Stimulation Of Somatic Nerves Research Articles

Acupuncture and Kidney Disease

Acupuncture as a complex therapeutic system has been used to treat a variety of diseases and pathological conditions. Although the exact mechanism(s) of acupuncture remains unknown, some evidence suggests a mechanism initially involving signal transduction through connective tissue, with secondary involvement of other systems including the nervous system. Acupuncture has become increasingly popular in the Western countries as a therapy for pain and several chronic disorders difficult to manage with conventional treatments. Acupuncture and acupuncture-like somatic nerve stimulation have been used in different kidney diseases and several complications related to them. The effect of acupuncture techniques in some kidney diseases is reviewed on the basis of clinical reports as well as mechanisms that may possibly explain the beneficial effects mediated by acupressure/acupuncture. The potential effect of acupressure techniques in renal inflammation and whether these effects could be mediated through the newly identified cholinergic anti-inflammatory pathway are discussed.

Partial nicotinic receptor blockade unmasks a modulatory role of nitric oxide on urethral striated neuromuscular transmission

The objective of this study was to investigate the possible modulatory role of endogenous nitric oxide (NO) production on the urethral striated muscle (USM) function in the sheep urethra. Significant NO synthase (NOS) activity was measured in both the particulate and cytosolic fractions of USM homogenates. NOS activity was calcium-dependent and showed greater inhibition by NOS inhibitors selective of the neural NOS isoform (nNOS). nNOS immunoreactivity was present in intramural nerves as well as in the sarcolemma of some striated fibers, being denser at the neuromuscular junction (NMJ). Double immunolabeling showed co-localization of nNOS with both alpha-bungarotoxin and choline acetyltransferase, at the USM endplates. For the first time, functional data support a role of NO on the USM contractility "in vitro," which became evident following partial nicotinic receptor inactivation with low concentrations of D-tubocurarine. Only under D-tubocurarine (0.25 microM) treatment, different NOS inhibitors, specially N(G)-propyl-L-arginine, as well as the guanylate cyclase inhibitor ODQ, all showed a significant enhancing effect on contractions induced by electrical field stimulation of intrinsic somatic nerves. These data suggest that local production of NO at the urethral NMJ may modulate release and/or action of acetylcholine on motor endplates by cyclic GMP-mediated effects. This modulatory action could be especially relevant when neuromuscular transmission at the USM is impaired.

Medullary substrate and differential cardiovascular responses during stimulation of specific acupoints.

Electroacupuncture (EA) at P5-P6 acupoints overlying the median nerve reduces premotor sympathetic cardiovascular neuronal activity in the rostral ventral lateral medulla (rVLM) and visceral reflex pressor responses. In previous studies, we have noted different durations of influence of EA comparing P5-P6 and S36-S37 acupoints, suggesting that point specificity may exist. The purpose of this study was to evaluate the influence of stimulating P5-P6 (overlying the median nerve), LI4-L7 (overlying branches of the median nerve and the superficial radial nerve), LI6-LI7 (overlying the superficial radial nerve), LI10-LI11 (overlying the deep radial nerves), S36-S37 (overlying the deep peroneal nerves), or K1-B67 (overlying terminal branches of the tibial nerves) specific acupoints, overlying deep and superficial somatic nerves, on the excitatory cardiovascular reflex and rVLM responses evoked by stimulation of chemosensitive receptors in the cat's gallbladder with bradykinin (BK) or direct splanchnic nerve (SN) stimulation. We observed point-specific differences in magnitude and duration of EA inhibition between P5-P6 or LI10-LI11 and LI4-L7 or S36-S37 in responses to 30-min stimulation with low-frequency, low-current EA. EA at LI6-LI7 and K1-B67 acupoints as well as direct stimulation of the superficial radial nerve did not cause any cardiovascular or rVLM neuronal effects. Cardiovascular neurons in the rVLM, a subset of which were classified as premotor sympathetic cells, responded to brief (30 s) stimulation of the SN as well as acupoints P5-P6, LI10-LI11, LI4-L7, S36-S37, LI6-LI7, or K1-B67, or underlying somatic pathways in a fashion similar to the reflex responses. In fact, we observed a significant linear relationship (r(2) = 0.71) between the evoked rVLM response and reflex change in mean arterial blood pressure. In addition, EA stimulation at P5-P6 and LI4-L7 decreased rVLM neuronal activity by 41 and 12%, respectively, for >1 h, demonstrating that prolonged input into the medulla during stimulation of somatic nerves, depending on the degree of convergence, leads to more or less inhibition of activity of these cardiovascular neurons. Thus EA at acupoints overlying deep and superficial somatic nerves leads to point-specific effects on cardiovascular reflex responses. In a similar manner, sympathetic cardiovascular rVLM neurons that respond to both visceral (reflex) and somatic (EA) nerve stimulation manifest graded responses during stimulation of specific acupoints, suggesting that this medullary region plays a role in site-specific inhibition of cardiovascular reflex responses by acupuncture.

