Effect of esophageal contraction on esophageal wall blood perfusion

Myocardial blood flow occurs during the diastolic phase of the cardiac cycle, because myocardial contraction during the systolic phase impedes myocardial perfusion. Using laser Doppler perfusion technique, we studied the effect of esophageal contraction on the esophageal wall perfusion. Studies were conducted in rats. A laser Doppler probe was anchored to the esophageal wall, and wall perfusion was studied under various experimental conditions. Increase and decrease in the systemic blood pressure induced by different pharmacological agents was associated with the increase and decrease in the esophageal wall perfusion, respectively. Esophageal contractions induced by electrical stimulation of the vagus nerve and electrical stimulation of the muscle directly resulted in a reduction in the esophageal wall perfusion, in a dose-dependent fashion. Esophageal wall perfusion could be monitored by placing the Doppler probe on the esophageal mucosa or on the outside of the esophageal wall. Esophageal contraction impedes entry of blood into the esophageal wall. Future studies may investigate if ischemia of the esophageal wall induced by sustained esophageal contractions/esophageal spasm is the cause of esophageal pain symptoms in humans.     

Deglutitive inhibition affects both esophageal peristaltic amplitude and shortening

Deglutitive inhibition attenuates ongoing esophageal contractions if swallows are separated by short time intervals. This study aimed to determine whether esophageal shortening, mediated by longitudinal muscle, was similarly affected. Eight healthy subjects with two distal esophageal segments demarcated by mucosal clips and manometric recording sites positioned within those segments underwent concurrent manometry and fluoroscopy. Peristaltic amplitude and change in distal segment lengths were quantified during single swallows, paired swallows separated by progressively prolonged intervals, and a series of rapid repetitive swallows. During grouped swallows, deglutitive inhibition with complete attenuation of both the manometric contraction and segment shortening was evident with short-interval swallows and rapid-sequence swallows. No inhibition of either was evident with long-interval pairs. With intermediate interswallow intervals, the occurrence and degree of deglutitive inhibition between peristaltic amplitude and segment shortening were closely correlated. Deglutitive inhibition affects both the longitudinal and circular muscle layers of the esophageal wall, and the occurrence of inhibition evident in one layer is strongly correlated with the other.     

Effect of dry swallows and wet swallows of different volumes on esophageal peristalsis.

The effect of dry swallows and wet swallows of various volumes on esophageal function was studied in normal subjects. An intraesophageal transducer assembly was used to measure the dynamics of esophageal peristalsis. The strength of esophageal contraction (amplitude) following a 1-ml liquid bolus was similar to that following a dry swallow but was significantly less than that following a wet swallow of a larger volume. There was no difference in strength of esophageal squeeze following swallows ranging from 2 to 20 ml. In addition, a wet swallow was associated with slower wave speed, greater duration of the contraction wave, and later time of appearance of the peristaltic wave in the distal esophagus than a dry swallow. Futhermore, the incidence of peristalsis was greater with a wet swallow than a dry swallow. The results of our studies indicate that although the act of swallowing alone in man initiates peristalsis, afferent information contributes to the regulation of primary peristalsis.     

Mechanics and hemodynamics of esophageal varices during peristaltic contraction

Our hypothesis states that variceal pressure and wall tension increase dramatically during esophageal peristaltic contractions. This increase in pressure and wall tension is a natural consequence of the anatomy and physiology of the esophagus and of the esophageal venous plexus. The purpose of this study was to evaluate variceal hemodynamics during peristaltic contraction. A simultaneous ultrasound probe and manometry catheter was placed in the distal esophagus in nine patients with esophageal varices. Simultaneous esophageal luminal pressure and ultrasound images of varices were recorded during peristaltic contraction. Maximum variceal cross-sectional area and esophageal luminal pressures at which the varix flattened, closed, and opened were measured. The esophageal lumen pressure equals the intravariceal pressure at variceal flattening due to force balance laws. The mean flattening pressures (40.11 +/- 16.77 mmHg) were significantly higher than the mean opening pressures (11.56 +/- 25.56 mmHg) (P < or = 0.0001). Flattening pressures >80 mmHg were generated during peristaltic contractions in 15.5% of the swallows. Variceal cross-sectional area increased a mean of 41% above baseline (range 7-89%, P < 0.0001) during swallowing. The peak closing pressures in patients that experience future variceal bleeding were significantly higher than the peak closing pressures in patients that did not experience variceal bleeding (P < 0.04). Patients with a mean peak closing pressure >61 mmHg were more likely to bleed. In this study, accuracy of predicting future variceal bleeding, based on these criteria, was 100%. Variceal models were developed, and it was demonstrated that during peristaltic contraction there was a significant increase in intravariceal pressure over baseline intravariceal pressure and that the peak intravariceal pressures were directly proportional to the resistance at the gastroesophageal junction. In conclusion, esophageal peristalsis in combination with high resistance to blood flow through the gastroesophageal junction leads to distension of the esophageal varices and an increase in intravariceal pressure and wall tension.     

