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PubMed1983

Prostanoids and cardiac reflexes of sympathetic and vagal origin.

Prostaglandins in concentrations too low to stimulate afferent nerve endings in the heart may sensitize them to chemical or mechanical stimuli that activate cardiac reflexes during myocardial ischemia. Bradykinin, which is released from the heart during ischemia, elicits sympathetically mediated reflex pressor effects and tachycardia when applied in low doses (0.1 to 1 microgram) to the epicardium of the left ventricle in open-chest, anesthetized dogs. The reflex pressor effects evoked by bradykinin are reduced after inhibition of prostaglandins biosynthesis with indomethacin and potentiated by concomitant topical application of low doses (0.1 to 0.3 microgram/min) of PGE1 or PGE2 and prostacyclin (PGI2). The pressor and tachycardic responses to bradykinin are also enhanced after temporary (10-minute) coronary occlusion; this potentiation is abolished by indomethacin treatment and can be restored by superfusing the ventricle with prostaglandins. Nicotine is known to excite mechanosensitive vagal receptors with afferent C fibers, which supply the left ventricle, and to elicit reflex hypotension and bradycardia. This depressor vagal reflex evoked by epicardial or intracoronary administration of nicotine (10 to 50 micrograms) was not affected by either indomethacin or by topical application of PGE1, PGE2, or PGI2. Also, intracoronary infusion of PGE2 (0.1 to 0.3 microgram/min), which enhanced the pressor reflex effects of bradykinin, was without effect on nicotine-induced depressor reflex. However, intracoronary infusion of PGI2 (0.1 to 0.3 microgram/min) significantly enhanced the hypotensive and bradycardic responses to nicotine and, at the same time, reduced sympathetically mediated reflex effects of bradykinin. The hypotensive effects induced by epicardial or intracoronary administration of nicotine were also significantly enhanced during intravenous infusion of subdepressor doses of PGI2 (5 to 20 ng/kg/min). Treatment with captopril, which enhances the endogenous production of prostaglandins, greatly enhanced the reflex depressor effects of nicotine; this potentiating effect of captopril was completely abolished by indomethacin treatment. An increase in the magnitude of nicotine-induced reflex depressor effects was also observed after intravenous injection (1 microgram/kg) or infusion (25 to 50 ng/kg/min) of prostaglandin D2. A working hypothesis is proposed to account for the role of prostanoids in activation of cardiac reflexes during myocardial ischemia.

Arteries↗
PubMed1990

Vagal afferent-mediated inhibition of a nociceptive reflex by intravenous serotonin in the rat. I. Characterization.

The effect of intravenous (i.v.) serotonin (5-HT) on nociception and blood pressure was examined in male Sprague-Dawley rats. Intravenous 5-HT produced a dose-dependent (6-192 micrograms/kg, i.v.) inhibition of the nociceptive tail-flick (TF) reflex in lightly pentobarbital-anesthetized (ED50 = 40 micrograms/kg) and conscious rats (ED50 = 44 micrograms/kg). In the lightly pentobarbital-anesthetized rat, the blood pressure response to i.v. 5-HT was typically a triphasic response with a marked Bezold-Jarisch reflex-induced decrease in pressure (associated with a brief period of apnea) followed by a pressor phase and a subsequent delayed hypotension. In the conscious rat, the response was typically biphasic with the late hypotensive phase absent. A variety of anatomical and pharmacological manipulations were performed to characterize the 5-HT-induced inhibition of the TF reflex and associated changes in blood pressure. Prevention of 5-HT-induced reflex apnea by artificial ventilation did not affect inhibition of the TF reflex produced by 5-HT. Pharmacological manipulations were performed to mimic, as closely as possible, the acute increases and decreases in blood pressure associated with i.v. 5-HT. Nitroprusside (8 micrograms/kg, i.v.) produced a decrease in blood pressure of similar magnitude and rate as that associated with the Bezold-Jarisch reflex-induced decrease in pressure produced by 72 micrograms/kg 5-HT, but did not change TF latency from baseline. Similarly, acute increases in pressure produced by phenylephrine (8 micrograms/kg, i.v.), intended to mimic the secondary pressor effect of 5-HT, did not change TF latency. The short-acting ganglion blocker trimethaphan (5 mg/kg, i.v.) closely mimicked the late hypotensive phase produced by 5-HT, but again resulted in no change in TF latency. Pretreatment with the ganglion blocker chlorisondamine (2.5 mg/kg) abolished all depressor responses to 72 micrograms/kg 5-HT, but did not significantly affect the TF reflex. These results indicate that acute changes in blood pressure and respiration associated with i.v. 5-HT do not contribute to inhibition of the TF reflex. This conclusion was confirmed in experiments in which bilateral vagotomy abolished approximately 70% of the 5-HT-induced inhibition of the TF reflex (and all depressor responses), and resulted in a significantly greater pressor response. Finally, low thoracic spinal cord transection (T9-10) abolished the inhibition of the TF reflex produced by i.v. 5-HT. Therefore, 5-HT stimulates vagal afferents and inhibits the TF reflex by activating descending inhibitory systems from the brainstem.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1992

