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PubMed1999

Autonomic denervations influence ocular dimensions and intraocular pressure in chicks.

Choroidal thickness and axial eye length in the chick undergo day/night fluctuations that can also be modulated by visual experience. In the present study, we tested the effect of parasympathetic and sympathetic denervations on both day/night and image dependent changes in ocular dimensions. We also correlated such changes with fluctuations in intraocular pressure. Parasympathectomy influenced choroidal thickness and its day/night fluctuation, but had no effect on vision dependent choroidal thickness modulation. Parasympathectomy also influenced-to a lesser extent-axial length and reduced the axial growth response to form vision deprivation. Sympathectomy had little effect on ocular dimensions, but reduced the day/night differences in intraocular pressure. We conclude that (a) the parasympathetic nervous system influences both choroidal thickness and axial length and participates in the neural control mechanism leading to form deprivation myopia and, (b) the day/night fluctuations of choroidal thickness and axial length are unlikely to be explained by fluctuations in intraocular pressure. For the regulation of choroidal thickness, we hypothesize the existence of two independent mechanisms. One involves the parasympathetic nervous system; it influences the day/night choroidal thickness fluctuation. The other uses a separate pathway and is driven by visual input.

Animals↗
PubMed1985

Changes in the vascular bed of submandibular glands after chronic autonomic denervation.

The effect of chronic sympathetic denervation (SCG) or parasympathetic decentralization (PSD) on the vascularization of the submaxillary gland (SM) of rat was studied in connection with morphological and functional changes. The resection of the superior cervical ganglion or the section of the chorda tympani was performed in adult male Wistar rats prior to the injection of Microfil MV Orange 3.25 cm3/kg. Once dissected, the glands were made transparent in increasing concentrations of methyl salicylate--alcohol. Three longitudinal sections were performed and the central one was projected in an automatic image analyzer (Kontron Zeiss), where vascular length and vascular volume were measured. Another group of animals was injected with Microfil after having received an injection of noradrenaline (10 g/kg) in SCG glands and methacholine in PSD glands. In SCG glands, vascular length underwent a 60% increase and the vascular volume increased from 0.26 +/- 0.15 cu mm/cu mm in controls to 0.54 +/- 0.15 cu mm/cu mm in SCG. The intravenous administration of noradrenaline prior to Microfil injection reverted the phenomenon. PSD caused a reduction of the vascular bed which resulted mainly in increased vascular volume. The administration of methacholine (10 g/kg) reverted the-response. It was concluded that SCG induced a loss of the existing vasoconstrictor tone, thus causing increase of vascular length and volume (passive vascular dilatation). Increased vascular volume after chronic PSD is compatible with vascular stasis and the absence of variations in vascular volume after the injection of methacholine would indicate that in the SM glands of rats there is no vascular dilatation tone.

Animals↗
PubMed1989

Autonomic denervation effects on the kallikrein and striated duct cells of the rat and cat submandibular glands.

Chronic preganglionic parasympathetic denervation in the rat submandibular gland increases kallikrein activity whereas post ganglionic sympathetic denervation has no effect. Ultrastructural morphology of the striated duct following either denervation remains unaltered. Chronic preganglionic parasympathetic denervation in the cat gland dramatically reduces kallikrein activity and causes disruption and disappearance of subcellular organelles. Chronic sympathetic denervation has no effect.

Animals↗
PubMed1989

Protection against autonomic denervation following acute myocardial infarction by preconditioning ischemia.

