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Phasic and tonic reflexes evoked in human antagonistic wrist muscles by tendon vibration.

The electromyographic reflex responses of the voluntarily contracting wrist flexor and extensor muscles to periods of vibration-evoked enhanced, Ia-dominated afferent discharge from flexor carpi radialis (FCR) were studied in normal human subjects. Three main response phases were characterised, namely, (i) phasic 'on' responses elicited at the commencement of stimulation, (ii) tonic response levels occurring during prolonged stimulation and (iii) phasic 'off' responses elicited at the termination of stimulation. The phasic 'on' reflex responses of FCR and extensor carpi radialis (ECR) comprised, respectively, a peak of autogenetic excitation of group mean latency 18.8 ms and a trough of reciprocal inhibition of group mean latency 38.0 ms. Prolonged (2 s) trains of FCR (agonist) vibration evoked a phase of tonic reflex excitation in FCR whose mean level was significantly increased, by 20%, above pre-stimulus activity and which did not change over the 0.5-2.0 s vibration period. Progressive reduction of the duration (from 2000 ms to 100 ms) of vibration trains demonstrated that phasic disfacilitatory 'off' troughs regularly occurred, with a consistent latency (mean 24.2 ms), on withdrawal of each period of enhanced Ia-input. This indicates that the responsible excitatory reflex mechanism was operational for the entire duration of each of the vibration periods tested. The extra latency (on average 5.4 ms) of phasic 'off' relative to 'on' responses may be attributed to factors (e.g. 5-10 ms duration of unitary muscle action potentials and afterdischarge in reflex pathways) which inevitably delay the appearance of overt disfacilitatory reductions in EMG rather than the involvement of different reflex pathways. Thus, short-latency, possibly monosynaptic, reflex excitation contributed throughout the entire tonic excitatory response. Sustained FCR (antagonist) vibration produced a significant tonic reciprocal inhibitory reflex depression, by 7% pre-stimulus EMG, of ECR activity which remained steady during the 0.5-2.0 s vibration period. The absence of well-defined phasic disinhibitory 'off' responses in ECR suggests that the contribution of oligosynaptic reflex inhibitory mechanisms to the tonic suppression of activity occurring during continuing vibration is relatively small.

Adult↗

Modular organization of excitatory and inhibitory reflex receptive fields elicited by electrical stimulation of the foot sole in man.

OBJECTIVES: The present study aimed to investigate how the inhibitory and excitatory reflex components of the human (polysynaptic) withdrawal reflex are organized depending on the stimulation site. The reflexes were elicited during a voluntary pre-contraction (between 10 and 20% of maximum voluntary contraction) of two antagonistic muscles. METHODS: Inhibitory and excitatory reflex receptive fields to tibialis anterior (TA) and soleus (SO) were mapped in 14 healthy subjects using randomized electrical stimulation at 16 sites of the foot sole. Low, non-painful (3x perception threshold), and high, painful (1.5x pain threshold), stimulus intensities were used. RESULTS: The inhibitory reflex receptive fields were organized in a highly functional manner supporting the action of the excitatory reflex. Together the two reflexes result in an optimal withdrawal from the stimulus. Low stimulation intensity was found sufficient to elicit the inhibitory reflex. High stimulation intensity caused a reversal of the inhibition to excitation in tibialis anterior. In soleus the inhibition was facilitated for stronger intensities. CONCLUSION: In conclusion, findings in animals of a modular organization of inhibitory reflexes are reproduced in humans.

Electric Stimulation↗

Reproducibility of tendon jerk reflexes during a voluntary contraction.

OBJECTIVES: The present study explored whether testing tendon jerks during voluntary contraction of the test muscle would improve reproducibility by effectively 'clamping' the excitability of the motoneurone pool at firing threshold. METHODS: Tendon jerk reflexes of soleus, tibialis anterior and vastus lateralis and the soleus H reflex were recorded in 12 healthy subjects at rest and during voluntary contractions of 10-20% of maximum. Recordings were repeated 8-10 times in 5 subjects, in whom reflex symmetry was also determined. RESULTS: Not all tendon jerk reflexes could be recorded at rest, and the variability of latency and amplitude was high. All reflexes could be recorded in each subject during contractions. The latency of tendon jerk reflexes decreased by approximately 2 ms during contractions, but H-reflex latency decreased by only 0.2-0.3 ms. For the tendon jerks, an asymmetry of >3.0 ms at rest and >2.5 ms contracting would be outside 3 SD of the normal mean. In repeat studies, the coefficient of variation of reflex latency was <4% for the tendon jerk. CONCLUSIONS: A voluntary contraction could potentiate the tendon jerk by a number of mechanisms, but the most important is probably enhancement of the excitability of the motoneurone pool. The present techniques should increase the value of tendon reflex testing when assessing possible peripheral nerve, plexus and root disturbances.