Relationship between esophageal muscle thickness and intraluminal pressure: an ultrasonographic study

A number of studies show a close temporal relationship between the rate of change in muscle thickness as detected by high-frequency intraluminal ultrasonography (HFIUS) and intraluminal pressure measured by manometry. There is a marked variability in esophageal contraction amplitude from one swallow to another at a given level in the esophagus and along the length of the esophagus. Furthermore, peristaltic pressures are higher in the distal compared with the proximal esophagus. The goal of this study was to evaluate the relationship between the baseline and peak muscle thickness and the contraction amplitude during swallow-induced contractions along the length of the esophagus. Fifteen normal subjects were studied using simultaneous esophageal pressures and HFIUS or HFIUS alone. Recordings were made during baseline and standardized swallows in the lower esophageal sphincter (LES) and at 2, 4, 6, 8, and 10 cm above the LES. HFIUS images were digitized, and esophageal muscle thickness and peak contraction amplitudes were measured. In the resting state, muscle thickness is higher in the LES compared with the rest of the esophagus. Baseline muscle thickness is also significantly higher at 2 cm vs. 10 cm above the LES. In a given subject and among different subjects, there is a good relationship between peak muscle thickness and peak peristaltic pressures (r = 0.55) at all sites along the length of the esophagus. The positive correlation between pressure and muscle thickness implies that the mean circumferential wall stress is fairly uniform from one swallow to another, irrespective of the contraction amplitude.     

Cholinergic stimulation induces asynchrony between the circular and longitudinal muscle contraction during esophageal peristalsis

In healthy subjects, a close temporal correlation exists between contractions of the circular muscle (CM) and longitudinal muscle (LM) layers of the esophagus. Patients with nutcracker esophagus show disassociation between the peak of contractions of the CM and LM layers and the peak of contraction 1-3 s apart (Jung HY, Puckett JL, Bhalla V, Rojas-Feria M, Bhargava V, Liu J, Mittal RK. Gastroenterology 128: 1179-1186, 2005). The purpose of the present study was to evaluate the effect of acetylcholinesterase inhibitor (edrophonium) and acetylcholine receptor antagonist (atropine) on human esophageal peristalsis in normal subjects. High-frequency intraluminal ultrasound imaging and manometry were performed simultaneously during swallow-induced peristalsis in ten normal subjects. Standardized 5-ml water swallows were recorded 2 cm above the lower esophageal sphincter under three study conditions: control, edrophonium (80 microg/kg iv), and atropine (10 microg/kg iv). A close temporal correlation exists between the peak pressure and peak wall thickness during the control period. The mean time lag between the peak LM and peak CM contraction was 0.03 s. After edrophonium administration, the mean contraction amplitude increased from 101 +/- 9 mmHg to 150 +/- 20 mmHg (P < 0.05) and mean peak muscle thickness increased from 3.0 +/- 0.2 mm to 3.6 +/- 0.3 mm (P < 0.01), and duration of both CM and LM contractions were also increased. Furthermore, the mean time difference between the peak LM and CM was increased to 1.1 s, (ranging 0.2 to 3.4 s) (P < 0.0001). We conclude that cholinomimetic agent induces discoordination between the two muscle layers of the esophagus.     