Inspiratory coupling to cardiac activity and to somatic afferent nerve stimulation in the anaesthetised rat

We examined the ability of somatic afferent nerve stimulation to entrain inspiratory onset in the anaesthetized spontaneously breathing rat, and compared features of this stimulus–ventilatory coupling to entrainment of inspiratory onset by cardiac activity. In 14 rats prior to stimulation, we commonly observed a constant temporal alignment between ECG R waves and inspiratory onset (cardioventilatory coupling). Stimulation of a hamstring nerve at rates close to the heart rate also caused coupling (a constant stimulus to inspiratory onset interval), although this was highly dependent upon frequency of stimulation, with small changes in frequency causing a loss of coupling. In experiments where stimuli were given at constant intervals after ECG R waves, we observed no augmentation of coupling. Our results indicate that both cardiac and somatic afferent nerve activity is able to entrain inspiratory onset. We have suggested that coupling causes respiratory frequency to increase, and it is possible that this is a general mechanism whereby non-respiratory afferents act as stimulants or pacemakers to respiratory rhythm. The role of non-respiratory activity in initiating inspiration needs to be more fully recognised and studied.

Cardiovascular responses to sciatic nerve stimulation are blocked by paratrigeminal nucleus lesion

The paratrigeminal nucleus (Pa5) receives primary sensory inputs from the vagus, glossopharyngeal, and trigeminal nerves and has efferent projections to the nucleus of the solitary tract (NTS), rostroventrolateral reticular nucleus (RVL), as well as to the nucleus ambiguus (Amb), lateral reticular (LRt), parabrachial (PB) and ventral posteromedial thalamic (VPM) nuclei, suggesting that it may play a significant role in cardiovascular responses to nociceptive stimuli. The aim of the present study was to evaluate the effects of unilateral lesions of the Pa5 on cardiovascular alterations induced by afferent somatic sensory nerve stimulation (SNS), also known as the somatosympathetic reflex (SSR). Cardiovascular responses were recorded in rats following either sham operation or unilateral lesions of the Pa5 with ibotenic acid. Mean arterial blood pressure (MAP) increased after SNS, which in sham-lesioned animals raised from 95±4 to 115±2 mmHg. Ipsilateral Pa5 lesion did not significantly reduce the pressor response to SNS (from 91±7 to 107±4 mmHg increase of baseline MAP). On the other hand, contralateral Pa5 lesion significantly reduced the response to SNS (from 99±5 to 104±2 mmHg). Sciatic nerve stimulation did not alter heart rate (HR) neither did ipsi- or contralateral Pa5 lesion HR baseline response level. These findings support a crucial role for the Pa5 in cardiovascular regulation, by relaying SSR input evoked by peripheral nerve stimulation.

Reflex cardiovascular responses originating in exercising muscles of mice.

