| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Department of Physiology, Graduate School of Health Sciences, Hiroshima University, Kasumi, Minami-ku, Hiroshima, Japan
Submitted 27 November 2006 ; accepted in final form 13 February 2007
 |
ABSTRACT |
|---|
 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
muscle thin fiber afferents; passive mechanical stretch; gadolinium; exercise; anesthetized rats
It appears that mechanical stimuli activate primarily group III afferents, whereas metabolic stimuli activate primarily group IV afferents (12–14). Group III afferents are expected to excite promptly at the onset of static muscle contraction, which may in turn induce the rapid reflex responses. When the reflex cardiovascular and sympathetic nerve responses were compared between static contraction and passive stretch in anesthetized or decerebrate animals, the time course and magnitude of the responses followed tension development and were almost the same between the two interventions despite the different changes in muscle length (16, 22, 23). Thus it will be postulated that the mechanoreceptors that contribute to the exercise pressor reflex are more sensitive to a change in muscle tension than a change in muscle length. If so, such mechanoreceptors may be located around the myotendinous junction in series with extrafusal muscle fibers like a Golgi tendon organ (5, 6). We hypothesized that the mechanosensitive receptors responsible for the reflex cardiovascular responses might be located at or close to the myotendinous junction to monitor tension development during muscular activity. To test this hypothesis, we examined the reflex cardiovascular responses to passive stretch of the triceps surae muscle with the three kinds of the experimental interventions: systemic injection of gadolinium, cutting the Achilles tendon, and local injection of lidocaine into the myotendinous junction. Passive stretch of the triceps surae muscle predominantly stimulates mechanosensitive receptors (11–14, 31). Gadolinium, a trivalent lanthanide, is known to block cation-selective mechanosensitive channels (3, 7, 9). Indeed, gadolinium attenuated the activation of group III mechanosensitive afferents to both static contraction and to tendon stretch and the resultant cardiovascular responses (10, 20, 29). Consequently, gadolinium can serve as a tool to determine a role played by mechanosensitive thin fiber afferents. First, we attempted to confirm the effect of gadolinium on the muscle mechanoreflex during passive stretch of the triceps surae muscle, precisely evaluating the muscle length-tension relationship. Second, to examine whether stimulation of mechanosensitive receptors in the tendon might evoke the cardiovascular responses during passive stretch, we conducted passive stretch of the triceps surae muscle with the cut and reconnected Achilles tendon. Afferent signals from the more distal part of the cut Achilles tendon during passive stretch of the triceps surae muscle would be eliminated by the intervention. If the responses to passive stretch under such condition would be attenuated compared with that with the intact tendon, mechanoreceptors located in the Achilles tendon might have an important role in evoking the reflex cardiovascular responses. Finally, to investigate whether mechanosensitive afferent fibers terminating at or passing through the myotendinous junction contribute to the exercise pressor reflex, passive stretch of the triceps surae muscle was conducted before and after injection of lidocaine into the myotendinous junction. Lidocaine is known to block excitation of small myelinated (group III) and unmyelinated (group IV) fibers. Although muscle afferent fibers passing through the myotendinous junction could not be excluded from the lidocaine experiments alone, contribution of those afferents would be revealed by cutting Achilles tendon experiments.
|
METHODS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
General Preparations
A mixture of 4% halothane, N2O, and O2 was used to initially anesthetize the rats in a plastic box, and then a face mask was attached. After the concentration of halothane was lowered to a level of 1.0–1.5% enough to keep anesthesia through the mask, surgery was started. ECG, heart rate (HR), and rectal temperature were continuously monitored. Respiratory thoracic movement was visually observed. Rectal temperature was maintained at 37.0–38.0°C with a heating pad. To maintain an appropriate level of surgical anesthesia, the concentration of halothane was usually preset in a range of 1.0–1.5%, but it was increased to 2.0–2.5% if an increase in HR and/or respiration and/or withdrawal of the limb in response to noxious pinch of the paw and/or a surgical procedure was observed. Catheters were inserted into the left external jugular vein for administration of drugs and into the left carotid artery for measurement of arterial blood pressure (AP). AP was continuously monitored with a pressure transducer (model DPT III, Baxter, Tokyo, Japan). The rats were given an initial dose of pentobarbital sodium (50 mg/kg) intraperitoneally. The trachea was exposed and, after halothane anesthesia was stopped, an endotracheal tube was inserted into the airway. A muscle relaxant, D-tubocurarine chloride (0.6 mg), was intravenously administered to eliminate muscle contraction. Then the lungs were artificially ventilated using a respirator (SN-480-7, Shinano, Tokyo, Japan). To maintain an appropriate level of anesthesia, pentobarbital sodium was administered (2–5 mg/kg iv) as necessary. Furthermore, a catheter was inserted via the right femoral artery into the iliac bifurcation of the abdominal aorta in five rats to administer gadolinium into the arterial supply of the left hindlimb.