To examine the effects of ischemic preconditioning on efferent autonomic responses following acute transmural myocardial ischemia/infarction (MI), the time course and extent of efferent sympathetic and vagal denervation were compared between control dogs that received a one-stage sustained coronary occlusion and preconditioned dogs that received four 5-minute coronary occlusions separated by 5 minutes of reperfusion before sustained occlusion. Effective refractory periods (ERP) basal and apical to MI were determined in the baseline state and during neural stimulation before and after preconditioning occlusions and 20, 60, 120, and 180 minutes after sustained occlusion by ligature ligation of diagonal branches of the left anterior descending coronary artery. In 10 control dogs with transmural MI, ERP shortening induced by bilateral ansae subclaviae stimulation (4-msec pulses, 2-4 Hz and 2-4 mA) was unchanged at basal sites but was attenuated at apical sites. Four of 40 apical test sites exhibited efferent sympathetic denervation (less than or equal to 2 msec shortening) 20 minutes after sustained occlusion. Thirteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, ERP shortening at apical sites was unchanged after preconditioning occlusions and during the first 60 minutes of sustained ischemia but was attenuated at 120 minutes. Three of 40 apical test sites became denervated during a 3-hour period. The cumulative percentage of denervated apical test sites was significantly less in the preconditioned group compared with the control group (p = 0.006) despite a comparable degree of subepicardial involvement in the MI (8.2 +/- 1.0% vs. 8.4 +/- 1.4%, the ratio to the left ventricular circumference, mean +/- SEM). In 11 control dogs tested for efferent vagal response after MI, ERP prolongation induced by bilateral vagal stimulation (4-msec pulses, 20 Hz with current strength 0.05 mA greater than that required to produce asystole) was unchanged at basal sites, but was attenuated at apical sites, and five of 44 test sites exhibited denervation (less than or equal to 1 msec prolongation) 20 minutes after sustained coronary occlusion. Fourteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, vagally induced ERP prolongation was unchanged both at basal and apical sites, and none of 36 apical test sites exhibited denervation after preconditioning and during a 3-hour period of sustained coronary occlusion (p less than 0.001 vs. control group) despite a comparable degree of subendocardial involvement in the MI (11.8 +/- 0.8% vs. 11.9 +/- 1.3%).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2003

Autonomic denervation after the Maze procedure.

The Maze III procedure is a surgical operation for curative treatment of AF. The procedure is extensive, however, with multiple incisions in both atria, and its effects on autonomic regulation of the heart rhythm are not known. This study comprises 17 patients, 10 with paroxysmal AF and 7 with chronic AF, who had no concurrent cardiac disease known to affect heart rate variability (HRV). A 24-hour Holter recording was performed preoperatively and 2 months (early) and 7 months (late) after surgery, for analysis of HRV in the time and frequency domains. Early after the Maze procedure all HRV components were markedly reduced compared to baseline (mean +/- 1 SD): SDNN 73 +/- 13 versus 148 +/- 50 (ms), total power 168 +/- 126 versus 560 +/- 1567 (ms2), low frequency (LF) power 47 +/- 67 versus 826 +/- 677 (ms2), high frequency (HF) power 47 +/- 40 versus 678 +/- 666 (ms2), and LF:HF 1.22 +/- 0.9 versus 2.55 +/- 1.4. Late after the Maze procedure all variables were still reduced. Only total power increased significantly between early and late follow-up (168 +/- 126 vs 496 +/- 435 ms2). Late after Maze surgery, values of the different HRV components did not differ between the patients with paroxysmal AF and chronic AF. Early after the Maze procedure there is a marked decrease of all HRV components, which is maintained 7 months after surgery, a pattern consistent with denervation of the heart.

Atrial Fibrillation↗
PubMed1984

Evaluation of topical phenol as a means of producing autonomic denervation of the liver.

Topical application of 90% phenol around the bile duct, portal vein, and hepatic artery, as well as along each of the three hepatic ligaments was tested for effectiveness of rapid and chronic denervation in cats. Because phenol produces nonselective nerve degeneration, it was assumed that proof of functional sympathectomy was adequate proof of disruption of parasympathetic and afferent nerves as well. Functional sympathetic neurons were evaluated by measuring physiological responses to direct electrical stimulation of the anterior hepatic plexus. Acute or rapid denervation was assessed by the degree of rise in portal blood pressure produced by nerve stimulation. Complete denervation appeared within 20 min and was still present by 80 min postapplication. Chronic denervation was tested by applying the phenol and recovering the cats for 6-14 days. An equal number (n = 6) of sham-denervated cats were compared. Phenol denervation did not alter basal glucose, insulin or glucagon levels, hematocrit, blood pressure, or hepatic glycogen levels. These variables are a good index of stress and metabolic status. Nerve stimulation in the chronic sham group raised portal pressure, arterial pressure, and blood glucose levels, whereas the chronic-denervated group showed no responses. The health of the two groups appeared normal with the sole difference being that the painted tissues were mildly discolored and more adhesions appeared in the phenol-denervated set. Thus phenol is a useful tool for producing hepatic denervation. It is less traumatic, faster, and more certain than surgical denervation. In addition, the hepatic lymphatics can be preserved using the topical application of phenol.

