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PubMed1999

Nitric oxide, atrial natriuretic factor, and dynamic renal autoregulation.

Inhibition of nitric oxide (NO) synthase by N(omega)-nitro-L-arginine methyl ester (L-NAME) increases arterial pressure (PA) and profoundly reduces renal blood flow (RBF). Here we report that L-NAME causes changes in the PA-RBF transfer function which suggest augmentation of the approximately 0.2 Hz autoregulatory mechanism. Attenuation of PA fluctuations from 0.06 to 0.11 Hz was enhanced, indicating increased efficacy of autoregulation. Also, the rate of gain reduction between 0.1 and 0.2 Hz increased while the associated phase peak became > or = pi/2 radians, indicating emergence of a substantial rate-sensitive component in this system so that autoregulatory responses to rapid PA changes become more vigorous. Infusion of L-arginine partly reversed the pressor response to L-NAME, but not the renal vasoconstriction or the changes in the transfer function. The ability of atrial natriuretic factor (ANF), which also acts via cGMP, to replace NO was assessed. ANF dose dependently reversed but did not prevent the pressor response to L-NAME, indicating additive responses. ANF did not restore RBF or reverse the changes in the transfer function induced by L-NAME. The rate-sensitive component that was enhanced by L-NAME remained prominent, suggesting that either ANF did not adequately replace cGMP or provision of a basal level of cGMP was not able to replace cGMP generated in response to NO. It is concluded that NO synthase inhibition changes RBF dynamics with the most notable change being increased contribution by a rate-sensitive component of the myogenic system.

Animals↗

PubMed2004

Randomized clinical trial of intra-anal electromyographic biofeedback physiotherapy with intra-anal electromyographic biofeedback augmented with electrical stimulation of the anal sphincter in the early treatment of postpartum fecal incontinence.

OBJECTIVE: The purpose of this study was to compare intra-anal electromyographic biofeedback alone with intra-anal biofeedback that was augmented with electrical stimulation of the anal sphincter in the treatment of postpartum fecal incontinence. A secondary aim was to examine the impact of the treatment on continence-related quality of life. STUDY DESIGN: Sixty symptomatic women were assigned randomly to receive intra-anal electromyographic biofeedback or electrical stimulation of the anal sphincter once weekly for 12 weeks and to perform daily pelvic floor exercises between treatments. Therapeutic response was evaluated with a symptom questionnaire to determine continence score, anal manometry, and endoanal ultrasound scanning. Quality of life was assessed before and after treatment with a validated questionnaire. RESULTS: Fifty-four women completed the treatment; 52 women (96%) had ultrasonic evidence of an external anal sphincter defect. After the treatment, both groups demonstrated significant improvement in continence score (P < .001) and in squeeze anal pressures (P < .04). Resting anal pressures did not alter significantly. Quality of life improved after the completion of physiotherapy, but there were no differences in outcome between intra-anal electromyographic biofeedback and electrical stimulation of the anal sphincter. CONCLUSION: Intra-anal electromyographic biofeedback therapy was associated with improved continence and quality of life in women with altered fecal continence after delivery. The addition of electrical stimulation of the anal sphincter did not enhance symptomatic outcome.

Adult↗

PubMed1986

Failure of electrical myofeedback to augment the effects of physiotherapy in stroke.

Electromyographic biofeedback has been used with some success to treat patients with disturbances of muscle tone resulting from neurological disease. The aim of this study was to incorporate electrical myofeedback as an integral part of a physiotherapeutic regime designed to improve quality of movement and function in limbs weakened or paralysed by stroke. A portable, inexpensive E. M. G. biofeedback machine was used. Stainless steel skin electrodes were applied which needed minimal skin preparation. Twelve adults, (five male, seven female, mean age 44.2 years and 51.3 years respectively) who were referred for treatment due to weakness of limb muscles due to disease of the brain or spinal cord, were treated. The mean time from onset of incidence to treatment was 75.5 days. Each patient received six weeks of treatment. This was divided into two phases. Phase 1, (weeks 1, 2, 3) and phase 2 (weeks 4, 5, 6). Physiotherapy, and physiotherapy with biofeedback was randomly allocated to either phase. Each patient acted as his/her own control. A validated assessment was carried out by an independent therapist at the start of treatment, after three weeks and after six weeks of treatment. General function, knee function, range of movement of the affected side and timed tests were measured. Results show an overall improvement in general function. The second phase of treatment was slightly more favourable to improvement, but there was no indication that biofeedback significantly improved the outcome. In three tests it was equally significant to the physiotherapy applied; in one test it improved the effectiveness of physiotherapy and in one test it reduced the effectiveness of physiotherapy. This suggests that a six week course of physiotherapy improved muscular function and range of movements in patients with weakness due to upper motor neurone disease, but that these effects are not enhanced by myofeedback.