The rats were placed in the lateral posture. The pelvis and the knee joints were clamped to prevent movement of the body trunk and hindlimbs. The triceps surae muscle, the Achilles tendon, and the calcaneus bone of either hindlimb were exposed. The calcaneus bone was sectioned, and the Achilles tendon was connected to a force transducer (model TU-CR 50N, TEAC) for measurement of muscle tension. The initial tension of the triceps surae muscle was preset at 70–100 g prior to any manipulation. The triceps surae muscle was stretched for 1 min with a manipulator, which allowed measuring a change in muscle length precisely. Three different magnitudes of tension (500, 750, and 1,000 g) were used to assess the relationship between tension development and the cardiovascular responses. Timing at the start and end of stretch was manually marked with an electric switch. HR was obtained from the R wave of ECG or AP pulse. HR, AP, muscle tension, and the marking signal were simultaneously recorded on an eight-channel pen-writing recorder (model 8M14, GE Marquette Medical Systems, Tokyo, Japan) and were also stored in a computer via an analog-to-digital converter (model MP100, BIOPACK system, Santa Barbara, CA) at a sampling frequency of 1 kHz.
Protocols
We conducted the three kinds of the experimental interventions; systemic injection of gadolinium, cutting the Achilles tendon, and locally injecting lidocaine into the myotendinous junction. Regarding the experimental order, we conducted first passive stretch of the triceps surae muscle with the cut or intact Achilles tendon. Next, passive stretch of the triceps surae muscle was conducted before and after injection of lidocaine into the myotendinous junction. The rats were allowed to recover from the effect of lidocaine prior to the gadolinium protocol. Finally, passive stretch of the triceps surae muscle was conducted before and after systemic injection of gadolinium. Four rats were involved in all protocols, and the remaining rats were involved at least in two protocols.
Intravenous or intra-arterial injection of gadolinium. To examine whether mechanical stimuli might play a role in evoking a pressor reflex during passive stretch, gadolinium was injected intravenously via the jugular vein (n = 11 rats) or intra-arterially via the iliac artery with (n = 3 rats) and without (n = 2 rats) venous occlusion. Gadolinium chloride hexahydrate (Aldrich Chemical, Milwaukee, WI) was dissolved in HEPES buffer with a concentration of 20 mM (pH 7.3–7.4) according to previous studies (3, 9, 10, 20, 29). Gadolinium was intravenously administered with a volume of 2.1 ± 0.3 ml/kg and intra-arterially with a volume of 3.0 ml/kg. A series of passive stretches of the triceps surae muscle were conducted before and 20–30 min after injection of gadolinium. On injection gadolinium intra-arterially with venous occlusion, a ligature around the left femur was tightened for 10–15 min to trap gadolinium in the hindlimb circulation as previously reported (29). A series of passive stretches were conducted 20–60 min after entrapment of gadolinium.
Cutting the Achilles tendon. If the triceps surae muscle with the sutured Achilles tendon were stretched acutely with the same tension development, the tendon would be ruptured again. Instead of this, we addressed the chronic experiments, because the cut and sutured Achilles tendon was able to heal with connective tissue a week after the surgery. In addition, because afferent fibers had not regenerated yet, afferent signals from the Achilles tendon below the cut level were expected to be eliminated. When we cut the left Achilles tendon (n = 10 rats), a mixture of 4% halothane, N2O, and O2 was used to initially anesthetize the rats in the plastic box and then the face mask was attached. After the concentration of halothane was lowered to a level of 1.0–1.5%, enough to keep anesthesia through the mask, surgery was started. ECG, HR, rectal temperature, and respiration were continuously monitored. Rectal temperature was maintained at 37.0–38.0°C with a heating pad. To maintain an appropriate level of surgical anesthesia, the concentration of halothane was usually preset in a range of 1.0–1.5%, but it was increased to 2.0–2.5% if necessary. The left Achilles tendon was exposed and cut at the proximal one-third level of the Achilles tendon (Fig. 1). Both ends of the cut Achilles tendon were sutured. Soon after recovery from anesthesia, the rats were able to perform daily activity as well as before achillotomy. Eight to 20 days after the surgery, the rats were anesthetized again. The cardiovascular responses during passive stretch of the triceps surae muscle with the cut Achilles tendon were compared with those during passive stretch with the right intact Achilles tendon.