Inhibition of a cutaneous nociceptive reflex by a noxious visceral stimulus is mediated by spinal cholinergic and descending serotonergic systems in the rat.

The present study examined the spinal pathway and receptors that mediate nocigenic inhibition of the tail-flick (TF) reflex produced by conditioning colorectal distension (CRD). Conditioning CRD (80 mmHg; 30 s) inhibited the TF reflex in all rats studied (n = 29). In 19 rats where intensity-dependent effects of CRD were studied, conditioning CRD in 7 rats facilitated the TF reflex at lesser, non-noxious intensities (mean 7.9 +/- 2.1 mmHg) and inhibited the TF reflex at greater, noxious intensities (40-100 mmHg); conditioning CRD at all intensities tested only inhibited the TF reflex in the other 12 rats. Inhibition of the TF reflex produced by 30 s CRD was short-lasting, repeatable and graded with the intensity of CRD. The mean threshold of CRD for inhibition of the TF reflex to cut off (10 s) was 61.4 +/- 3.3 mmHg (n = 29). Intrathecal pretreatment with atropine or methysergide significantly attenuated the inhibitory effect of CRD on the TF reflex; the effects were time- and dose-related. Intrathecal pretreatment with mecamylamine, phentolamine or naloxone was without effect. Intrathecal administration of physostigmine, an acetylcholinesterase inhibitor, significantly reduced the threshold intensity of conditioning CRD necessary to inhibit the TF reflex to cut off (mean 36.0 +/- 4.0 mmHg; n = 5). Bilateral transections of the spinal dorsolateral funiculi (DLF) did not affect the inhibitory effect of CRD in 4/7 rats and attenuated the inhibitory effect of CRD in the other 3 rats. The antagonistic effect of methysergide on CRD-produced inhibition of the TF reflex was abolished following the DLF transections, while scopolamine retained its efficacy in rats with bilateral DLF transections. These findings provide evidence for involvement of spinal cholinergic interneurons as well as a descending serotoninergic pathway traveling in the DLF in CRD-produced inhibition of the TF reflex.

Animals↗
PubMed1986

Phasic stretch reflex of the abdominal muscles.

This analysis of the abdominal stretch reflex (ASR) evoked by a tap to the abdomen was designed to explore how abdominal motoneurons process signals from respiratory and nonrespiratory sources. We recorded surface EMGs from the external and internal oblique muscles in standing subjects. Amplitudes of the abdominal stretch reflex varied despite constant tap forces, but strong taps evoked a larger reflex than weak taps. Trunk rotation toward the recording side, or voluntary contraction of the external and internal oblique muscles increased the reflex amplitudes, whereas contralateral rotation reduced their occurrence. An abdominal stretch reflex during a voluntary contraction was followed by a silent period of 40 to 80 ms. Often a late wave followed a reflex by 20 to 40 ms. Amplitudes during breathholds at residual lung volume were larger than those evoked during a breathhold at functional residual capacity, suggesting that abdominal stretch reflex amplitudes are inversely proportional to static lung volume. During quiet breathing the reflex amplitude reached a maximum slightly before end-expiration and decreased progressively to a minimum close to end-inspiration. During rebreathing, background abdominal activity was augmented with highest activity in late expiration. Abdominal stretch reflex amplitudes continued to wax and wane in phase with respiration, and the maximal reflex occurred progressively earlier in expiration. In summary, the abdominal stretch reflex reflects strong control from abdominal muscle spindles, lung proprioceptors, and chemoreceptors. The relative contributions of these inputs need to be determined.