Adolescent↗

PubMed1998

Effect of cerebellar inactivation by lidocaine microdialysis on the vestibuloocular reflex in goldfish.

Vestibuloocular reflex performance and adaptation were examined during vestibulocerebellar inactivation by localized lidocaine microdialysis or injection in goldfish. In the light, eye velocity perfectly compensated for head velocity (Vis-VOR) during sinusoidal yaw rotation (1/8 Hz +/- 20 degrees). In the dark, the reflex (VOR) gain was slightly reduced (gain approximately 0.8-0.9). In neither Vis-VOR nor VOR, was gain altered after 1 h of lidocaine microdialysis in the vestibulocerebellum. Before adaptation of reflex gain, the initial suppression or augmentation of Vis-VOR reflex gain produced by in-phase or out-of-phase visual-vestibular stimulation was also unaffected by cerebellar inactivation. Subsequently, 3 h of adaptive reflex training in either the in-phase or out-of-phase paradigm (acquisition phase) respectively decreased (0.30 +/- 0.09) or increased (1.60 +/- 0.08) VOR gain during artificial cerebral spinal fluid (CSF) microdialysis. However, microdialysis of lidocaine completely blocked adaptive gain changes during a 3-4 h period of continuous application. This effect was reversible because VOR gain changes were produced 1 h after lidocaine was replaced with CSF as the dialysate. After adaptive training, bilateral CSF injections (0.25 microl/side) into the vestibulocerebellum did not alter the normal retention or decay of adapted gain changes during a 3 h period in the dark (retention phase). However, injection of lidocaine into the vestibulocerebellum completely blocked retention of the adapted VOR gain returning the gain to values recorded before adaptation. In contrast to either acute or chronic surgical removal, lidocaine inactivation of the cerebellum by microdialysis did not alter either Vis-VOR and VOR behavior or interactive Vis-VOR performance over a wide range of gain extending from 0.3 to 1.4. Thus short-term VOR motor learning is a dynamic process requiring either continuous operation of brain stem cerebellar loops or, alternatively, modifiable sites within or directly influenced by the cerebellum. Our data supports the latter hypothesis, because the direct brain stem VOR pathways appear to be unaltered after cerebellar inactivation, and, hence, independent of the VOR-adapted state.

Adaptation, Ocular↗

PubMed1993

Mandatory neuropeptide-steroid signaling for the preovulatory luteinizing hormone-releasing hormone discharge.

In this article I have examined various aspects of the complex spatio-temporal patterning of peptidergic signaling that lead to synchronized development of neural events for the preovulatory LHRH discharge on proestrus. Undoubtedly, the integration of these events is orchestrated by both ovarian steroids, E2 and P. Evidence accumulated in recent years has failed to affirm the perceived notion that E2 is an adequate peripheral signal for the timely, robust discharge of LHRH on proestrus. The current understanding is shaped by the thesis that the concerted central actions of E2 and P are mediated by a host of regulatory peptides produced locally in the hypothalamus, and steroids, in general, augment the production and release of both inhibitory and excitatory peptides in a timely fashion to facilitate the preovulatory LHRH discharge. Since these peptidergic pathways appear mandatory for signal transfer, considerable recent research has been devoted first to identifying the signals that selectively participate in the induction of preovulatory LHRH (LH) surge, and then to trace the route of signal transmission that ultimately leads to LHRH hypersecretion on the afternoon of proestrus (Fig. 1). The peptidergic pathways that propagate and transmit impulses for the preovulatory LHRH discharge reside in the SCN-MPN-MPOA-ARC-ME neural complex (Fig. 1). The timely initiation of these impulses is entrained to the photo-periodic input reaching the SCN by the retino-hypothalamic tract. The evidence is already in place to show that further information processing is transduced in the MPN; however, the nature of neurochemical signaling between the two sites remains to be deciphered. The available evidence favors a mandatory participation of inhibitory (EOP and NPK) and excitatory (NPY, GAL, NT, and AII) messenger molecules within the SCN-MPN-MPOA-ARC-ME complex (Fig. 1). It is possible that the relevant information from the SCN-MPN is conveyed caudally to the ARC in order to initiate a chain of events for disinhibition/excitation of the NPY-EOP network and to affect LHRH neurosecretion at the perikaryal level in the MPOA and at axon terminals in the ME. Also, either concurrently or on a time-delayed basis, the relevant information from the MPN may be relayed to the MPOA via the local peptidergic network comprised of NT, EOP, NPK, and GAL. This transmission may initially be critical for elicitation of antecedent neurosecretory events in the ME and to ultimately evoke the preovulatory LHRH surge.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