Sleeve sensor versus high-resolution manometry for the detection of transient lower esophageal sphincter relaxations

Transient lower esophageal sphincter relaxations (TLESRs) are the most important mechanism by which gastroesophageal reflux occurs, and sleeve sensor manometry is the gold standard for detection of TLESRs. The aim of this study was to evaluate manometry with closely spaced sideholes (high-resolution manometry) for the detection of TLESRs as an alternative. In 12 patients with gastroesophageal reflux disease, a 90-min postprandial manometry was performed by using a catheter incorporating both a sleeve sensor and closely spaced sideholes in the esophagogastric junction. TLESRs recorded with both techniques were scored. Reflux during TLESRs was detected by using manometry (common cavity), intraluminal impedance, and pH monitoring. A total of 145 TLESRs were detected by using both techniques, 117 with high-resolution manometry and 108 with sleeve sensor manometry [not significant (NS)]. Manometric signs of reflux during TLESRs detected with high-resolution and sleeve sensor manometry were found in 62.4 and 56.5%, NS, respectively, versus 38.5 and 35.2%, NS on pH-metry and 70.1 and 60.2%, NS on impedance monitoring. TLESRs recognized only with high-resolution manometry were more often accompanied by reflux, as detected with manometry (59.5%) and impedance monitoring (67.6%), than TLESRs recognized only with sleeve sensor manometry (32.1 and 28.6%). High-resolution manometry is at least as accurate as sleeve sensor manometry for the detection of TLESRs.     

Determinants of transpyloric fluid transport: a study using combined real-time ultrasound,manometry, and impedance recording

Intraluminal impedance recording has made it possible to record fluid transport across the pylorus during the interdigestive state without filling the stomach. During antral phase II, fluid transport occurs with and without manometrically detectable antral contraction. Our aim was to investigate the relationships between ultrasonographic patterns of antral contraction, manometric pressure waves, and transpyloric fluid transport during antral phase II. Antral wall movements were recorded by real-time ultrasound (US) in eight healthy volunteers (mean age 24 +/- 7 yr) during 17 +/- 5 min of antral phase II. Concomitantly, a catheter positioned across the pylorus, monitored by transmucosal potential difference measurement, recorded five impedance signals (1 antral, 1 pyloric, and 3 duodenal) and six manometric signals (2 antral, 1 pyloric, and 3 duodenal). Antral contractions detected by US at the level of the two antral impedance electrodes were classified according to their association with a pyloric opening or a duodenal contraction. Transpyloric liquid transport events (impedance drop of >40% of the baseline with an antegrade or retrograde propagation) and manometric pressure waves (amplitude and duration) were identified during the whole study and especially during each period of US antral contraction. A total of 110 antral contractions was detected by US. Of these, 79 were also recorded by manometry. Fluid transport across the pylorus was observed in 70.9% of the US-detected antral contractions. Pyloric opening was observed in 98.6% of the contractions associated with fluid transport compared with 50% in the absence of fluid transport (P < 0.05). Antral contractions associated with fluid transport were significantly (P < 0.05) more often propagated to the duodenum (92%) than those without fluid transport (53%). Pressure waves associated with fluid transport were of higher amplitude (208 mmHg, range 22-493) and longer duration (7 s, range 2.5-13.5 s) than those not associated with fluid transport (102 mmHg, range 18-329 mmHg, and 4.1 s, range 2-8.5 s; P < 0.05). The propagation of the antral contractions in the duodenum in US was always associated with a pyloric opening, whereas only 8 of the 25 contractions without duodenal propagation were associated with a pyloric opening (P < 0.05). The presence of duodenal contractile activity before the onset of an antral contraction in US was always accompanied by pyloric opening and with fluid transport in 93.3%, compared with 56.8% in its absence (P < 0.05). In antral phase II, US is the most sensitive technique to detect antral contractions. Transpyloric fluid transport observed in relation to antral contractions occurs mainly in association with contractions of high amplitude and long duration and is associated with pyloric opening and/or duodenal propagation.     

Relationship between esophageal muscle thickness and intraluminal pressure in patients with esophageal spasm

We previously showed, in normal subjects, a positive correlation between the esophageal contraction amplitude and peak muscle thickness. The goal of this study was to determine the relationship between esophageal muscle thickness and contraction amplitude in patients with high-amplitude peristaltic and simultaneous contractions. Eleven patients with high-amplitude peristaltic contractions, 8 with diffuse esophageal spasm (DES), 7 with nonspecific (NS) motor disorder of the esophagus, and 10 normal subjects were studied using simultaneous pressure and ultrasound imaging. Pressure was recorded by manometry and ultrasound imaging with a high-frequency ultrasound probe catheter. Recordings were performed in the lower esophageal sphincter (LES) and at 2, 4, 6, 8, and 10 cm above the LES during resting state and swallow-induced contractions. Baseline esophageal muscle was thicker in the distal, compared with the proximal esophagus both in normal subjects and patient groups. Patients with DES and nutcracker esophagus (NC) have a higher baseline muscle thickness compared with normal and NS patients. Correlation between the peak pressure and the peak muscle thickness was weaker in patients with NC and DES compared with normal subjects and patients with NS. Whereas normal subjects have good correlation between delta (difference between peak and baseline) muscle thickness and peak pressures, this relationship was absent in patients with NC and DES. Increase in contraction amplitude in patients with NC and DES was associated with an increase in baseline thickness of esophageal muscularis propria. Increase in baseline thickness was specific to patients with spastic motor disorders and was not seen in patients with NS.     