Abdominal Muscles↗
PubMed1996

Elicitation and modification of the rabbit's nictitating membrane reflex following prenatal exposure to cocaine.

The nictitating membrane (NM) reflex was assessed in adult Dutch-belted rabbits exposed to cocaine in utero. The intensity threshold for eliciting the reflex was increased in cocaine progeny and the amplitude of the reflex was decreased at the lower stimulus intensities. However, cocaine and saline progeny showed equivalent rates of habituation of the NM reflex when tested with a suprathreshold eliciting stimulus. Reliable modification of the NM reflex was obtained when the reflex-eliciting stimulus was preceded by an auditory stimulus at intervals of 100-800 ms. Cocaine and saline progeny exhibited an increase in the peak amplitude of the reflex, a shortening of the latency of the reflex, and a shortening of the latency to achieve peak amplitude of the reflex as a function of increases in the interstimulus interval. Furthermore, cocaine progeny showed significantly longer response latencies than saline progeny across all interstimulus intervals, although neither the peak amplitude nor the latency to achieve peak amplitude was affected. Thus, prenatal exposure to cocaine affected elicitation of the defensive NM reflex to an aversive stimulus but did not affect the sensorimotor integration necessary for modification of the reflex by antecedent stimulation.

Animals↗
PubMed1980

Effects of anaesthetics on reflexes elicited in the sudomotor system by stimulation of Pacinian corpuscles and of cutaneous nociceptors.

Sudomotor neurones supplying sweat glands in the hairless skin of the cat's paws can be activated by the cutaneous afferent inputs deriving from vibrational receptors (Pacinian corpuscles) in the paws and from cutaneous nociceptors. Both reflexes probably have separate spinal pathways. In the present investigation the effects of the anaesthetics ketamine, methohexital, chloralose, halothane and Althesin on both types of sudomotor reflexes were examined. For this purpose the skin potentials were recorded from the hairless skin of the paws with Ag--AgCl-electrodes. Before application of any anaesthetic the cats were in a state of light ketamine anaesthesia. The following results were obtained: (1) the resting activity in the sudomotor system and the synchronization of the activity between both hindpaws and between hind- and forepaws were depressed by all anaesthetics to a variable degree. After chloralose application large synchronous potentials of low frequency appeared; (2) ketamine (18--25 mg/kg injected intramuscularly) enhanced the reflexes on vibrational stimulation and depressed the reflexes on noxious stimulation of skin; (3) methohexital (3--10 mg/kg injected intramuscularly) mostly depressed the reflexes on vibrational stimulation and enhanced the reflexes on noxious cutaneous stimuli; (4) chloralose (4.5--20 mg/kg injected intraperitoneally) enhanced both types of reflexes; (5) halothane (1--1.5 vol. %) and Althesin (2.5--5 mg/kg injected intramuscularly) depressed both types of reflexes; (6) in chronic spinal cats ketamine, methohexital and chloralose had a slightly depressive effect on the resting activity of the sudomotor system, but practically no influence on the reflexes induced by cutaneous stimuli; and (7) these results argue that the effects of anaesthetics on the sudomotor system depend on the type of reflex tested and the type of anaesthetic used. They indicate furthermore that the anaesthetics affect largely supraspinal structures and influence the spinal reflex pathways via descending spinal pathways.

Adrenergic Fibers↗
PubMed1992

Characteristics of sympathetic reflexes evoked by electrical stimulation of phrenic nerve afferents.

