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PubMed1989

Parasagittal thalamic knife-cuts and cardiac changes.

Rabbits received knife-cuts either medial or lateral to the mediodorsal nucleus of the thalamus (MD), and had stimulating electrodes implanted in MD. These animals were compared to animals with sham knife-cuts for (1) the cardiac component of the orienting reflex (OR) to novel tone stimuli; (2) differential pavlovian heart rate (HR) conditioning, utilizing tones of different frequencies as CSs and paraorbital shock as the US; and (3) heart rate, blood pressure, electromyographic activity, and respiration changes elicited by electrical stimulation in MD. Medial knife-cuts led to faster habituation of the OR, and to somewhat attenuated HR conditioning, but had no effect on stimulation-elicited changes. Lateral knife-cuts, on the other hand, enhanced the stimulation-elicited HR response, but had little effect on the HR OR. The HR CR was unaffected by lateral cuts during an initial conditioning session, but was attenuated in both knife-cut groups during a second session, compared to sham control animals.

Afferent Pathways↗
PubMed1994

Assessment of local sympathetic function in patients with erectile dysfunction.

Fifty men with erectile dysfunction (ED) were urologically investigated for autonomic deficit by evaluation of the sympathetic skin response at the penis. They were additionally subjected to thorough urological, vascular, psychiatric and neurological examinations, and well-established neurophysiological tests of the somatosensory, sympathetic, and parasympathetic function. Patients with clinical evidence of neurological deficit showed abnormal results (68%) in at least one test of the autonomic nervous system. The sympathetic skin response at the penis was absent in 11 cases (37%) with clinical evidence of neuronal aetiology of the erectile dysfunction and was normal in all cases with positive evidence of a psychiatric origin of erectile dysfunction and no clinical indication of a neuronal deficit. Moreover, the sympathetic skin response at the penis was abnormal in three cases with normal results in the other neurophysiological tests. The results emphasize that the local sympathetic skin response at the penis is a useful extension of autonomic testing in ED patients since this method tests local sympathetic pathways and is sometimes the only evidence for autonomic deficit. From a clinical viewpoint, the sympathetic skin response at the penis is a very simple and time-saving neurophysiological method suitable for clinical routine and also for the investigation of outpatients.

Adult↗
PubMed2006

Autonomic dysreflexia after spinal cord injury: central mechanisms and strategies for prevention.

Spinal reflexes dominate cardiovascular control after spinal cord injury (SCI). These reflexes are no longer restrained by descending control and they can be impacted by degenerative and plastic changes within the injured cord. Autonomic dysreflexia is a condition of episodic hypertension that stems from spinal reflexes initiated by sensory input entering the spinal cord caudal to the site of injury. This hypertension greatly detracts from the quality of life for people with cord injury and can be life-threatening. Changes in the spinal cord contribute substantially to the development of this condition. Rodent models are ideal for investigating these changes. Within the spinal cord, injury-induced plasticity leads to nerve growth factor (NGF)-dependent enlargement of the central arbor of a sub-population of sensory neurons. This enlarged arbor can provide increased afferent input to the spinal reflex, intensifying autonomic dysreflexia. Treatments such as antibodies against NGF can limit this afferent sprouting, and diminish the magnitude of dysreflexia. To assess treatments, a compression model of SCI that leads to progressive secondary damage, and also to some white matter sparing, is very useful. The types of spinal reflexes that likely mediate autonomic dysreflexia are highly susceptible to inhibitory influences of bulbospinal pathways traversing the white matter. Compression models of cord injury reveal that treatments that spare white matter axons also markedly reduce autonomic dysreflexia. One such treatment is an antibody to the integrin CD11d expressed by inflammatory leukocytes that enter the cord acutely after injury and cause significant secondary damage. This antibody blocks integrin-mediated leukocyte entry, resulting in greatly reduced white-matter damage and decreased autonomic dysreflexia after cord injury. Understanding the mechanisms for autonomic dysreflexia will provide us with strategies for treatments that, if given early after cord injury, can prevent this serious disorder from developing.

Afferent Pathways↗
PubMed1993

Localization of NADPH-diaphorase in pelvic afferent and efferent pathways of the rat.