Bolus transit patterns in healthy subjects: a study using simultaneous impedance monitoring, videoesophagram, and esophageal manometry

Impedance monitoring (Imp) measures bolus transit. Combining Imp with manometry (EM) allows the effect of contractile patterns on transit to be assessed. The objective of this study is to identify bolus transit patterns in normal subjects, correlate Imp findings with the gold standard barium esophagram (Ba), and compare bolus transit with concomitant EM findings. Simultaneous Ba-Imp-EM was performed for 2 min in 15 normal volunteers (women, 11; age, 43 yr). Combined impedance-pressure sites were 5, 10, 15, 20 cm above the lower esophageal sphincter (LES). Boluses (10 ml) of 45% barium mixed with 0.9% NaCl were swallowed at > or = 20-s intervals (5-6 swallows/subject). Imp and Ba showed three bolus transit patterns, and the two methods were in agreement on the pattern type in 97% (83/86) of swallows. Normal bolus transit was found in 73% (61/83), and each had normal peristalsis and contraction amplitude. Stasis in the proximal esophagus occurred in 7 of 83 swallows despite normal manometric parameters in 4 of 7 swallows. Retrograde escape of a residue of incompletely cleared bolus from just above the LES to the site 5 cm above occurred in 14 of 83 swallows. Retrograde escape was triggered by the next swallow, occurred despite normal manometric parameters, and did not occur if the swallow interval was >30 s. In 55% (47/86) of swallows, air accumulated in the distal esophagus and persisted there for a mean of 3.6 s until cleared into the stomach. We conclude that impedance monitoring is a valid transit test and describe bolus transit patterns in normal subjects for comparison with patients with esophageal motility disorders.     

Effect of hyperglycemia on triggering of transient lower esophageal sphincter relaxations

Acute changes in blood glucose concentration have major effects on gastrointestinal motor function. Patients with diabetes mellitus have an increased prevalence of gastroesophageal reflux. Transient lower esophageal sphincter (LES) relaxation (TLESR) is the most common sphincter mechanism underlying reflux. The aim of this study was to investigate the effect of acute hyperglycemia on triggering TLESRs evoked by gastric distension in healthy volunteers. TLESRs were stimulated by pressure-controlled and volume-controlled (500 ml) gastric distension using an electronic barostat and performed on separate days. On each day, esophageal manometry was performed in the sitting position during gastric distension for 1 h under euglycemia (5 mM), and either marked hyperglycemia (15 mM) or physiological hyperglycemia (8 mM) in randomized order was maintained by a glucose clamp. Marked hyperglycemia doubled the rate of TLESRs in response to both pressure-controlled [5 (3-10.5, median or interquartile range) to 10 (9.5-14.5) per hour, P < 0.02] and volume-controlled [4 (2.5-7.5) to 10.5 (7-12.5) per hour, P < 0.02] gastric distension but had no effect on basal LES pressure. Physiological hyperglycemia had no effect on the triggering of TLESRs or basal LES pressure. In healthy human subjects, marked hyperglycemia increases the rate of TLESRs. Increase in the rate of TLESRs is independent of proximal gastric wall tension. Mechanisms underlying the effect remain to be determined. Hyperglycemia may be an important factor contributing to the increased esophageal acid exposure in patients with diabetes mellitus.     