In chloralose-anaesthetized cats, sympathetic reflex responses were recorded in left cardiac and renal nerve during stimulation of afferent fibres in the ipsilateral phrenic nerve. In cardiac nerve, a late reflex potential with a mean onset latency of 75.6 +/- 13.8 ms was regularly recorded which, in 20% of the experiments, was preceded by an early, very small reflex component (latency between 35 and 52 ms). In contrast, in renal nerve only a single reflex component after a mean latency of 122.1 +/- 13.1 ms was observed. Bilateral microinjections of the GABA-agonist muscimol into the rostral ventrolateral medulla oblongata resulted in a nearly complete abolition of sympathetic background activity and in an 88% reduction of the late reflex amplitude with only small effects on the latency of the evoked potentials. Under this condition, an early reflex component was never observed to appear. After subsequent high cervical spinalization, the residual small potentials which persisted after bilateral muscimol injections were completely abolished and in cardiac nerve an early reflex potential with a mean latency of 45 +/- 10 ms was observed in all but one experiment. The early reflex was therefore referred to as a spinal reflex component which, however, is suppressed in most animals with an intact neuraxis. In the renal nerve a spinal response was only observed in one experiment after spinalization. The results suggest that sympathetic reflexes evoked by stimulation of phrenic nerve afferent fibres possess similar spinal and supraspinal pathways as previously described for somato-sympathetic and viscero-sympathetic reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Cutaneous nerve-evoked cholinergic inhibition of monosynaptic reflex in the neonatal rat spinal cord: involvement on M2 receptors and tachykininergic primary afferents.

The mechanisms of a cutaneous nerve-evoked inhibition of monosynaptic reflex were investigated in an isolated spinal cord-peripheral nerve preparation of the neonatal rat. Conditioning stimulation of the saphenous nerve, with five pulses at 50 Hz and a strength sufficient to activate C fibers, evoked an inhibition lasting about 20 s of the monosynaptic reflex that was elicited by stimulation of the nerve branch to quadriceps femoris muscle and recorded from the L3 ventral root. This inhibition of monosynaptic reflex was potentiated by an anticholinesterase, edrophonium, and mostly blocked by atropine. Application of acetylcholine, muscarine, bethanechol, carbachol, arecoline and oxotremorine induced an inhibition of monosynaptic reflex. From the effects of muscarinic antagonists, pirenzepine, AF-DX 116, and 4-diphenylacetoxy-N-methylpiperidine on the agonist-evoked and primary afferent-evoked inhibition of monosynaptic reflex it was concluded that the muscarinic receptors involved in the cutaneous nerve-evoked inhibition of monosynaptic reflex are of M2 type. When monosynaptic reflexes were evoked by two successive stimuli with intervals of 15 ms to 1 s, the second response was smaller than the first. This depression of monosynaptic reflex became less pronounced when the reflex was reduced by application of oxotremorine or arecoline or by conditioning stimulation of primary afferents, suggesting that the inhibition of monosynaptic reflex is presynaptic in nature. The late phase of the cutaneous nerve-evoked inhibition of monosynaptic reflex (5-20 s after conditioning stimulation) was markedly depressed by a tachykinin antagonist, spantide. Perfusion of the spinal cord with capsaicin (1 microM) for 1 h also abolished the late phase of the inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed2005

Aging-related neuromuscular changes characterized by tendon reflex system properties.

OBJECTIVE: To quantitatively evaluate changes in neuromuscular reflex system properties that are associated with aging. DESIGN: Controlled, experimental. SETTING: Research laboratory in a rehabilitation hospital. PARTICIPANTS: Fourteen elderly (age, 69.4+/-7.1 y) and 18 young (age, 29.9+/-6.5 y) healthy subjects. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: With the subject relaxed, an instrumented reflex hammer was used to tap the Achilles tendon and record the tapping force, whereas the ankle plantarflexion torque and plantarflexor muscle electromyographic activity were recorded isometrically as measures of the reflex responses. Tendon reflex system properties were evaluated by using system identification techniques. Tendon tapping force was designated as system input and reflex-mediated torque and electromyographic activity as outputs. The dynamic relations between input and output were characterized by the system parameters of reflex-mediated torque and electromyographic gains, contraction and excitation rate, reflex-mediated torque and electromyographic delays, and electromechanic delay. RESULTS: Various aging-related changes were found in the tendon reflex system properties, including decreased tendon reflex gain ( P =.029), slower contraction and half-relaxation rates ( P </=.018), and longer electromyographic activation delay, electromechanical delay and overall torque reflex delay ( P </=.025). In contrast, changes in the electromyographic properties were not significant, except for the longer electromyographic activation delay. CONCLUSIONS: Aging is associated with significant changes in the neuromuscular reflex system properties. The changes were mainly associated with weaker and slower muscle force generation but not with significant decrease in motoneuronal excitability.