The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 +/- 1.9 mmHg) and heart rate (33.5 +/- 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 +/- 3.5, 20.9 +/- 4.0, 21.7 +/- 2.6, and 25.8 +/- 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O(2)-90% N(2)) elicits increases in blood pressure (11.7 +/- 2.6 mmHg) and heart rate (42.7 +/- 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.

Somatic nerve stimulation and cholera-induced net fluid secretion in the small intestine of the rat: Evidence for an opioid effect

The effects of somatic nerve stimulation on cholera toxin induced secretion was investigated in vivo in anaesthetised rats. Small intestinal secretion was induced with cholera toxin and measured by a gravimetric technique. Afferent stimulation (pulse frequency within train; 100 Hz; train duration: 50 ms; train frequency: 3 Hz) of the sciatic nerve over 30 min significantly reduced the net fluid secretion both during ( P<0.05) and after cessation of the stimulation ( P<0.01). The greatest effect was obtained immediately after the termination of the nerve stimulation when the secretion was reversed to net fluid absorption. The opioid receptor antagonist naloxone (10 mg kg −1 i.v.) administrated during the stimulation, significantly inhibited the antisecretory effect seen after the stimulation, thus no significant difference was seen between the control period and the periods after cessation of the stimulation. The opioid receptor antagonist naloxone methiodide (10 mg kg −1 i.v.), which does not cross the blood–brain barrier, partly inhibited the antisecretory effects but not with the same magnitude as naloxone, thus the net fluid secretion was still significantly inhibited after the stimulation ( P<0.05). We conclude that afferent stimulation of the sciatic nerve strongly inhibits the cholera toxin induced secretion in the small intestine. This inhibition involves primarily a central opioid mechanism and to a lesser extent peripheral opioid mechanism.

Modification of the cardiovascular response to hemorrhage by somatic afferent nerve stimulation with special reference to gut and skeletal muscle blood flow.

Tissue injury modifies heart rate and blood pressure responses to hemorrhage. The effect of concomitant injury on the hemorrhage-induced redistribution of cardiac output is much less clear. However, if injury elicits the visceral alerting response of the defense reaction, then a change in this redistribution of peripheral blood flow might be expected. If such a change compromised the gut circulation, then it might explain the deleterious effects of injury on the ability to withstand hemorrhage. Immature pigs anesthetized with Saffan were bled 30% of blood volume with or without concomitant somatic afferent (brachial) nerve stimulation (to mimic injury). In addition to global cardiovascular and oxygen transport variables, blood flow was measured in the cranial mesenteric (gut) and right femoral (skeletal muscle) arteries after a 60-minute stabilization period after surgery, at the end of the 30-minute hemorrhage, and after a 30-minute shock period. Hemorrhage induced the expected cardiovascular and oxygen transport changes accompanied by a reduction in skeletal muscle blood flow and a 55% increase in skeletal muscle vascular resistance, but gut blood flow and vascular resistance were unchanged. However, in the presence of brachial nerve stimulation, the pattern of response to hemorrhage was modified, such that gut blood flow was now reduced and gut vascular resistance increased. The sparing of the gut circulation after hemorrhage was abolished in the presence of "injury." This finding is consistent with injury eliciting the defense reaction and may help explain the deleterious effects of injury on resistance to hypovolemia.

Somatic electrical nerve stimulation regulates the motility of sphincter of Oddi in rabbits and cats: evidence for a somatovisceral reflex mediated by cholecystokinin.