Temporal relationships between wall motion, intraluminal pressure, and flow in the isolated rabbit small intestine

Intraluminal manometry is a tool commonly used to record motility in the human digestive tract. The recorded signal results from a combination of factors, including the hydrodynamic pressure transmitted through the intestinal contents due to contraction of the gut wall and the force of the gut wall acting on the sensors in regions of a luminal occlusion. However, the actual relationships between small bowel wall contraction, the measured intraluminal pressure, and the resultant flow have not been directly addressed. Video recording and high-resolution fiber-optic manometry were used to create spatiotemporal video maps of diameter and intraluminal pressure from isolated segments of rabbit small intestine. In the unstimulated gut, longitudinal muscle contractions were the only detectable motor pattern; circular muscle contractions were elicited by distension or erythromycin (1 μM). Longitudinal muscle contractions were not lumen-occlusive, although they caused measurable low-amplitude changes in pressure. Localized nonpropagating circular muscle contractions caused small localized, nonpropagating peaks of intraluminal pressure. Propagating contractions of circular muscle evoked larger, propagating pressure changes that were associated with outflow. Propagating circular muscle contractions often caused dilation of aboral receiving segments, corresponding to "common cavities"; these were propulsive, despite their low intraluminal pressure. The highest-amplitude pressure events were caused by lumen-occlusive circular muscle contractions that squeezed directly against the catheter. These data allow us to define the complex relationships between wall motion, intraluminal pressure, and flow. A strong correlation between circular and longitudinal muscle contraction and intraluminal pressure was demonstrated. Common-cavity pressure events, caused by propulsion of content by circular muscle contractions into a receptive segment, were often of low amplitude but were highly propulsive. Studies of wall motion in isolated preparations, combined with manometry, can assist in interpretation of pressure recordings in vivo.     

Effects of electrocardiography contamination and comparison of ECG removal methods on upper trapezius electromyography recordings

Electromyography (EMG) recordings from the trapezius are often contaminated by the electrocardiography (ECG) signal, making it difficult to distinguish low-level muscle activity from muscular rest. This study investigates the influence of ECG contamination on EMG amplitude and frequency estimations in the upper trapezius during muscular rest and low-level contractions. A new method of ECG contamination removal, filtered template subtraction (FTS), is described and compared to 30 Hz high-pass filter (HPF) and averaged template subtraction (ATS) methods. FTS creates a unique template of each ECG artifact using a low-pass filtered copy of the contaminated signal, which is subtracted from contaminated periods in the original signal. ECG contamination results in an over-estimation of EMG amplitude during rest in the upper trapezius, with negligible effects on amplitude and frequency estimations during low-intensity isometric contractions. FTS and HPF successfully removed ECG contamination from periods of muscular rest, yet introduced errors during muscle contraction. Conversely, ATS failed to fully remove ECG contamination during muscular rest, yet did not introduce errors during muscle contraction. The relative advantages and disadvantages of different ECG contamination removal methods should be considered in the context of the specific motor tasks that require analysis.     

Upper esophageal sphincter impedance as a marker of sphincter opening diameter

The measurement of the physical extent of opening of the upper esophageal sphincter (UES) during bolus swallowing has to date relied on videofluoroscopy. Theoretically luminal impedance measured during bolus flow should be influenced by luminal diameter. In this study, we measured the UES nadir impedance (lowest value of impedance) during bolus swallowing and assessed it as a potential correlate of UES diameter that can be determined nonradiologically. In 40 patients with dysphagia, bolus swallowing of liquids, semisolids, and solids was recorded with manometry, impedance, and videofluoroscopy. During swallows, the UES opening diameter (in the lateral fluoroscopic view) was measured and compared with automated impedance manometry (AIM)-derived swallow function variables and UES nadir impedance as well as high-resolution manometry-derived UES relaxation pressure variables. Of all measured variables, UES nadir impedance was the most strongly correlated with UES opening diameter. Narrower diameter correlated with higher impedance (r = -0.478, P < 0.001). Patients with <10 mm, 10-14 mm (normal), and ≥ 15 mm UES diameter had average UES nadir impedances of 498 ± 39 Ohms, 369 ± 31 Ohms, and 293 ± 17 Ohms, respectively (ANOVA P = 0.005). A higher swallow risk index, indicative of poor pharyngeal swallow function, was associated with narrower UES diameter and higher UES nadir impedance during swallowing. In contrast, UES relaxation pressure variables were not significantly altered in relation to UES diameter. We concluded that the UES nadir impedance correlates with opening diameter of the UES during bolus flow. This variable, when combined with other pharyngeal AIM analysis variables, may allow characterization of the pathophysiology of swallowing dysfunction.     