The NADPH diaphorase histochemical reaction was used in combination with retrograde axonal transport of Fluorogold (FG) from the major pelvic ganglion (MPG) to determine if NADPH diaphorase is contained within afferent and preganglionic efferent pathways to pelvic visceral organs. In L6 and S1 dorsal root ganglia, 68.5% and 62.2%, respectively, of FG-labeled afferent neurons were NADPH-diaphorase positive. In the sacral parasympathetic nucleus (SPN) of the L6 and S1 spinal cord segments, 49.4% and 51.7%, respectively of FG labeled preganglionic efferent neurons were NADPH-diaphorase positive. NADPH-diaphorase-positive neurons were also observed in laminae I and II of the dorsal horn, around the central canal and in the dorsal commissure. In addition, fiber-like NADPH diaphorase staining was present in superficial dorsal horn, Lissauer's tract and the lateral edge of the dorsal horn extending into the region of the SPN. If NADPH diaphorase activity in neurons does indicate a physiological function of nitric oxide, then nitric oxide may have a role as a neuromodulator or neurotransmitter within visceral afferent and preganglionic efferent pathways to the pelvic viscera in the rat.

Afferent Pathways↗
PubMed1984

[Sweating-related tears--a new syndrome?].

Two years after operative correction of a middle third fracture of the face, a patient suffered unilateral tearing and homolateral rhinorrhea as soon as he started sweating. This is explained by abnormal regeneration of autonomic nerve fibres. The possible anatomic pathways are discussed and compared with similar syndromes in the literature.

Adult↗
PubMed2000

Abnormal cerebral processing of oesophageal stimuli in patients with noncardiac chest pain (NCCP).

In noncardiac chest pain (NCCP), altered visceral perception may result from abnormal cerebral processing of sensory input rather than abnormalities of afferent pathways. However, the interactions between symptoms, autonomic function and oesophageal stimuli are poorly studied. Oesophageal stimulation elicits reproducible cortical evoked potentials [CEP] and modulates heart rate variability via vagal pathways, as visible on power spectrum analysis of heart rate variability [PS-HRV]. These methods are increasingly used to study the function of visceral afferent neural pathways in human. The aim of this study was to compare EP and PS-HRV during oesophageal stimuli in NCCP and controls. Twelve healthy volunteers (one female, 11 male; aged 24-51 years; mean 32 +/- 8 years), and eight NCCP patients (three female, five male; age range 26-58, mean 40.5 +/- 10 years) were studied. Electrical oesophageal stimulation (EOS; 200 microseconds, 0.2 Hz, 25 stimuli) was applied to the oesophageal wall 5 cm above the lower oesophageal sphincter (LOS), and perception thresholds (measured in mA) determined. EP responses were recorded using 22 standard electroencephalogram scalp electrodes. Autonomic activity was assessed using PS-HRV, before, during, and after oesophageal stimulation. Measured PS-HRV indices included high frequency (HF; 0. 15-0.5 Hz) and low frequency (LF; 0.06-0.15 Hz) power, respectively, assessing vagal and sympathetic activity, and the LF/HF ratio. EOS perception occurred at lower thresholds in NCCP than in controls (3. 6 +/- 1 vs. 7.8 +/- 2 mA, P < 0.05). EP amplitude was greater (13 +/- 2 vs. 6 +/- 1 microV, P < 0.0001), and latency longer in controls vs. NCCP (191 +/- 7 ms vs. 219 +/- 6 ms, P < 0.001). In NCCP, EOS decreased sympathetic outflow (low frequency peak on PS-HRV) and increased cardiovagal activity (high frequency peak, P < 0.02) to a significantly higher degree in comparison with controls. During EOS, heart rate decreased in NCCP from 68 vs. 62 beats min-1 (P < 0.003) but not in controls. In NCCP patients, EOS was perceived at lower intensities and was associated with a greater cardiovagal reflex response. EP responses associated with EOS were smaller in NCCP than in controls, suggesting that an increased perception of oesophageal stimuli results from an enhanced cerebral processing of visceral sensory input in NCCP, rather than from hyperalgesic responses in visceral afferent pathways.

Adult↗
PubMed2002

A characterization of the effects of Dpp signaling on cell growth and proliferation in the Drosophila wing.