Adult↗

H-reflex modulation during walking in spastic paretic subjects.

Hoffman (H) reflexes were elicited from the soleus muscle during treadmill walking in 21 spastic paretic patients. The soleus and tibialis anterior muscles were reciprocally activated during walking in most patients, much like that observed in healthy individuals. The pattern of H-reflex modulation varied considerably between patients, from being relatively normal in some patients to a complete absence of modulation in others. The most common pattern observed was a lack of H-reflex modulation through the stance phase and slight depression of the reflex in the swing phase, considerably less modulation than that of normal subjects under comparable walking conditions. The high reflex amplitudes during periods of the step cycle such as early stance seems to be related to the stretch-induced large electromyogram bursts in the soleus in some subjects. The abnormally active reflexes appear to contribute to the clonus encountered during walking in these patients. In three patients who were able to walk for extended periods, the effect of stimulus intensity was examined. Two of these patients showed a greater degree of reflex modulation at lower stimulus intensities, suggesting that the lack of modulation observed at higher stimulus intensities is a result of saturation of the reflex loop. In six other patients, however, no reflex modulation could be demonstrated even at very low stimulus intensities.

Adult↗

On the role of 5-HT1B/1D receptors in modulating transmission in a spinal reflex pathway in the decerebrated rabbit.

1. In decerebrated rabbits, the selective 5-HT1B/1D receptor antagonist GR 127,935 had no significant effects on reflexes evoked in medial gastrocnemius motoneurones by electrical stimulation of the sural nerve, or on arterial blood pressure or heart rate when given by the intrathecal (up to 543 nmol cumulative) or intravenous (up to 1.8 micromol cumulative) routes. 2. In decerebrated, spinalized rabbits, intrathecal GR 127,935 in doses of up to 543 nmol, had no effect on the sural-gastrocnemius reflex. Furthermore, this drug failed to alter enhancement of the sural-gastrocnemius reflex induced by 8-hydroxy-2-(di-n-propyl)aminotetralin (8-OH-DPAT), given at 300 nmol kg-1 i.v. 3. In decerebrated, spinalized rabbits, the selective 5-HT1B/1D receptor agonists L-694,247 (cumulative doses of 2 - 243 nmol kg-1 i.v.) and L-741,604 (cumulative doses of 3 - 307 nmol kg-1 i.v.), each caused the sural-gastrocnemius reflex to increase to 140% of pre-drug levels, and arterial blood pressure to rise by about 10 mmHg. Subsequent administration of GR 127,935 at 0.9 - 1.8 micromol kg-1 reversed the pressor effect of the agonists but not the increase in reflexes. The 5-HT1A receptor antagonist WAY-100,635 (185 nmol kg-1 i.v.) also failed to reverse the increase in reflexes, but the 5-HT1B/1D/5-HT2/5-HT7 ligand ritanserin (1.6 micromol kg-1 i.v.) restored reflexes to pre-drug control values after L-741,604 (it was not tested against L-694,247). 4. These data indicate that 5-HT1B/1D receptors do not significantly modulate transmission in the sural-gastrocnemius reflex pathway, and that the enhancement of reflexes by 8-OH-DPAT and L-741,604 is probably mediated by 5-HT7 receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Speech performance, dysphagia and oral reflexes in cerebral palsy.

The adequacy of biting, sucking, swallowing, and chewing as well as the presence or absence of nine infantile oral reflexes were assessed in 60 cerebral-palsied individuals. The effect of the asymmetric tonic neck reflex and the Moro reflex on the infantile oral reflexes was also studied. There was a trend for subjects with more adequate feeding skills to achieve higher levels of overall speech proficiency and articulatory competency, but this trend was not completely systematic. Fifteen subjects displayed abnormal oral reflexes, but these reflexes could not be elicited consistently. The effect of the ATNR and Moro reflex on the oral reflexes seemed limited. Results generally supported the value of the widespread prescription of improving feeding in cerebral palsy, but the need to modify abnormal oral reflexes received less support. The question of using prespeech oromotor training to reduce possible future dysarthria is discussed in terms of the findings.