Aged↗
PubMed2004

Differential modulation of withdrawal reflexes by a cannabinoid in the rabbit.

Inhibition of spinal and trigeminal withdrawal reflexes by morphine and by the cannabinoid agonist HU 210 has been studied in anaesthetized and in decerebrated rabbits. In intact, pentobarbitone-anaesthetized animals, the jaw-depressor reflex (JDR) evoked by stimulation of the tongue, and the reflex elicited in the ankle flexor tibialis anterior (TA) by stimulation of the toes were inhibited to the same extent by morphine (1-30 mg kg(-1) i.v. cumulative). In spinalized, anaesthetized rabbits morphine depressed the JDR to the same level as in non-spinal preparations, but the effect of the opioid on the TA reflex was significantly reduced. All effects of morphine were reversed by naloxone (0.25 mg kg(-1), i.v.). In anaesthetised intact animals, HU 210 depressed the JDR at a dose of 100 nmol kg(-1) i.v. cumulative, reduced reflexes evoked in the knee flexor muscle semitendinosus (ST) by stimulation at the toes at a dose of 30 nmol kg(-1) i.v. cumulative, but had no consistent or significant effects on the TA reflex to toe stimulation. The same results were obtained in spinalized, anaesthetised animals. In decerebrated, spinalized rabbits with no anaesthesia, HU 210 (30 nmol kg(-1)) depressed both ST and TA reflexes evoked by toe stimulation. These data reveal that trigeminal and spinal withdrawal reflexes are equally sensitive to morphine provided the spinal cord is intact, suggesting that at least part of the action of systemic morphine is due to activation of descending inhibition. The present results also show for the first time that cannabinoid agonists can inhibit trigeminal withdrawal reflexes. HU 210 had differential effects on the three reflexes studied depending on the presence or absence of anaesthesia. This is the first occasion on which we have found pharmacological distinctions between withdrawal reflexes, and indicates that spinal sensorimotor processing is more heterogeneous than has been suspected previously.

Animals↗
PubMed2005

Postural uncertainty leads to dynamic control of cutaneous reflexes from the foot during human walking.

Cutaneous reflexes evoked by stimulation of nerves innervating the foot are modulated in a phase-dependent manner during locomotion. The pattern of modulation of these reflexes has been suggested to indicate a functional role of cutaneous reflexes in assisting to maintain stability during walking. We hypothesized that if cutaneous reflexes assist in maintaining stability during gait, then these reflexes should be modulated in a context-dependent manner when subjects are asked to walk in an environment in which stability is challenged. To do this, we asked subjects to walk on a treadmill under five conditions: (1) normally, (2) with the arms crossed, (3) while receiving unpredictable anterior-posterior (AP) perturbations, (4) with the arms crossed while receiving unpredictable AP perturbations, and (5) with the hands holding onto fixed handles. Cutaneous reflexes arising from electrical stimulation of the superficial peroneal (SP; relevant to stumbling) or distal tibial (TIB; relevant to ground contact sensation) nerves were recorded bilaterally, at four points in the step cycle. Reflexes evoked with SP nerve stimulation showed marked facilitation during the most unstable walking condition in 4 of the 7 muscles tested. SP nerve-evoked reflexes in the muscles of the contralateral leg also showed suppression during the most stable walking condition. Reflexes evoked with TIB nerve stimulation were less affected by changes in the walking task. We argue that the specific adaptation of cutaneous reflexes observed with SP nerve stimulation supports the hypothesis that cutaneous reflexes from the foot contribute to the maintenance of stability during walking.