|
6% of the triceps surae muscle volume was stained as shown in Fig. 1. Because the dye did not spread over the triceps surae muscle, it is likely that lidocaine influenced afferent signals from or through the myotendinous junction. Data Analysis
To quantify the reflex cardiovascular responses in a given passive stretch trial, we measured both peak and integrated increases in HR and MAP. The integrated values of the increases in HR and MAP over the 1-min passive stretch were denoted as integrated 
HR and MAP, respectively. The integrated HR and MAP and the change in muscle length were compared using a paired t-test in each of the three interventions: 1) passive stretch before and after gadolinium, 2) passive stretch between the intact and cut Achilles tendons, and 3) passive stretch before and after local injection of lidocaine into the myotendinous junction. The level of statistical significance was defined as P < 0.05 in all cases. The data are expressed as means ± SE.
|
RESULTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
The baseline values of HR and MAP were 492 ± 10 beats/min and 83 ± 2 mmHg, respectively, which were not affected by intravenous injection of gadolinium (n = 11 rats). HR and MAP increased during passive stretch of the triceps surae muscle as shown in Fig. 2. The tension development of the triceps surae muscle was in proportion to the extent of the increase in muscle length. The more muscle tension was developed, the more HR and MAP were augmented. The integrated HR during 1,000-g-tension stretch was significantly decreased by gadolinium to 64% of the control response, though the integrated tension was the same (Fig. 2). The integrated MAP were also decreased to 74–78% of the control at 750-g-tension stretch and at 1,000-g-tension stretch. Similarly, the peak values of the increases in HR and MAP were blunted by gadolinium to 67 and 58–80% of the control values, respectively. The changes in muscle length at 500- and 750-g-tension stretch were not affected by intravenous injection of gadolinium. The muscle length change at 1,000-g-tension stretch became smaller (control vs. gadolinium; 6.5 ± 0.2 vs. 5.7 ± 0.2 mm); i.e., the resting length-tension relationship was altered by gadolinium.
|
HR and MAP to 11–37 and 16–34% of the control responses, respectively; the intra-arterial injection of gadolinium without venous occlusion also decreased the integrated HR and MAP to 14–24 and 30–49%, respectively. The baseline values of HR and MAP did not change following intra-arterially injection of gadolinium, irrespective of venous occlusion. Cutting the Achilles Tendon
In Fig. 3, the reflex cardiovascular responses during passive stretch of the triceps surae muscle were compared between the intact tendon and the cut Achilles tendon in the same rat. On the intact side, as tension was developed, HR and AP were increased by 11 beats/min and 12 mmHg, respectively; the integrated HR over the passive stretch was 293 beats·min–1·s and the integrated MAP was 383 mmHg·s. During passive stretch of the triceps surae muscle with the cut Achilles tendon, the similar cardiovascular responses were obtained; HR and AP were increased by 16 beats/min and 12 mmHg, respectively. The integrated HR was 281 beats·min–1·s, and the integrated MAP was 454 mmHg·s.
|
HR, integrated MAP, and the integrated increase of tension and the changes in muscle length during passive stretch of the triceps surae muscle were summarized with the cut and intact Achilles tendons in Fig. 4. The tension of the triceps surae muscle with the cut Achilles tendon was developed in proportion to lengthening of the muscle, suggesting that the muscle length-tension relationship was not disturbed by the achillotomy (Fig. 4). The average integrated HR and MAP during passive stretch of the triceps surae muscle with the cut Achilles tendon were similar to those with the intact Achilles tendon. The peak increases in HR and MAP during passive stretch were also the same between the cut and intact Achilles tendons.
|
Typical changes in HR and AP during passive stretch before and after injection of lidocaine into the myotendinous junction of the Achilles tendon are shown in Fig. 5. Lidocaine blunted the reflex cardiovascular responses to passive stretch of the triceps surae muscle. The average increases in HR and MAP during passive stretch before and after lidocaine are summarized in Fig. 6. Because the tension of the triceps surae muscle was similarly developed in proportion to lengthening of the muscle following lidocaine, the length-tension relationship was not affected by lidocaine. The integrated HR during passive stretch was significantly decreased by lidocaine to 49% of the control value at 750-g-tension stretch and to 63% at 1,000-g-tension stretch in Fig. 6. Similarly, the integrated MAP during passive stretch was significantly decreased to 66% at 750-g-tension stretch and to 73% at 1,000-g-tension stretch. The reduction in the peak increases in HR and MAP was smaller than the reduction in their integrated increases. Indeed, the peak increase in HR was blunted by lidocaine to 78–88% (from 24 ± 4 to 21 ± 5 beats/min at 750-g-tension stretch and from 40 ± 9 to 31 ± 7 beats/min at 1,000-g-tension stretch); the peak rise in MAP was blunted to 78% (from 23 ± 4 to 18 ± 4 mmHg at 750-g-tension stretch and from 32 ± 5 to 25 ± 5 mmHg at 1,000 g-tension stretch).