Adolescent↗

Newborn acoustic reflexes to noise and pure-tone signals.

A variable-frequency probe-tone acoustic-impedance bridge has been developed to enable an artifact-free pure-tone acoustic reflex study to be carried out on neonates. Contralateral reflex thresholds for pure tones, broadband noise, and filtered noise were measured in 28 newborns aged 4-8 days. The mean reflex threshold for the broadband noise was 73 dB SPL, 4 dB lower than the reflex threshold for the 2600-Hz low- and high-pass noise bands. Reflex activation at 500, 1000, 2000, and 4000 Hz gave responses that closely followed the normal adult pattern although reflex thresholds were approximately 10 dB higher. Two infants failed to demonstrate reflexes. One of these failed a behavioral-response test using the Auditory Response Cradle and was found to have mild jaundice. The second infant passed the behavioral test and had measurable reflexes 5 weeks later. A third baby with elevated reflex thresholds also was jaundiced but had normal behavioral responses and was discharged. Discussion of these results emphasizes their value to those engaged in neonatal auditory assessment.

Hearing Tests↗

Tympanometric and acoustic-reflex studies in neonates.

Tympanograms and acoustic reflexes for a broadband noise and for a 1000-Hz tone were measured in normal neonates. Notched tympanograms were typical of neonatal ears for a 220-Hz probe tone. A single-peaked tympanogram was most characteristic for a probe frequency of 660 Hz. Ipsilateral and contralateral acoustic reflexes were present more frequently for a 660-Hz probe tone compared to a 220-Hz probe tone, but acoustic-reflex thresholds were not significantly different between probe tones. As with adults, acoustic-reflex thresholds for the noise were significantly lower than for the tone, and ipsilateral reflex thresholds were lower than contralateral reflex thresholds. Reliability of acoustic-reflex and tympanometric measures was high. Age change from 2 to 4 days had no significant effect on tympanometric or acoustic-reflex characteristics. There was no apparent relation between tympanometric pattern and acoustic-reflex characteristics.

Acoustic Impedance Tests↗

The spatial organization of central sensitization of hind limb flexor reflexes in the decerebrated, spinalized rabbit.

This study was designed to investigate the relationship between the location of a noxious stimulus and the magnitude and duration of the plastic effects induced by that stimulus in withdrawal reflexes acting about the knee and the ankle, in rabbits. Reflexes were evoked in the nerves to the anterior tibial and semitendinosus flexor muscles by electrical stimulation at the toes. Repetitive, high intensity electrical stimulation of nerve trunks (sural, medial gastrocnemius, superficial peroneal, tibial, 100 pulses, 20 V, 1 ms at 0.5 Hz) was generally found to be a poor method for inducing central sensitization in these flexor reflexes. 'Natural' noxious stimulation induced more reliable enhancement of both reflexes. Mechanical (clamp) or chemical (mustard oil) stimulation of the heel induced prolonged (median duration >30 min) increases in reflexes to both muscles. Mechanical (clamp and superficial pinch) or chemical (mustard oil) stimulation of the toes, and injection of bradykinin into the gastrocnemius muscles or into the soft tissues of the sole of the foot, also led to enhancement of both reflexes, with the median duration of potentiation between 7 and 30 min. The effects obtained from deep tissue stimulation were generally weaker than those obtained after stimulation of superficial structures. These data show that there were no major differences in the effects obtained from the heel vs the toes, or between the two reflexes. It appears that the spatial organization of the spinal mechanisms underlying central sensitization of flexor withdrawal reflexes is rather more crudely drawn than that pertaining to the reflexes themselves. Furthermore, the data indicate that in the present preparation, afferents from deep tissues are no more effective in generating central sensitization than those from superficial structures.

Afferent Pathways↗

Effect of opioid active therapeutics on the ascending reflex pathway in the rat ileum.