Administration, Topical↗
PubMed2006

Impact of liver transplantation on cardiac autonomic denervation in familial amyloid polyneuropathy.

Familial amyloid polyneuropathy (FAP) is a rare and severe hereditary form of amyloidosis, due to the deposition of a genetic variant transthyretin essentially produced by the liver, and characterized by both sensorimotor and autonomic neuropathy. Liver transplantation (LT) is the most effective treatment to stop the progression of the disease. Cardiac amyloid infiltration is usually associated with cardiac denervation, restrictive cardiomyopathy, conduction disturbances, and sometimes sudden death. Whether the cardiac involvement related to amyloid deposition may be altered after LT remains unclear. We conducted the present study to define the outcome of cardiac involvement after LT in 31 patients with FAP (age, 39 +/- 12 yr). Patients were evaluated before and after LT (24 +/- 15 mo). Cardiac sympathetic denervation was assessed by both iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy and heart rate variability (HRV) analysis. The scintigraphic importance of sympathetic denervation was evaluated globally on planar imaging using heart-to-mediastinum activity ratio (H/M) measured 4 hours after injection, and regionally using single-photon emission tomography (SPET) imaging. Amyloid myocardial infiltration was assessed by echocardiography. Diffuse sympathetic denervation was found when using cardiac MIBG planar imaging in patients evaluated before LT and compared with 12 control subjects (H/M: 1.45 +/- 0.29 vs. 1.98 +/- 0.35, p < 0.001). On SPET images, defects were diffuse in 12 patients and focal in 19 patients, with predominance at the inferior and apical segments. No change in sympathetic innervation was found in patients after LT as assessed either with planar imaging (H/M after LT: 1.46 +/- 0.28, p = not significant vs. H/M before LT) or with SPET imaging. HRV nonspectral indexes showed that the standard deviation of all cycles was significantly lower in patients compared with control subjects, and remained unchanged after LT. Conduction disturbances and ventricular arrhythmias were associated with low cardiac MIBG uptake, and progressed after LT. The left ventricular wall was slightly thickened in patients, and a further increase was observed after LT (posterior wall from 9.2 +/- 1.8 to 10.1 +/- 2.3 mm, p = 0.02; septal wall from 10.6 +/- 2.7 to 12.1 +/- 4, p = 0.046). Neurologic status stabilized in 26 patients, but worsened in the 5 patients who had the most severe cardiac sympathetic denervation before LT as measured by MIBG imaging. The magnitude of the cardiac sympathetic denervation remained stable 2 years after LT in patients with FAP, whereas the cardiac amyloid infiltration progressed. The importance of cardiac sympathetic denervation found in FAP patients before LT was associated with a neurologic worsening after LT.

3-Iodobenzylguanidine↗
PubMed2000

Augmented sympathetic response to bradykinin in the diabetic heart before autonomic denervation.