Cholecystokinin (CCK) plays an important role in regulating the biliary motility in herbivorous and carnivorous animals. Little is known about how the motility of the sphincter of Oddi (SO) is regulated through a somatic stimulation. It was our aim to test the hypothesis that somatic electrical nerve stimulation (SENS) affects SO motility in animals with different types of SO through CCK-related mechanisms. The activity of SO in anesthetized rabbits and cats was measured by using a continuously perfused open-tip manometric method. SENS was brought about by applying an electric current (2/15 Hz alternatively, 20 min) to two needles positioned near spinal nerves in the 6th and 7th intercostal space in the right midclavicular line. The SO motility before and X min after the start of SENS, designated as pre-SENS and SENS-X respectively, were recorded and saved in a computer equipped with off-line analysis software. The SO activity in rabbits, in terms of phasic contraction pressure and duration of summation peak during SENS were significantly higher than that before SENS. The phasic contraction pressure of pre-SENS, SENS-10, and SENS-16 were 6.83 +/- 0.39 mm Hg, 9.23 +/- 0.83 mm Hg and 10.46 +/- 0.81 mm Hg, respectively (P < 0.03, N = 13). The duration of summation peak in pre-SENS, SENS-10, and SENS-16 were 7.26 +/- 0.41 sec, 10.22 +/- 0.46 sec, and 13.49 +/- 2.31 sec, respectively (P < 0.05, N = 13). The SENS-induced SO hyperactivity was not inhibited by pretreatment with atropine, propranolol, phentolamine, or naloxone, but was blocked by pretreatment with the CCK receptor antagonist, proglumide, and by injection of anti-CCK-8 antibody during SENS in a dose-dependent manner. In contrast, SENS induced an inhibitory SO response in cats. However, in both circumstances, an obvious elevation of plasma CCK level determined by radioimmunoassay was noted after SENS. We conclude that SENS causes secretion of CCK, which in turn affects biliary tract motility in animals with different types of SO. This provides an easily applicable method for those patients who have hyperactive SO function.

Neural mechanisms of autonomic responses elicited by somatic sensory stimulation.

All evidence introduced here indicates that, in anesthetized animals in which emotional factors have been eliminated, somatic afferent nerve stimulation can regulate various visceral functions by responses that are reflex in nature. One conclusion emerging from the evidence presented is that the effects of somatic afferent stimulation are dependent upon the particular organs and on the spinal afferent segments. When the central nervous system is intact, the responses are sometimes general, as seen in cerebral cortical blood flow, heart rate, and adrenal medullary hormonal secretion and splenic immune function, whereas sometimes they have a strong segmental organization, as seen in gastric motility and urinary vesical contractility (Fig. 8). Needless to say, in the spinalized preparation all responses are strongly segmental. The contribution of the sympathetic and parasympathetic efferent nerves to the somato-visceral reflexes depends on the organs. It is difficult for us to state specifically or to generalize upon which autonomic component, the sympathetic or parasympathetic, will dominate as the efferent path in these reflexes, because this depends on the individual organ, the site being stimulated, and the nature or mode of the stimulation. The somatically-induced reflex responses of autonomic, hormonal and immune functions demonstrated in anesthetized animals, as have been discussed herein, appear to function even during conscious states. We need further studies to evaluate the physiological meaning of these somato-autonomic reflex responses. The analysis of neural mechanisms of these reflex responses seems to be very important for clinical application to regulate visceral function by physical treatment.

Attention and distraction: Effects on gut perception

BACKGROUND & AIMS: Paying attention to the gut may magnify perception of abdominal symptoms, but the actual influence of attention by anticipatory knowledge and distraction on gut perception remains poorly defined. The aim of this study was to determine whether mental activity, attention vs. distraction, affects intestinal perception and whether mental effects are synergistic with other modulatory mechanisms.METHODS: Perception of 1-minute intestinal balloon distentions applied at 7-13-minute random intervals was measured in healthy subjects. First, distentions were tested during attention by anticipatory knowledge and during distraction (n = 8). Because somatic transcutaneous electrical nerve stimulation (TENS) reduces gut perception, distentions were then tested during attention alone, attention plus somatic TENS, and during distraction plus TENS (n = 8).RESULTS: Perception of intestinal distentions was higher during attention than during distraction (3.3 +/- 0.2 vs. 2.9 +/- 0.1 [mean +/- SEM]; P < 0.05). The area of somatic projection was greater during attention (P < 0.05). Intestinal compliance and oral reflex relaxation remained unchanged. During application of somatic TENS, perception of intestinal distention was higher during attention than distraction (2.4 +/- 0.3 vs. 1.7 +/- 0.2; P < 0.05). However, TENS did not alter the perception score during attention.CONCLUSIONS: Mental activity may modulate gut perception and overrides the effects of somatic TENS on gut perception.(Gastroenterology 1997 Aug;113(2):415-22)

