction of a salivary protein, cystatin S (a cysteine proteinase inhibitor), by a diet containing papain (a cysteine proteinase) in rats. GL denervation largely inhibited the induction of cystatin S in the rat submandibular glands by papain. These results collectively suggest that chemosensory information conveyed by the GL nerve plays important roles on recognition of both nutrient and toxic compounds in the diet and induction of biological responses that protect the animal from both nutritional deficiency and exogenous toxic compounds.

Animals↗
PubMed1987

Postnatal development of the lung following denervation.

We asked to what extent pulmonary innervation influences the postnatal development of the lung. To this end we performed cervical vagotomy and sympathectomy either on the right or on the left side in young rats and rabbits and rats after weaning. One to four weeks later we examined the lungs of the denervated side, the contralateral intact side of the same animal, and sham-operated controls. Dry lung weight, lung volume and the size of subpleural alveoli were not different among the three groups. Lung mechanical properties (static and dynamic lung compliances, lung resistance, frequency dependence of compliance), measured in rabbits, were also not different among groups of lungs, suggesting that neither central nor peripheral airways were markedly affected by the denervation. The breathing pattern, measured in the rats after weaning, was characterized by a larger tidal volume in the denervated animals than in controls, as expected after the partial pulmonary afferent denervation. The absence of major structural and functional changes in the lungs of these animals suggests that an increase in the mechanical stretch to the lung above that normally occurring during resting breathing does not influence the lung structure. We conclude that pulmonary innervation does not play an important role in the postnatal development of the lung.

Animals↗
PubMed1987

Differences in respiratory patterns after acute and chronic pulmonary denervation.

The role of pulmonary vagal information in the control of respiratory patterns was assessed in awake and anaesthetised rats in which pulmonary denervation was effected by bilateral cervical vagotomy or by right cervical vagotomy combined with left pneumonectomy or left intrathoracic vagotomy. Acute denervation led to increases of tidal volume (VT), inspiratory duration (TI) and expiratory duration (TE) in both awake and halothane anaesthetised animals; in awake rats the increase of TE rapidly subsided. Chronic pulmonary denervation produced markedly smaller increases of VT and TI and no change of TE from control values. In hypercapnia, awake animals with combined pneumonectomy and vagotomy consistently increased respiratory frequency by reductions in TI and TE; awake animals with combined intrathoracic and cervical vagotomy showed no increase in f because decreases in TI offset increases in TE; in anaesthetised rats with acute bilateral cervical vagotomy there was a consistent fall in respiratory frequency due to an expiratory pause. The results demonstrate that (1) the role of vagal activity in the production of respiratory patterns is unlikely to be accounted for solely in terms of influences arising from pulmonary stretch receptors; (2) vagal influences of TE are transitory; (3) under halothane anaesthesia hypercapnia induces an expiratory pause; and (4) the combination of pneumonectomy with contralateral vagotomy makes possible studies in awake rats although pulmonary denervation is less complete than with bilateral intrathoracic vagotomy.

Animals↗