For a long time therapeutic agents that interact with opioid receptors have been used in antidiarrheal therapy. The action of the opioid active substances on motility and transit have already been characterized; however, their effects on myenteric reflexes and their possible luminal action have not yet been investigated. Loperamide, fedotozine and beta-casomorphin-4, as well as the casomorphin-analogue beta-CM-4027, are, or have been, suggested as therapeutic agents and were studied in the isolated rat ileum for their effect on the ascending reflex pathway. beta-CM-4027 > fedotozine > loperamide > beta-casomorphin-4 caused a concentration-dependent inhibition of the ascending contractile reflex response with an IC(50)of 1.4x10(-7)M, 1.5x10(-6)M, 4.1x10(-6)M and 4.5x10(-6)M respectively. At the same time as the oral contractile reflex response was inhibited, all four opioid agonists (CM-4027 > beta-casomorphin-4 > fedotozine > loperamide) increased the latency of the reflex response. Both effects were blocked by naloxone, indicating the involvement of opioid receptors. These results demonstrate that opioid-active drugs and substances modify the peristaltic reflex by reducing the efficacy of the reflex response and modulating the timing of the reflex pathway. In a second series of experiments, luminal application of opioid-active drugs was compared with serosal application. beta-casomorphine-4 caused a concentration-dependent inhibition of the oral reflex response with an IC(50)of 3x10(-3)M which was 750 times higher than after serosal application. In contrast, a stable and highly selective kappa opioid agonist (U-50,488), which caused potent inhibition upon serosal application (IC(50): 2.3x10(-7)M), showed no inhibitory effect after luminal application up to a concentration of 10(-2)M. Thus casomorphins could have a local effect on the gut wall with no need for systemic absorption. This might be used for a possible therapeutic application.

Animals↗

Operant conditioning of H-reflex in spinal cord-injured rats.

Operant conditioning of the spinal stretch reflex or its electrical analog, the H-reflex, is a new model for exploring the mechanisms of supraspinal control over spinal cord function. Both rats and primates can gradually increase (HRup conditioning mode) or decrease (HRdown conditioning mode) soleus H-reflex magnitude when exposed to an operant conditioning task. This study used H-reflex operant conditioning to assess and modify spinal cord function after injury. Soleus H-reflexes were elicited and recorded with chronically implanted electrodes from rats that had been subjected to calibrated contusion injuries to the spinal cord at T8. From 18 to 140 days after injury, background EMG, M response amplitude, and initial H-reflex amplitude were not significantly different from those of normal rats. HRdown conditioning was successful in some, but not all, spinal cord-injured rats. The H-reflex decrease achieved by conditioning was inversely correlated with the severity of the injury as assessed histologically or by time to return of bladder function. It was not correlated with the length of time between injury and the beginning of conditioning. The results confirm the importance of descending control from supraspinal structures in mediating operantly conditioned change in H-reflex amplitude. In conjunction with recent human studies, they suggest that H-reflex conditioning could provide a sensitive new means for assessing spinal cord function after injury, and might also provide a method for initiating and guiding functional rehabilitation.

Animals↗

The bulbocavernosus reflex. A single motor neuron study.

Reflex latency variability was established for single motor neuron discharges in the bulbocavernosus reflex, as elicited by electrical stimuli to the dorsal penile nerve and recorded by a single fibre EMG electrode in the bulbocavernosus muscle. Whereas many reflex responses had a rather large latency variability of above 1000 microseconds (expressed as SD of mean latency) there was a group of motor neurons with a variability of around 500 microseconds. Single motor neuron reflex responses with shorter latencies tended to show less variability. No habituation of single motor neuron reflex discharges was observed on prolonged regular repetitive stimulation. Both absence of habituation and the relatively low latency variability of bulbocavernosus reflex responses for single motor neurons suggest similarities between this reflex and the first component of the blink reflex; we postulate that the shortest bulbocavernosus reflex pathway is oligosynaptic.

Adult↗

Soleus Hoffmann-reflex modulation during walking in healthy elderly and young adults.

Soleus Hoffmann-reflex (H-reflex) modulation during walking was examined in 7 young and 13 elderly adults. H-reflex size was measured in 16 equal time divisions (phases) of the step cycle. In both the elderly and the young groups, the H reflex was minimal at the time of heel contact, rose to a maximum shortly after midstance, decreased rapidly as toe-off neared, then was minimal during swing. There was a significant interaction between age group and step cycle phase (p < .05). During midstance of walking, the elderly participants had a smaller H-reflex size during two of the 16 time phases of the step cycle (p < .05), despite no significant difference in H-reflex size between the age groups while standing. The smaller H-reflex size during the stance phase of walking may reflect changes in central reflex mechanisms that may impact stretch reflex contribution to ankle extensor neural drive and ankle stiffness in elderly persons during walking.