Differential regional sympathetic responses to somatic stimulation in anesthetized dogs

The present study was designed to determine whether regional differences exist in sympathetic responses to somatic nerve stimulation and whether the baroreceptor reflex modulates this somato-sympathetic reflex. The cardiac (CNA), renal (RNA), hepatic (HNA), splenic (SpNA) and adrenal (AdNA) sympathetic postganglionic nerve activities (SNA) were simultaneously recorded in anesthetized dogs with intact ( n = 7) or bilaterally sectioned ( n = 8) carotid sinus and vagus nerves. In the intact group, electrical stimulation of the left peroneal nerve at low intensity and low frequency (5 V, 5 Hz) produced a fall in mean arterial pressure (MAP) (−9.7 ± 2.7 mmHg) and a decrease in each SNA with no regional differences RNA (79.2 ± 8.5%), AdNA (82.7 ± 5.4%), HNA (89.4 ± 4.5%), CNA (87.5 ± 3.5%), SpNA (84.2 ± 3.2%). In contrast, stimulation at high intensity and high frequency (25 V, 50 Hz) produced a rise in MAP (+21.4 ± 3.8 mmHg) and increases in SNA with quantitative predominance of RNA (178.6 ± 13.6%) and AdNA (158.3 ± 16.1 %) over HNA (129.0 ± 4.2%), CNA (117.7 ± 7.6%), and SpNA (112.0 ± 6.2%). Similar responses were observed when the left ulnar nerve was stimulated. The changes in SNA (ΔSNA) at 10 s after the start of stimulation were plotted as a function of the changes in MAP (ΔMAP) and the regression curves were determined. The best fit regression curve was a logistic sigmoid curve in the intact group and a linear one in the baroreceptor denervated group. Furthermore, ΔRNA/ΔMAP and ΔAdNA/ΔMAP during the somato-pressor response were significantly smaller in the intact group than in the denervated group. In conclusion, there are regional differences of sympathetic response during the somato pressor response but not during somato depressor response. The baroreceptor reflex may suppress the somato-sympathetic reflex of RNA and AdNA.

Desflurane Attenuates the Somatosympathetic Reflex in Rats

Arterial blood pressure and heart rate changes after afferent somatic sensory nerve stimulation are termed the "somatosympathetic reflex" (SSR). Inhibition of the SSR may partially represent an antinociceptive action. This investigation examined the actions of the volatile anesthetic, desflurane, on the SSR evoked by peripheral nerve stimulation. Rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) were mechanically ventilated and cannulated with arterial and venous catheters for monitoring arterial pressure and for fluid administration, respectively. The sciatic (n = 7) or tibial (n = 6) nerves were isolated and stimulated at one, two, and four times the voltage threshold required to elicit a change in systemic hemodynamics. These cardiovascular responses were recorded before, during, and after varying concentrations of desflurane, 1.8% (0.25 minimum alveolar anesthetic concentration [MAC]), 3.6% (0.5 MAC), 7.2% (1.0 MAC), and 10.8% (1.5 MAC). Desflurane decreased arterial pressure at 1.0 and 1.5 MAC and heart rate (at more than 0.5 MAC) compared to baseline levels. Tibial nerve stimulation decreased mean arterial pressure (MAP) with no consistent changes in heart rate. Desflurane significantly attenuated this depressor response to tibial nerve stimulation (MAP decrease: control; -20 +/- 2 mm Hg versus 1.0 MAC desflurane; -6 +/- 4 mm Hg). The increases in MAP after sciatic nerve stimulation were also significantly inhibited by increasing concentrations of desflurane. At more than 0.5 MAC desflurane, the pressor response to sciatic nerve stimulation was significantly converted to a depressor response in four of seven rats (MAP: control; increase 24 +/- 2 mm Hg versus 1.0 MAC desflurane; decrease -2 +/- 4 mm Hg). Sciatic nerve stimulation also elicited increases in heart rate which were significantly attenuated by desflurane (control; 37 +/- 6 bpm versus 1.5 MAC desflurane; 0 +/- 2 bpm). These findings demonstrate that desflurane produces dose-dependent cardiovascular depression in rats and, despite previous reports of sympathoexcitation, desflurane significantly attenuated both excitatory and inhibitory types of SSR. The results of this study also support a potential antinociceptive action for this anesthetic.