We studied whether diabetes mellitus affects the bradykinin (BK)-induced release of norepinephrine (NE) from rat cardiac sympathetic endings in situ. Three groups were studied. Group A (n=12) was rendered diabetic with streptozotocin (STZ), group B (n=13) received STZ and insulin, and group C (n=14) received citrate buffer only. NPH insulin was given to group B from day 7 after STZ. Atria were paced (3Hz) with rectangular voltage pulses at mechanical threshold intensity (0.15 V/cm). The release of NE was assessed through its effects on contractile force in the presence of atropine (1 micromol/L). Intensifying the field stimulation above the neural threshold ( approximately 0.4 V/cm) produced a graded positive inotropic effect that was due to the release of NE from sympathetic nerve endings. The additional effect of 0.1 micromol/L BK on the force of contraction was determined at half-maximal neural stimulation (ie, at approximately 0.65 V/cm). Then, after washing out BK and lowering the stimulation intensity to mechanical threshold, a cumulative dose-response curve for added NE was generated, allowing the positive inotropic effects of neural stimulation (with or without BK) to be expressed in terms of an equivalent inotropic concentration of added NE ([NE(eq)]). Neural stimulation, in the absence of BK, gave an [NE(eq)] of 32+/-3 nmol/L in group A, 44+/-6 nmol/L in group B, and 37+/-6 nmol/L in group C. BK increased [NE(eq)] by a factor of 6.2+/-0.9 in group A, 4.5+/-0.5 in group B, and 3.7+/-0.3 in group C. This factor was greater in group A than in group C but indistinguishable in groups B and C. Atria from normal and diabetic rats were incubated in (3)[H]NE for 60 minutes. Excess tracer was removed, and atria were stimulated during a series of 1-minute episodes at half-maximal neural stimulation to cause exocytotic (3)[H]NE release. BK augmented (3)[H]NE release in normal (n=4) and in diabetic (n=4) atria. This BK-induced increase of (3)[H]NE overflow (expressed as a fraction of tissue (3)[H]NE radioactivity) was 4 times greater in diabetic than in normal preparations. The response to BK in releasing sympathetic neurotransmitter is augmented in diabetic rats, recovering in a manner dependent on insulin.

Animals↗
PubMed1992

Nerve growth factor effects on inhibition by submandibular gland ablation or autonomic denervation of activity-induced parotid growth.

Present data confirm our earlier report that an increase in [3H]thymidine incorporation into DNA of parotid gland occurs with reintroduction of solid chow to rats previously maintained on liquid diet; if, however, the submandibular-sublingual glands are removed prior to the dietary substitution, the increase is prevented (present data and [19]). In addition, present data show that administration of nerve growth factor (NGF) to partially sialoadenectomized rats during the 2-day period of dietary change from liquid to solid diet restores thymidine values to the high levels observed following the dietary change in intact animals. However, the increase in gland size that accompanied the change in dietary consistency was not prevented by prior submandibular gland ablation, and administration of NGF had no influence on gland size or cell size. The removal of both the sympathetic and parasympathetic nerves to the parotid gland prior to the dietary manipulation also suppressed [3H]thymidine incorporation into parotid, and values did not differ from chow controls. The data show that NGF, a submandibular growth factor, has a prominent role in regulation of the autonomically-mediated hyperplastic response. However, neither the submandibular gland nor NGF has an important role in regulation of the increase in gland size that also accompanies the dietary change.

Aging↗
PubMed1994

Extent of cardiac autonomic denervation in relation to angina on exercise test in patients with recent acute myocardial infarction.

According to the current concept, anginal pain results from stimulation of sympathetic nerves within the heart. In this study, we evaluated the role of cardiac adrenergic denervation in exercise-induced angina pectoris in 15 men with recent acute myocardial infarction. Before discharge from the hospital, the patients were subjected to a symptom-limited exercise test. Three months after the infarction, cardiac scintigraphic studies using I-123 metaiodobenzylguanidine (MIBG), I-123 paraphenylpentadecanoic acid (pPPA), and Tc-99m sestamibi (MIBI) were performed in order to determine the extent of denervated myocardium, the size of infarction, and myocardium with reduced perfusion, respectively. MIBG defect (17.2 +/- 7.6% of left ventricular mass) (defect defined as an activity distribution < or = 30% of the maximal myocardial activity) was larger than pPPA defect (8.3 +/- 8.8%, p < 0.001) in all patients, which indicates that the area of myocardial necrosis was surrounded by viable myocardium with sympathetic denervation. The extent of viable but denervated myocardium was significantly greater in patients who developed angina pectoris than in patients without angina pectoris during the early exercise test (13.3 +/- 4.4% vs 5.0 +/- 2.4%, p < 0.001). In addition, patients with silent ischemia tended to have smaller areas of viable but denervated myocardium than patients with painful ischemia (5.7 +/- 3.8% vs 13.8 +/- 5.1%, p = 0.07). Thus, contrary to expectations, the extent of viable but denervated myocardium seems to be associated with increased pain sensitivity in patients with recent myocardial infarction.

Adrenergic Fibers↗