Adult↗
PubMed2005

Effect of spinal cord injury severity on alterations of the H-reflex.

The monosynaptic motoneuron response to stimulation of Ia afferents is known to be altered by spinal cord injury (SCI). Although the Hoffman (H)-reflex is a tool that is often used to measure this reflex in patients, there has not been a systematic study investigating the effect of SCI severity and time on the H-reflex. We used a clinically relevant model of spinal cord contusion (Mild and Moderate) as well as complete surgical transection to measure the H-reflex at 1, 4 and 8 weeks after injury. The H-reflex was recorded from rat hindpaw plantar muscles in order to measure the baseline reflex amplitude and its response to increased stimulus frequency, i.e. rate depression. We correlated the reflex amplitude at each frequency to spared white matter at the injury epicenter, hindlimb function and serotonin immunoreactivity associated with retrogradely labeled plantar muscle motoneurons. The three injury groups displayed different behavioral deficits and amount of spared white matter at all three times tested. H-reflex rate depression was abnormal in all three injury groups at all three time points. At 8 weeks, transected animals displayed more H-reflex rate depression than those with a mild contusion. Baseline H-reflex amplitude was increased in both contusion groups at 4 weeks and showed a positive linear correlation with serotonin immunoreactivity. This baseline amplitude was not increased after transection. Furthermore, in the contusion group, there was a U-shaped relationship between behavioral scores and H-reflex rate depression, suggesting that an intermediate sensitivity of the motoneuronal pool to afferent input is associated with better recovery of hindlimb function.

Analysis of Variance↗
PubMed2004

Anticipatory modulation of neck muscle reflex responses induced by mechanical perturbations of the human forehead.

The aim of this study was to test whether anticipation of upcoming head blow stimuli, which elicit reflex responses in the neck muscle, makes the reflex responses greater or not. In nine healthy subjects the reflex responses were elicited in the sternocleidomastoid (SCM) muscle in the eyes-open (EO) and eyes-closed (EC) conditions, which corresponded to the predictable and unpredictable conditions, respectively. The subjects were instructed not to resist the perturbations after the impact. The results demonstrated that the reflex response of the SCM muscle was significantly smaller in the predictable EO condition than in the unpredictable EC condition (P < 0.05), although no significant differences were observed in either the background EMG activities or the head accelerations. Further, this effect of anticipation was observed only in the later reflex EMG component, which most probably mediated the stretch reflex pathway. In contrast, no significant difference was observed in the early component, which was presumed to be the vestibular-collic reflex. The reduced stretch reflex response was suggested to be functionally relevant to the task requirement, i.e., to let the neck extension movement occur, and not to resist after the impact of the head blow. It was concluded that the anticipation has an effect on reducing the stretch reflex responses in the neck muscle, but does not have any effect on the presumed vestibular-collic reflex under the present experimental paradigm. It is suggested that the gain of the stretch reflex pathway is modulated by anticipatory information of upcoming mechanical event.

Adult↗
PubMed2006

Prevalence and associations of enhanced retinal arteriolar light reflex: a new look at an old sign.