Single electrical shock of a somatic afferent nerve elicits A- and C-reflex discharges in gastric vagal efferent nerves in anesthetized rats

The possibility that single electrical shock stimulation of somatic afferent nerves could evoke a reflex response in vagal efferent nerves innervating the stomach was examined using anesthetized, artificially-ventilated rats. A single shock to a hindlimb afferent nerve (tibial nerve) produced two distinct reflex components in gastric vagal efferent nerves; namely (1) A-reflex discharges with a latency of about 120 ms and a duration of about 200 ms elicited by stimulation of myelinated A afferent fibers, and (2) C-reflex discharges with a latency of about 360 ms and a duration of about 200 ms elicited by stimulation of unmyelinated C afferent fibers. A single shock to a first lumbar spinal afferent nerve produced only a weak reflex component with a latency of about 120 ms and a duration of about 190 ms in gastric vagal efferent nerves. Limb afferents appear to have stronger central pathways functionally connecting to gastric vagal efferent preganglionic neurons in the brainstem, than do abdominal afferents.

Renal sympathetic nerve responses to somato-sensory nerve stimulation in normotensive rats

Blood pressure, heart rate and renal sympathetic nerve activity were recorded in groups of chloralose/urethaneanaesthetised intact, vagotomised and carotid sinus denervated Wistar rats before and during bilateral somatic afferent nerve stimulation from 0.1 to 3.2 Hz. Renal sympathetic nerve activity was subjected to power spectral and cross correlation analysis. Haemodynamic and integrated renal nerve responses to graded brachial nerve stimulation were not altered by either bilateral vagotomy or carotid sinus denervation and total power of the spectra, from 0–10 Hz, was similar in each group. The percentage power peak at heart rate in intact rats decreased with increasing stimulus frequency, from a control value of 19.2 ± 1.9% to a minimum of 2.8 ± 0.7% at 1.6 Hz, while coherence and phase were not altered. Conversely, the peak at the stimulus frequency rose with increasing stimulus frequency reaching 35.3 ± 2.0% at 3.2 Hz. In the vagotomised group, power at heart rate was significantly lower at each stimulus frequency compared to intact rats although coherence was similar and the phase difference was larger. The peak power at stimulus frequency, coherence and phase difference were similar to those obtained in the intact rats. In the carotid sinus denervated rats, the percentage power at heart rate, coherence and phase difference were significantly smaller than in intact rats. The peak at the stimulus frequency and the phase difference were similar to those obtained in the intact rats whereas coherence was lower. These findings demonstrate that the pattern of renal nerve activity can be changed from one modulated by the baroreceptor to one driven by somatic afferent nerve activity. The vagus appears to play a minor role in the overall pattern of renal nerve activity with the primary controller being the carotid sinus baroreceptors. The data also show that the renal nerve response to somatic afferent nerve stimulation is independent of the afferent nerve input arising from either the atrial or the carotid sinuses.