Cell proliferation and patterning must be coordinated for the development of properly proportioned organs. If the same molecules were to control both processes, such coordination would be ensured. Here we address this possibility in the Drosophila wing using the Dpp signaling pathway. Previous studies have shown that Dpp forms a gradient along the AP axis that patterns the wing, that Dpp receptors are autonomously required for wing cell proliferation, and that ectopic expression of either Dpp or an activated Dpp receptor, Tkv(Q253D), causes overgrowth. We extend these findings with a detailed analysis of the effects of Dpp signaling on wing cell growth and proliferation. Increasing Dpp signaling by expressing Tkv(Q253D) accelerated wing cell growth and cell cycle progression in a coordinate and cell-autonomous manner. Conversely, autonomously inhibiting Dpp signaling using a pathway specific inhibitor, Dad, or a mutation in tkv, slowed wing cell growth and division, also in a coordinate fashion. Stimulation of cell cycle progression by Tkv(Q253D) was blocked by the cell cycle inhibitor RBF, and required normal activity of the growth effector, PI3K. Among the known Dpp targets, vestigial was the only one tested that was required for Tkv(Q253D)-induced growth. The growth response to altering Dpp signaling varied regionally and temporally in the wing disc, indicating that other patterned factors modify the response.

Animals↗
PubMed1980

Inhibition and facilitation in parasympathetic ganglia of the urinary bladder.

Neurons in vesical parasympathetic ganglia receive excitatory and inhibitory inputs from both divisions of the autonomic nervous system. Sacral parasympathetic pathways (cholinergic) provide the major excitatory input to these ganglia via activation of nicotinic receptors. Parasympathetic pathways also activate muscarinic inhibitory and excitatory receptors, which may exert a modulatory influence on transmission. Cholinergic transmission is relatively inefficient when preganglionic nerves are stimulated at low frequencies (< 1 Hz). However, excitatory postsynaptic potentials (EPSPs) and postganglionic firing markedly increase during repetitive stimulation at frequencies of 1-10 Hz. It is concluded that enhanced transmitter release accounts for the temporal facilitation and that vesical ganglia function as "high pass filters" that amplify the parasympathetic excitatory input to the detrusor muscle during micturition. Transmission in vesical ganglia is also sensitive to adrenergic inhibitory and facilitatory synaptic mechanisms elicited by efferent pathways in the hypogastric nerves. The effects of exogenous norepinephrine indicate that adrenergic inhibition is mediated by alpha receptors and reflects primarily a presynaptic depression of transmitter release although postsynaptic adrenergic hyperpolarizing and depolarizing effects have also been noted. Adrenergic facilitation is mediated by beta receptors as well as unidentified receptors. Norepinephrine also can inhibit or excite spontaneously active neurons in vesical ganglia. The existence of inhibitory and facilitatory synaptic mechanisms in vesical ganglia provides the basis for a complex ganglionic modulation of the central autonomic outflow to the bladder.

Animals↗
PubMed2006

calderón encodes an organic cation transporter of the major facilitator superfamily required for cell growth and proliferation of Drosophila tissues.

The adaptation of growth in response to dietary changes is essential for the normal development of all organisms. The insulin receptor (InR) signalling pathway controls growth and metabolism in response to nutrient availability. The elements of this pathway have been described, although little is known about the downstream elements regulated by this cascade. We identified calderón, a gene that encodes a protein with highest homology with organic cation transporters of the major facilitator superfamily, as a new transcriptional target of the InR pathway. These transporters are believed to function mainly in the uptake of sugars, as well as other organic metabolites. Genetic experiments demonstrate that calderón is required cell autonomously and downstream of the InR pathway for normal growth and proliferation of larval tissues. Our results indicate that growth of imaginal cells may be modulated by two distinct, but coordinated, nutrient-sensing mechanisms: one cell-autonomous and the other humoral.

Amino Acid Sequence↗
PubMed2005

Glutathione-S-transferase M1, obesity, statins, and autonomic effects of particles: gene-by-drug-by-environment interaction.