Enhancement of antral contractions and vagal afferent signaling with synchronized electrical stimulation

Gastric filling activates vagal afferents involved in peripheral signaling to the central nervous system (CNS) for food intake. It is not known whether these afferents linearly encode increasing contractions of the antrum during antral distension (AD). The aim of this study was to investigate effects of AD and electrically enhanced antral contractions on responses of vagal afferents innervating the antrum. Single-fiber recordings were made from the vagal afferents in anesthetized male Long-Evans rats. Antral contractions were measured with a solid-state probe placed in the antrum. A nonexcitatory electrical stimulation (NES) inducing no smooth muscle contractions was applied during the ascending phase of antral contractions to enhance subsequent antral contractions. Fifty-six fibers identified during AD (1 ml for 30 s) were studied through different types of mechanical stimuli. Under normal conditions, one group of fibers exhibited rhythmic firing in phase with antral contractions. Another group of fibers had nonrhythmic spontaneous firing. Responses of 15 fibers were tested with NES during multiple-step distension (MSD). NES produced a mean increase in antral contraction amplitude (177.1 +/- 35.3%) and vagal afferent firing (21.6 +/- 2.6%). Results show that both passive distension and enhanced antral contractions activate distension-sensitive vagal afferents. Responses of these fibers increase linearly to enhanced antral contraction induced by NES or MSD up to a distending volume of 0.6 ml. However, responses reached a plateau at a distending volume >0.8 ml. We concluded that enhanced contraction of the antrum can activate vagal afferents signaling to the CNS.     

Muscle contraction-blood flow interactions during upright knee extension exercise in humans.

To test for evidence of a muscle pump effect during steady-state upright submaximal knee extension exercise, seven male subjects performed seven discontinuous, incremental exercise stages (3 min/stage) at 40 contractions/min, at work rates ranging to 60-75% peak aerobic work rate. Cardiac cycle-averaged muscle blood flow (MBF) responses and contraction-averaged blood flow responses were calculated from continuous Doppler sonography of the femoral artery. Net contribution of the muscle pump was estimated by the difference between mean exercise blood flow (MBFM) and early recovery blood flow (MBFR). MBFM rose in proportion with increases in power output with no significant difference between the two methods of calculating MBF. For stages 1 and 5, MBFM was greater than MBFR; for all others, MBFM was similar to MBFR. For the lighter work rates (stages 1-4), there was no significant difference between exercise and early recovery mean arterial pressure (MAP). During stages 5-7, MAP was significantly higher during exercise and fell significantly early in recovery. From these results we conclude that 1) at the lightest work rate, the muscle pump had a net positive effect on MBFM, 2) during steady-state moderate exercise (stages 2-4) the net effect of rhythmic muscle contraction was neutral (i.e., the impedance due to muscle contraction was exactly offset by the potential enhancement during relaxation), and 3) at the three higher work rates tested (stages 5-7), any enhancement to flow during relaxation was insufficient to fully compensate for the contraction-induced impedance to muscle perfusion. This necessitated a higher MAP to achieve the MBFM.     

Seasonal changes in the effects of arginine vasotocin and stretch on Anolis uterine contractions in vitro

We determined the effects of acute stretch on spontaneous and arginine vasotocin (AVT)-driven contractions of the Anolis carolinensis uterus in vitro. Whole uteri from reproductively inactive females (October) were placed in a bath of oxygenated 32 degrees C Anolis "Ringer's." Two initial tensions were utilized, 1.5 g or 15 g, the latter being an estimate of the tension on the wall of a uterine compartment. Uteri were then exposed to either saline or AVT (50 ng/ml), and spontaneous or AVT-driven contractions were recorded for 20 min with the use of a strain gauge and physiograph. A similar experiment was performed on uteri from reproductively active females in the summer (June). Our results indicate that the effects of acute stretch and AVT on uterine contractility were qualitatively similar in summer and fall. That is, AVT induced a tonic contraction; stretch decreased the duration of the tonic contraction; the saline-treated uteri exhibited spontaneous rhythmic contractions; AVT increased the amplitude of the rhythmic contractions, but only at the lower tension; there were no effects of AVT on the timing (contraction interval, duration, rest interval) of the rhythmic contractions; and stretch increased the frequency of the rhythmic contractions. Season greatly influenced the magnitude of these contractile phenomena. Uteri tested during the breeding season exhibited greater distensibility, an increase in the amplitude and duration of the AVT-driven tonic contraction, and an increase in the frequency of both spontaneous and AVT-driven rhythmic contractions because of a decrease in both contraction duration and rest interval.(ABSTRACT TRUNCATED AT 250 WORDS)     