PURPOSE: To assess the prevalence, associated risk factors and prognosis (mortality) of the enhanced retinal arteriolar light reflex sign in an older Australian population. DESIGN: Population-based cross-sectional study. PARTICIPANTS: Three thousand six hundred fifty-four participants (82.4% response) ages >/=49 years from Australia's Blue Mountains region. METHODS: Retinal photographs of participants were graded for presence and severity of the enhanced arteriolar light reflex sign by comparison with standard photographs. Associations with systemic factors (subject-specific) and ocular variables (eye-specific) were assessed by logistic regression. Mortality data were obtained using the Australian National Death Index. Hazard ratios were calculated using Cox regression. MAIN OUTCOME MEASURES: Prevalence of enhanced arteriolar light reflex and associations with demographic variables (age, gender), blood pressure, blood parameters, health risk behaviors, cataract, retinal vessel wall signs, retinopathy, and 10-year incident mortality. RESULTS: The enhanced arteriolar light reflex sign was found in 1053 participants (31.7%, including 28.8% graded as mild and 2.9% as marked). Prevalence decreased with age (36.0%, 37.7%, 28.0%, and 18.8% for age groups < 60, 60-69, 70-79 and > or = 80 years, respectively, P(trend)<0.0001); odds ratio (OR) 0.78; and 95% confidence interval (CI) 0.72 to 0.85 per decade. Persons with cataract were less likely to have mildly enhanced light reflex (OR, 0.74; CI 0.64-0.87). After multivariate adjustment, mildly enhanced light reflex was significantly associated with serum glucose (OR 1.11 per SD increase), total cholesterol (OR 1.11), low-density lipoprotein (OR 1.55), triglycerides (OR 1.11), platelets (OR 0.89), and body mass index (OR 1.12). Markedly enhanced light reflex was significantly associated with mean arterial blood pressure (OR 1.24), heavy alcohol consumption (OR 2.66, > or = 40 grams alcohol per day), and serum glucose (OR 1.16). Strong associations were demonstrated between presence of mildly enhanced light reflex and either arteriovenous nicking (OR 3.12) or retinopathy (OR 1.96). There was no association between mildly or markedly enhanced light reflex and either all-cause or vascular mortality. CONCLUSIONS: In this older population, the enhanced retinal arteriolar light reflex sign was a relatively common finding. Although some associations of this sign with vascular risk factors were found, only a marked level of enhanced light reflex was correlated with elevated blood pressure, but not with poor survival.

Aged↗
PubMed1997

Conditions for excitatory or inhibitory masseteric reflexes elicited by tooth pressure in man.

The reflex responses evoked by slowly rising pressure "push' stimuli to an upper lateral incisor tooth in human masseter muscle were studied. Factors such as the preload (the static force applied to the tooth by the stimulus probe before the start of the push stimulus) and the shape of the stimulus wave affected the outcome of the reflex response. When the stimulating probe did not apply preload to the tooth before the push stimulus took place, the force profile exhibited a large fast component as the probe took up the 'slack' in the periodontium. The fast component in the force profile was found to be responsible for inducing the inhibitory reflex (sole inhibitory reflex). When preload was applied, the size of the fast component in the force profile was reduced and the change in force rate became slower and smoother. This slower stimulus profile induced the sole excitatory reflex significantly more often (58% vs 21%) and the sole inhibitory reflex significantly less often (15% vs 52%) than in the experiments that used no preload. The shape of the stimulus wave that drove the stimulus probe was also of importance. Provided that a 0.5-N preload was applied to the tooth, the smoothest stimulus wave induced the sole excitatory reflex most often. Fitting a rubber attachment to the up of the probe made the push-force profile even smoother and thence more successful in inducing the sole excitatory reflex. Furthermore, the rubber tip reduced the possibility of the probe slipping off the tooth due to small and unavoidable movements of the participant's head. It is concluded that the periodontal mechanoreceptors can induce both excitatory and inhibitory reflexes on the jaw closers. The excitatory reflex becomes dominant when a smooth force is applied with preload. The inhibitory reflex becomes dominant when fast-force changes are applied on the tooth and/or no preload is used.

Adult↗
PubMed1997

Facilitation and inhibition of the urethrogenital reflex in spinal cord-transected rats.

It was evaluated in the spinal cord-transected rats whether the urethrogenital (UG) reflex shows some of the features that are present during ejaculation in intact animals. It was found that the UG reflex was facilitated after its first elicitation: the latency of the reflex was shorter than the previous one and low intensity of stimulation was needed to produce the reflex. In addition, a change in the latency of the reflex was found that was correlated with the number of stimulation trials. The latency change showed a J-shaped curve that is similar to that found for the ejaculation latency in a copulatory series. An inhibition of the reflex appeared after several trials: the reflex could not be elicited after three continuous trials. The reflex could be elicited again if the intensity of stimulation was increased. The UG reflex also showed 'exhaustion': it could not be elicited, even with high intensities of stimulation, after 3 h of rest. All these findings were present when the UG reflex was elicited by applying pressure to the urethra or when it was evoked by the electrical stimulation to the pudendal nerve. According to these findings, it can be concluded that the UG reflex maintains some of the features that are found during ejaculation in intact animals. According to this view, it can be speculated that some of the mechanisms that control ejaculation in intact animals can be localized at a spinal level.