RATIONALE: Air pollution by particulate matter (PM) has been associated with cardiovascular deaths, although the mechanism of action is unclear. One proposed pathway is through disturbances of the autonomic control of the heart. OBJECTIVES: We tested the hypothesis that such disturbances are mediated by PM increasing oxidative stress by examining the association between PM and the high-frequency (HF) component of heart rate variability as modified by the presence or absence of the allele for glutathione-S-transferase M1 (GSTM1) and the use of statins, obesity, high neutrophil counts, higher blood pressure, and older age. METHODS: We examined the association between particles less than 2.5 microM in aerodiameter (PM2.5) and HF in 497 participants in the Normative Aging Study, using linear regression controlling for covariates. MAIN RESULTS: A 10-microg/m3 increase in PM2.5 during the 48 h before HF measurement was associated with a 34% decrease in HF, 95% confidence interval (-9%, -52%), in subjects without the allele, but had no effect in subjects with GSTM1 present. Among GSTM1-null subjects, the use of statins eliminated the effect of PM2.5. Obesity and high neutrophil counts also worsened the PM effects with or without GSTM1. CONCLUSION: The effects of PM2.5 on HF appear to be mediated by reactive oxygen species. This may be a key pathway for the adverse effects of combustion particles.

Age Factors↗
PubMed1987

Transient requirement for prolactin as a growth initiator following treatment of autonomous Nb2 node rat lymphoma cell cultures with butyrate.

A previous study described the development of cultures of Nb2 node rat lymphoma cells which specifically require a lactogenic hormone, e.g., prolactin (PRL), as a growth factor. In the present study, sublines of these cultures have been established, including clones, which do not depend on exogenous lactogens for growth; the cells do not appear to produce autocrine, PRL-like substances. Although these autonomous cells grew readily in the complete absence of lactogens, their growth rate was stimulated (up to approximately 30%) by PRL concentrations greater than or equal to 0.1 ng/ml. When cultures of the lactogen-dependent and of the cloned, autonomous lymphoma cells were incubated for 3 days with sodium n-butyrate (NaBT; 2 mM), cells were arrested in the G1 phase of the cell cycle, as shown by flow cytometric analysis. A substantial proportion of the G1-arrested cells was viable and readily resumed growth, within 1 day, when transferred to NaBT-free medium containing PRL (1-100 ng/ml). The resumption of growth of the cells from the lactogen-dependent cultures was critically dependent on PRL; in its absence cells lysed. Surprisingly, the rapid recovery of the cells from the lactogen-independent cultures also depended on the presence of PRL in the medium; in its absence growth did not resume for at least 2.3 days. The acquired need of the NaBT-treated, autonomous cells for PRL was only transient, since such cells reverted fully to the PRL-independent state within about 3 days of culturing in PRL-containing, NaBT-free medium. It is proposed, as a working hypothesis, that the autonomous lymphoma cells can be mitogenically activated by two different pathways, one requiring exogenous lactogens and another which is independent of lactogens; the latter pathway recovers much more slowly from the treatment with NaBT than the lactogen-dependent pathway. This model could explain the sensitivity of the autonomous lymphoma cells to PRL and their transient dependency on exogenous lactogens during their recovery from NaBT treatment. NaBT would appear to be a useful agent for studying the mechanism(s) by which the autonomous lymphoma cells circumvent the need for mitogenic lactogens.

Animals↗
PubMed1994

Differential effect of esmolol on the fast and slow AV nodal pathways in patients with AV nodal reentrant tachycardia.

INTRODUCTION: AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting ("slow") pathway and retrograde conduction over a rapidly conducting ("fast") pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. METHODS AND RESULTS: Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 micrograms/kg for 1 minute, 150 micrograms/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 micrograms/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 +/- 75 msec at baseline to 453 +/- 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 +/- 26 msec to 310 +/- 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 +/- 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 +/- 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 +/- 46 msec to 376 +/- 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). CONCLUSION: The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.

Adrenergic beta-Antagonists↗
PubMed2004

Nitric oxide and thyroid gland: modulation of cardiovascular function in autonomic-blocked anaesthetized rats.