Lowered oesophageal sensory thresholds in patients with symptomatic but not excess gastro-oesophageal reflux: evidence for a spectrum of visceral sensitivity in GORD.

Some patients undergoing ambulatory oesophageal pH monitoring to investigate symptoms suggestive of gastro-oesophageal reflux disease (GORD) are found to have oesophageal acid exposure within the physiological range but show a close correlation between their symptoms and individual reflux episodes. It is suggested that these patients might exhibit enhanced oesophageal sensation, akin to the heightened perception of both physiological and provocative stimuli in the gut that has been described in patients with functional gastrointestinal disorders. This study tested the hypothesis by measuring the sensory thresholds for oesophageal balloon distension and discomfort in 20 patients with symptoms of GORD, in whom ambulatory pH monitoring had shown normal acid exposure times, but in whom the symptom index for reflux events was 50% or greater, and compared these with 15 healthy volunteer controls, and with control groups with confirmed excess reflux. The study group showed lower thresholds both for initial perception of oesophageal distension, and for discomfort, compared with healthy controls (median ml (range)); 7.5 (2-19) v 12 (6-30) (p = 0.002) and 10 (5-20) v 16 (8-30) (p < 0.0001), respectively. Sensory thresholds in the study group were also significantly lower than in patients with excess reflux, and than patients with Barrett's oesophagus, who also exhibited significantly higher sensory thresholds than healthy controls. No differences in sensory thresholds for somatic nerve stimulation were found between the study group and health controls. The results show a spectrum of visceral sensitivity in GORD, with enhanced oesophageal sensation in patients with symptomatic but not excess gastro-oesophageal reflux, suggesting that their symptoms result from a heightened perception of normal reflux events.

Selective dysfunction of mechanosensitive intestinal afferents in irritable bowel syndrome

Background/Aims : Experimental studies have shown gut hypersensitivity in irritable bowel syndrome. The aim of this study was to determine whether heightened perception of gut distention in irritable bowel syndrome is related to either decreased gut compliance, altered mechanosensitive afferents, or nonspecific sensory dysfunction. Methods : In 17 patients with irritable bowel syndrome and 15 healthy controls, stimulus-related perception of (1) intestinal balloon distentions, (2) transmucosal electrical nerve stimulation (15 Hz, 100 μs), and (3) somatic transcutaneous electrical nerve stimulation (100 Hz, 100 μs) was measured. Individual stimuli of 1-minute duration were randomly applied at 5-minute intervals. Results : Patients tolerated smaller intestinal volumes than controls (33 ± 3 mL vs. 43 ± 4 mL, respectively; mean ± SE; P < 0.05), whereas both intestinal compliance and perception of transmucosal electrical nerve stimulation were normal (patients tolerated 58 ± 5 mA and healthy subjects tolerated 69 ± 5 mA). Interestingly, patients perceived both stimuli more diffusely than controls; 48% ± 9% distentions and 52% ± 9% electrical stimuli were perceived over more than one abdominal region vs. 21% ± 9% and 18% ± 6%, respectively, in controls ( P < 0.05 for both). In contrast to gut distentions, patients showed higher tolerance of somatic stimuli than controls (68 ± 7 mA vs. 42 ± 6 mA, respectively; P < 0.05). Conclusions : Patients with irritable bowel syndrome show selective hypersensitivity of intestinal mechanosensitive pathways associated with a nonspecific, probably central dysfunction of viscerosomatic referral.

The effects of halothane on pressor and depressor responses elicited via the somatosympathetic reflex: a potential antinociceptive action.