Animals↗
PubMed1998

The H-reflex in the passive human soleus muscle is modulated faster than predicted from post-activation depression.

The purpose of the present study was to investigate the influence of afferent activity (mainly homonymous Ia-afferent activity) on the modulation (post-activation depression) of the soleus H-reflex during isolated and passive sinusoidal ankle joint rotations at a speed and amplitude comparable to slow walking. The H-reflex modulation was measured in the relaxed soleus muscle on human subjects during different imposed patterns of 20 degrees haversine ankle joint rotations (0.5-0.6 Hz) while they were sitting comfortably in a chair. Eighteen healthy males and four male patients with clinically complete spinal cord lesion above the soleus motoneuron pool participated in the study. During a single dorsi-plantar flexion rotation the H-reflex was depressed to 27+/-7% (mean+/-S.E.M.) of the initial level within 600 ms. The course of this depression was reversed when the dorsi-flexion velocity started to decrease. At the end of the dorsi-flexion movement the depression was already relieved to a level of 73+/-6% of the initial level. The H-reflex returned more slowly to the initial level within 2 s after the end of the movement cycle. During two consecutive ankle joint rotations and continuous ankle joint rotations both at 0.5 Hz the H-reflex was modulated but also generally depressed while the movement was imposed. The reflex only returned to the reference level after the movements were stopped. These observations indicate the action of a fast and a slow mechanism in the post-activation depression of the soleus H-reflex. The H-reflex modulations observed in the spinal cord injured patients were comparable to the reflex modulations observed in the healthy subjects, except the depressions were smaller. This suggests that a major part of the amplitude of the H-reflex modulation observed in healthy subjects was caused by peripheral and spinal influences. The fast 500 ms recovery of the H-reflex had a time course comparable to presynaptic inhibition. The slow 2 s recovery after the end of a given imposed movement may be explained by a change in the probability of transmitter release from the homonymous soleus Ia-afferent synaptic terminals after repeated activations.

Adult↗
PubMed2000

Nociceptin and the micturition reflex.

The i.v. administration of nociceptin (10-100 nmol/kg) inhibits the micturition reflex in a naloxone-resistant manner. The effects induced by i.v. nociceptin were not observed in capsaicin-pretreated animals indicating that i.v. nociceptin inhibits the micturition reflex by inhibiting afferent discharge from capsaicin-sensitive nerves. Supporting this interpretation, nociceptin also inhibited the reflex but not the local bladder contraction induced by topical capsaicin and protects this reflex (but not the local contraction) by desensitization. Intrathecal nociceptin (10 nmol/rat) produces urodynamic modifications similar to those induced by the i.v. administration. Intracerebroventricular (i.c.v.) administration of nociceptin (0.3-1 nmol/rat) also inhibited the micturition reflex in a naloxone-resistant manner suggesting a direct effect on supraspinal sites controlling the micturition. Beyond the inhibitory effects exerted by nociceptin on the micturition reflex, a peripheral excitatory effect mediated by capsaicin-sensitive fibers was also detected. The application of nociceptin (5-50 nmol/rat) onto the bladder serosa when the intravesical volume was subthreshold for the triggering of the micturition reflex, activated the reflex in a dose-dependent manner; the same treatment produced a biphasic effect on the ongoing reflex. In addition to the triggering of micturition reflex, topical nociceptin evokes a local tonic-type contraction that was abolished by the coadministration of tachykinin NK(1) and NK(2) receptor antagonists. Altogether these results indicate that ORL(1) receptors are present at several sites for the integration of the micturition reflex, and that their activation may produce both excitatory or inhibitory effects, depending on the route of administration and the experimental conditions.

Animals↗