Adult↗

Isoflurane, but not mild hypothermia, depresses the human pupillary light reflex.

The pupillary light reflex is often evaluated in the perioperative period as a measure of cranial nerve and midbrain integrity. Although surgical concentrations of some anesthetic agents and severe hypothermia qualitatively alter the light reflex, confounding factors frequently present during postanesthetic recovery have not been specifically quantified. We therefore studied 12 volunteers to determine the effects of residual isoflurane concentrations and typical (mild) hypothermia on the human pupillary light reflex. Young, healthy volunteers were assigned to one of three treatments: 1) normothermic isoflurane-oxygen anesthesia; 2) isoflurane-oxygen anesthesia with 2.2 +/- 0.5 degree C central hypothermia; and 3) central hypothermia (1.6 +/- 0.3 degree C) without anesthesia, induced by internal jugular infusion of iced lactated Ringer's solution. In normothermic anesthetized volunteers, the amplitude of the light reflex was depressed 80-90% at end-tidal concentrations greater than 0.5% isoflurane: reflex (percent of control) = 14 - 67.log (percent isoflurane); r = -0.92. In the mildly hypothermic anesthetized volunteers, pupillary responses were not statistically different from those in anesthetized normothermic volunteers: reflex (percent of control) = 16 - 62.log (percent isoflurane); r = -0.97. Hypothermia alone did not alter the magnitude of the light reflex. Our data suggest that mild hypothermia does not depress the light reflex but that isoflurane reversibly depresses the light reflex in a dose-related manner.

Adult↗

Acetazolamide and amiloride inhibit pentobarbital-induced facilitation of nocifensive reflexes.

BACKGROUND: Neuronal excitation may result from stimulation of gamma-aminobutyric acid A (GABA(A)) receptors that prolong the channel opening, depolarizing the postsynaptic membrane. Drugs such as acetazolamide or amiloride can block GABA depolarization. Barbiturates facilitate nociceptive reflexes and also prolong the GABA(A) channel open-time. To evaluate the possible mechanism, the authors studied the impact of acetazolamide and amiloride on pentobarbital-induced nocifensive reflex facilitation. Because nitric oxide (NO) is a mediator of reflex facilitation, the authors evaluated the effects of NO synthase inhibition. METHODS: Nocifensive reflex thresholds were quantified with the hind paw withdrawal latency from radiant heat (HPW latency) in the rat. Nocifensive reflexes were facilitated with intraperitoneal injection of pentobarbital (30 mg/kg). The authors tested the roles of GABA-mediated depolarization and NO in reflex facilitation by pretreatment with acetazolamide and amiloride and inhibition of NO synthase with L-NAME and 7-NI, respectively. Sedative effects of pentobarbital were evaluated with the righting reflex, the response to vibrissal stimulation, and plasma drug concentrations. RESULTS: Pentobarbital decreased the hind paw withdrawal latency from 11.2+/-1 to 8.3+/-1 s (P < 0.001). Pretreatment with each of the four test drugs limited the reduction in reflex facilitation after pentobarbital to 1.3 s or less, similar to the reduction seen after saline injection, without altering sedation. L-NAME increased plasma pentobarbital concentrations by 10% without changing the concentration associated with return of responsiveness. CONCLUSIONS: Pentobarbital-induced nocifensive reflex facilitation was inhibited by all four tested drugs without evidence of increased sedation. The results are consistent with a role for GABA(A) receptor-mediated depolarization in barbiturate-induced hyper-reflexia.

Acetazolamide↗

Electrically elicited stapedius reflex in cochlear implant patients.