The specific stimulation of various somatic sensory afferent nerves results in significant changes in autonomic responses, including systemic arterial pressure (AP) and heart rate (HR). These reflexively mediated responses have been termed the "somatosympathetic reflex" (SSR). The SSR is mediated at spinal and supraspinal sites within the central nervous system (CNS), and may, in part, represent a nociceptive response. The present investigation examined the actions of the volatile anesthetic, halothane, on the SSR evoked by electrical stimulation of peripheral nerves resulting in pressor or depressor alterations in AP and associated changes in HR. Experiments were completed in rats anesthetized with alpha-chloralose (50 mg/kg) and urethane (500 mg/kg) and mechanically ventilated. After nerve isolation, either the tibial nerve or the sciatic nerve was stimulated 1, 2, and 4 times the voltage threshold required to elicit a change in hemodynamics. Cardiovascular responses to nerve stimulation were recorded prior to, during, and after increasing concentrations of halothane (0.25%, 0.5%, and 1.0%). Halothane, as expected, produced dose-dependent decreases in AP and HR as compared to baseline controls. Electrical stimulation of the tibial nerve during control resulted in graded decreases in mean arterial pressure (MAP) with increasing current densities. Halothane significantly attenuated the depressor response to tibial nerve stimulation (decrease in MAP at maximal stimulation: 3 +/- 2 mm Hg with 1.0% halothane vs 21 +/- 2 mm Hg during control). Stimulation of the sciatic nerve resulted in current-dependent increases in AP which were significantly inhibited in the presence of halothane (increase in MAP at maximal stimulation: 7 +/- 3 mm Hg with 1.0% halothane vs 34 +/- 5 mm Hg during control).(ABSTRACT TRUNCATED AT 250 WORDS)

Selective gastric hypersensitivity and reflex hyporeactivity in functional dyspepsia

Background/Aims: We have previously shown that patients with functional dyspepsia are hypersensitive to gastric distention. The aim of this study was to establish whether this sensory disturbance was confined to the stomach and whether it was associated with gut reflex dysfunction. Methods: In 10 selected patients with dyspepsia and 12 healthy controls, perception and gut reflex responses to gastric distention, duodenal distention, and somatic stimulation were measured. Standardized distentions at fixed pressures were performed by gastric and duodenal barostats. Perception was scored by a detailed symptom questionnaire; gut reflex responses were measured as isobaric volume changes by each barostat. Somatic transcutaneous electrical nerve stimulation was produced on the hand. Individual stimuli (2-minute duration) were randomly applied at 10-minute intervals in stepwise increments in search of the respective threshold for discomfort. Results: Patients with dyspepsia had gastric hypersensitivity to distention (discomfort threshold at 6.4 ± 0.4 mm Hg vs. 8.3 ± 0.6 mm Hg in controls; mean ± SE; P < 0.05), whereas duodenal and somatic sensitivity was normal. Furthermore, patients with dyspepsia explicitly recognized their clinical symptoms in all gastric but only in 58% ± 12% of the duodenal distention trials. In addition, patients with dyspepsia showed defective gastric relaxatory responses to duodenal distention (68 ± 30 ml gastric expansion vs. 239 ± 12 mL in controls; P < 0.05). Conclusions: Patients with dyspepsia are selectively hypersensitive to gastric distention; this sensory dysfunction is associated with impaired reflex reactivity of the stomach.

Responses of neurones in the nucleus paragigantocellularis lateralis to somatic nerve stimulation

Among the seventy-eight extracellularly recorded neurones in the nucleus paragigantocellularis lateralis (PGL), 30 and 31 of them were excited by the stimulation of superficial (SPN) and deep (DPN) peroneal nerve, respectively. In the other 17 neurones, convergent inputs from both nerves to a single neurone were found, and a post-excitatory inhibition was also observed. The consequence of the integrated responses to the stimulation of both nerves depended on the time interval of the stimuli to them. Excitatory post-synaptic potentials (EPSP) were recorded in neurones excited by the stimulation of both nerves. In conclusion, the stimulation of SPN and DPN can excite neurones in PGL, at least partially, via EPSP through their respective pathways; the integrated responses of PGL neurones to both nerves are related to the arrival time of impulses from them.