Residual force enhancement following eccentric induced muscle damage

During lengthening of an activated skeletal muscle, the force maintained following the stretch is greater than the isometric force at the same muscle length. This is termed residual force enhancement (RFE), but it is unknown how muscle damage following repeated eccentric contractions affects RFE. Using the dorsiflexors, we hypothesised muscle damage will impair the force generating sarcomeric structures leading to a reduction in RFE. Following reference maximal voluntary isometric contractions (MVC) in 8 young men (26.5±2.8y) a stretch was performed at 30°/s over a 30° ankle excursion ending at the same muscle length as the reference MVCs (30° plantar flexion). Surface electromyography (EMG) of the tibialis anterior and soleus muscles was recorded during all tasks. The damage protocol involved 4 sets of 25 isokinetic (30°/s) lengthening contractions. The same measures were collected at baseline and immediately post lengthening contractions, and for up to 10min recovery. Following the lengthening contraction task, there was a 30.3±6.4% decrease in eccentric torque (P<0.05) and 36.2±9.7% decrease in MVC (P<0.05) compared to baseline. Voluntary activation using twitch interpolation and RMS EMG amplitude of the tibialis anterior remained near maximal without increased coactivation for MVC. Contrary to our hypothesis, RFE increased (～100-250%) following muscle damage (P<0.05). It appears stretch provided a mechanical strategy for enhanced muscle function compared to isometric actions succeeding damage. Thus, active force of cross-bridges is decreased because of impaired excitation-contraction coupling but force generated during stretch remains intact because force contribution from stretched sarcomeric structures is less impaired.     

Cholinergic receptors in the Aplysia gill

Acetylcholine has been suggested as a neurotransmitter released in the Aplysia gill by peripheral afferents of central neurons and by peripheral neurons within the gill. The perfused gill, isolated from the abdominal ganglion, was examined. At concentrations greater than 1 microM, acetylcholine elicited a slowly developing tonic contraction of the afferent vein that reversed upon washout. This effect was observed on both quiescent and active preparations. At concentrations less than 1 microM, acetylcholine perfusion resulted in a reduction of gill tone. The excitatory effect of acetylcholine was reduced 80 and 60% by the cholinergic antagonists atropine and hexamethonium, respectively. The acetylcholine-evoked contraction was potentiated 2.5-fold when curare was coinfused. Carbachol did not mimic the excitatory effects of acetylcholine. At all concentrations examined (1-100 microM), carbachol infusion reduced baseline tension, the amplitude of spontaneous contractions and contractions evoked by FMRFamide and dopamine. Contractions evoked by perfusion of p-chlorophenylthiocyclic AMP were greatly reduced when carbachol was added to the perfusate. Further addition of curare reversibly blocked carbachol inhibition of the cyclic AMP-evoked contractions. These findings suggest that excitatory and inhibitory cholinergic receptors are involved in the regulation of gill contractile behavior by acetylcholine.     

MRI measures of perfusion-related changes in human skeletal muscle during progressive contractions.

Although skeletal muscle perfusion is fundamental to proper muscle function, in vivo measurements are typically limited to those of limb or arterial blood flow, rather than flow within the muscle bed itself. We present a noninvasive functional MRI (fMRI) technique for measuring perfusion-related signal intensity (SI) changes in human skeletal muscle during and after contractions and demonstrate its application to the question of occlusion during a range of contraction intensities. Eight healthy men (aged 20-31 yr) performed a series of isometric ankle dorsiflexor contractions from 10 to 100% maximal voluntary contraction. Axial gradient-echo echo-planar images (repetition time = 500 ms, echo time = 18.6 ms) were acquired continuously before, during, and following each 10-s contraction, with 4.5-min rest between contractions. Average SI in the dorsiflexor muscles was calculated for all 240 images in each contraction series. Postcontraction hyperemia for each force level was determined as peak change in SI after contraction, which was then scaled to that obtained following a 5-min cuff occlusion of the thigh (i.e., maximal hyperemia). A subset of subjects (n = 4) performed parallel studies using venous occlusion plethysmography to measure limb blood flow. Hyperemia measured by fMRI and plethysmography demonstrated good agreement. Postcontraction hyperemia measured by fMRI scaled with contraction intensity up to approximately 60% maximal voluntary contraction. fMRI provides a noninvasive means of quantifying perfusion-related changes during and following skeletal muscle contractions in humans. Temporal changes in perfusion can be observed, as can the heterogeneity of perfusion across the muscle bed.