Electrically elicited stapedius reflexes were examined in 25 deaf patients who had received a 22-channel Clark/NUCLEUS cochlear implant. Using an apical, a medial and a basal electrode pair, different stimulation positions within the cochlea and different stimulation modes were examined. For threshold determination, 10 reflexes were averaged with reflexes recorded on the nonoperated side. Reflexes were elicited in 19 of the 25 patients (76%); a saturation of reflex amplitude could be recorded in 14 (56%) subjects. In two additional cases, a reflex could be obtained by increasing the bipolar stimulation width (changing the stimulation mode). In comparison with different stimulation positions within the cochlea, the stimulation of apical electrodes produced more distinctive reflexes and required lower current levels. An increase in the bipolar stimulation width also decreased the intensity required for stapedius reflex threshold. Our data suggest that stapedius reflex evaluation may be a useful tool for speech processor fitting.

Adult↗

Suppression of a somatosympathetic reflex by the gamma-aminobutyric acid agonist muscimol and by clonidine.

gamma-Aminobutyric acid (GABA) and GABA agonists, e.g., muscimol, reduce blood pressure and sympathetic outflow and inhibit the "carotid occlusion reflex." In contrast, muscimol exerted only marginal effects on postural reflexes in a prior study. The somatosympathetic reflex, i.e., potentials evoked in sympathetic nerves in response to sensory nerve stimulation, is a useful model for studying centrally acting drugs. Effects of muscimol on the reflex were examined in anesthetized normotensive rats. At doses which had previously been shown to reduce blood pressure but to produce only minimal attenuation of postural reflexes in conscious hypertensive rats, muscimol, administered intracerebroventricularly, reduced blood pressure and inhibited the somatosympathetic reflex in the present study. The time course of the evoked potential was not altered. Baroreceptor activation and intracerebroventricular clonidine also suppressed the reflex. The inhibitory effect of muscimol but not that of clonidine was prevented by pretreatment with the GABA antagonist bicuculline. Thus, the marked suppression of the somatosympathetic reflex by muscimol and by clonidine, in contrast to minimal effects on postural reflexes, point to the selectivity of their central inhibitory actions.

Animals↗

"Skin-CNS-bladder" reflex pathway for micturition after spinal cord injury and its underlying mechanisms.

PURPOSE: A "skin-CNS-bladder" reflex pathway for inducing micturition after spinal cord injury has been established in cat. This reflex pathway which is basically a somatic reflex arc with a modified efferent limb that passes somatic motor impulses to the bladder, has been designed to allow spinal cord injured patients to initiate voiding by scratching the skin. MATERIALS AND METHODS: The skin-CNS-bladder reflex was established in the cat by intradural microanastomosis of the left L7 ventral root (VR) to the S1 VR while leaving the L7 dorsal root (DR) intact to conduct cutaneous afferent signals that can trigger the new micturition reflex arc. After allowing 11 weeks for axonal regeneration, urodynamic, pharmacological and electrophysiological studies were conducted in pentobarbital or chloralose anesthetized animals. RESULTS: A detrusor contraction was initiated at short latency by scratching the skin or by percutaneous electrical stimulation in the L7 dermatome. Maximal bladder pressures during this stimulation were similar to those activated by bladder distension in control animals. Electrophysiological recording revealed that single stimuli (0.3 to 3 mA, 0.02 to 0.2 msec duration) to the left L7 spinal nerve in which the efferent axons had degenerated evoked action potentials (0.5 to 1 mV) in the left S1 spinal nerve distal to the anastomosis. In addition, increases in bladder pressure were elicited by trains of the stimuli (5 to 20 Hz, 5 seconds) applied to the L7 spinal nerve. Urodynamic studies including external sphincter EMG recording demonstrated that the new reflex pathway could initiate voiding without detrusor-external urethral sphincter dyssynergia. Atropine (0.05 mg./kg., i.v.) or trimethaphan (5 mg./kg., i.v.), a ganglionic blocking agent, depressed the bladder contractions elicited by skin stimulation. The skin-CNS-bladder reflex could also be elicited after transecting the spinal cord at the L2-L3 or L7-S1 levels. CONCLUSION: The cross-wired somato-autonomic bladder reflex is effective in initiating bladder contractions and coordinated voiding in cats with an intact neuraxis and can also induce bladder contractions after acute transection of the lumbar spinal cord. The new pathway is mediated by cholinergic transmission involving both nicotinic and muscarinic receptors. It is concluded that somatic motor axons can innervate bladder parasympathetic ganglion cells and thereby transfer somatic reflex activity to the bladder smooth muscle.

Anastomosis, Surgical↗