We have previously reported that acute administration of N(G)-nitro-l-arginine methyl ester (L-NAME) increases the mean arterial pressure (MAP) and heart rate (HR) in autonomic-blocked (CAB) anaesthetized rats. In the present study we examined whether thyroid and adrenal glands are involved in these pressor and chronotropic responses. Sprague-Dawley rats were studied after bilateral vagotomy and ganglionic blockade with hexamethonium (10 mg kg(-1)), and stabilization of MAP with infusion of phenylephrine (PE) (6 microg kg(-1) min(-1)). The rats were divided into groups: L, CAB; PE, CAB + PE bolus (6 microg kg(-1)); L-TX, thyroidectomy + CAB; L-AX, adrenalectomy + CAB; TX, only thyroidectomy; C, CAB. L, L-AX and L-TX groups received a bolus of l-NAME (7.5 mg kg(-1)). Triiodothyronine (T3), thyroxin (T4) and thyrotropin (TSH) levels were measured in L and L-TX rats before and after l-NAME administration. Reduced nicotamide adenine dinucleotide (NADPH) diaphorase activity was determined in heart and aorta of the TX group. The pressor response induced by l-NAME was similar in all groups. l-NAME-induced-tachycardia was associated with this rise in MAP. Adrenalectomy did not modify this chronotropic response, but it was attenuated by thyroidectomy. Thyroidectomy by itself decreased the circulating levels of T3 but it had no effect on the plasma levels of T4 and TSH. L and L-TX groups showed similar levels of circulating T4 and TSH, meanwhile the plasma level of T3 decreased in the L group. Nitric oxide synthase (NOS) activity in atria as well as in aorta was greater in the TX group compared with C. When autonomic influences are removed, the thyroid gland modulates intrinsic heart rate via a mechanism that involves, at least in part, the nitric oxide pathway.

Anesthesia↗
PubMed1987

Infestation in the dog by the paralysis tick Ixodes holocyclus. 1. Clinical and histological findings.

Under laboratory conditions 8 dogs were infested with Ixodes holocyclus and the clinical signs and histological findings were recorded. Seven of the dogs developed clinical signs of the disease, died and were subjected to a post-mortem examination, while the eighth dog remained normal. The clinical signs were consistent between animals and enabled the course of the disease to be subdivided into 5 stages to facilitate analysis of data in future experiments. The most prominent feature of the disease was dysfunction of the efferent motor system although some disturbance of the afferent pathways and involvement of the autonomic nervous system did occur. The period elapsing between attachment of the ticks and onset of signs varied from 5.5 to 7 days, while the mean duration of the disease was 23.3 h. The histopathology demonstrated moderate to severe congestion of the liver, kidney and lungs, and in some lung sections pulmonary oedema was present.

Animals↗
PubMedDate not supplied

The role of nitric oxide in carotid chemoreception.

Immunocytochemical and histochemical studies of cat and rat carotid bodies have revealed a plexus of nitric oxide synthase (NOS)-positive nerve fibers associated with lobules of chemosensory type I cells as well as with the carotid body vasculature. NOS-positive fibers originate from (1) autonomic neurons located in the carotid body and distributed along the carotid sinus nerve (CNS) and IXth cranial nerve which terminate in the adventitial layer of carotid body blood vessels, and (2) from unipolar sensory neurons of the petrosal (IXth nerve) ganglion. Carotid bodies incubated with the NO precursor, 3H-arginine, yield 3H-citrulline, the detectable coproduct of NO synthesis. Furthermore, electrical stimulation of the CNS or exposure of carotid bodies to hypoxic incubation media elevates 3H-citrulline formation. Millimolar concentrations of L-arginine inhibit chemoreceptor activity evoked by hypoxia, an effect which is reversed by the specific NOS antagonist, L-NG-nitroarginine methylester (L-NAME, 0.1 mM). Electrical stimulation of CNS C fibers elevates cyclic GMP in the carotid body vasculature and lobules of type I cells. Cyclic GMP production is reduced during stimulation in the presence of L-NAME, a finding consistent with the known ability of NO to activate a soluble form of guanylate cyclase. Further studies showed that brief (< 1 min) stimulation of CNS C fibers inhibits basal chemoreceptor discharge in a perfused/superfused in vitro carotid body preparation, whereas prolonged (> 5 min) stimulation is required to inhibit the response to hypoxia. The inhibitory effect is reversed by L-NAME. Our combined anatomical, neuropharmacological and electrophysiological data suggest that NO plays a dual role in mediating CNS inhibition, one via its actions on the organ's vasculature and the other through direct effects on the chemosensory type I cells. The former pathway involves cholinergic/NOS presumptive parasympathetic autonomic neurons, while the latter may be mediated by axon reflex or primary affarent depolarization of chemosensory nerve terminals.

Afferent Pathways↗