|
|
|
DISCUSSION |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
Effect of Gadolinium on the Cardiovascular Responses During Passive Stretch
We confirmed that gadolinium significantly blunted on the reflex responses in HR and MAP to passive stretch of the triceps surae muscle in agreement with previous studies (10, 20, 29), indicating that the reflex cardiovascular responses to passive stretch were evoked by stimulation of muscle mechanosensitive receptors. Indeed, Hayes and Kaufman (10) reported that gadolinium attenuated the responses of group III afferents from the triceps surae muscle to tendon stretch, suggesting that gadolinium might exert its effect on group III skeletal muscle mechanoreceptors by blocking stretch-activated ion channels. Furthermore, we found that gadolinium altered the resting length-tension relationship. After injecting gadolinium, the change in muscle length at 1,000-g-tension stretch became smaller than before gadolinium, suggesting that resting muscle stiffness is augmented by gadolinium. Because a muscle relaxant was administered in the present study, muscle contraction induced by stretch reflex was not relevant. Gadolinium is considered to act as a calcium analog (19) and may affect the calcium ion transduction system of skeletal muscle. However, a precise mechanism for the increased muscle stiffness remains to be solved.
Because arterial baroreceptors in the cardiovascular system are mechanosensitive and spontaneously active, gadolinium may influence mechanoelectrical transduction in arterial baroreceptors. If so, systemic administration of gadolinium might affect baseline hemodynamics; for example, decreased activity in arterial baroreceptors will cause an increase in sympathetic nerve activity and raise HR and MAP. Recently, our laboratory reported that gadolinium (55 µmol/kg iv) did not alter the baseline values of HR and MAP in both conscious and anesthetized cats (20). Furthermore, gadolinium (42 µmol/kg) in this study and a smaller dose of gadolinium (20–40 µmol/kg) (3, 9) had no significant effect on baseline hemodynamics in anesthetized animals. Therefore, it is likely that systemic administration of gadolinium less than 50 µmol/kg does not alter the ongoing activity of arterial mechanosensitive baroreceptors. Indeed, when we recently conducted a preliminary study on the effect of systemically administered gadolinium on aortic baroreceptor activity in anesthetized cats, we found that the same dose of gadolinium (40–50 µmol/kg) did not change the stimulus-response curve of aortic baroreceptors (unpublished observation). The discrepancy regarding the effect of gadolinium on baroreceptor activity may be partly explained by a difference in the drug injection method (intra-arterial vs. intravenous) and accordingly by a difference in concentration of gadolinium in the carotid sinus and aortic regions.
Mechanoreceptors Located at the Myotendinous Junction Evoke Reflex Responses
Mense and Meyer (25) distinguished two types of group III mechanoreceptors in the cat triceps surae muscle. One was low-threshold pressure-sensitive receptors responding to innocuous indentation of the tissue and distributing widely over the muscle and tendon, which were relatively insensitive to stretch and contraction. The other was contraction-sensitive receptors responding to active contraction and innocuous passive stretch of the muscle, whose exact location was not identified because the contraction-sensitive mechanoreceptors were relatively insensitive to local pressure stimulation. At first, the mechanoreceptors eliciting the exercise pressor reflex might exist in the Achilles tendon, because group III afferent fibers terminate within blood and lymphatic vessel walls and between collagen fibers in the Achilles tendon (2, 4, 25, 30, 32). To examine this possibility, we conducted passive stretch of the triceps surae muscle with the cut Achilles tendon. When comparing the reflex cardiovascular responses to passive stretch between the cut Achilles tendon and the intact Achilles tendon, we observed the same cardiovascular responses (Figs. 3 and 4). This result suggested that mechanoreceptors, which ended in the more distal part of tendon than the cut level, did not contribute to the reflex cardiovascular responses. Mense and Meyer (25) reported that the low-threshold pressure-sensitive mechanoreceptors existed in the Achilles tendon did not respond to both passive stretch and muscle contraction. Therefore, mechanoreceptors evoking the reflex cardiovascular responses should locate in the more proximal part than the cut level, i.e., within the muscle and/or near the myotendinous junction.
It has been reported that some group III afferent fibers terminate in intramuscular connective tissues (5) and within muscle spindles (30), implying a possibility that the mechanoreceptors within the muscle might respond to tendon stretch and the resultant cardiovascular responses. On the other hand, the myotendinous junction of the Achilles tendon is innervated by not only group Ib afferent fibers but also thin afferent fibers (1, 30). Abrahams et al. (1) reported that some group III receptors lie in or close to intramuscular tendinous material in dorsal neck muscle of the cat. Therefore, it is likely that mechanoreceptors evoking the exercise pressor reflex might exist within the muscle and/or in the myotendinous junction. To investigate this, we addressed passive stretch of the triceps surae muscle before and after injecting lidocaine into the myotendinous junction. The injection of lidocaine into the myotendinous junction did not abolish but reduced the cardiovascular responses by approximately one-third. Because lidocaine did not spread over the triceps surae muscle, lidocaine influenced only mechanoreceptors located near and at the myotendinous junction. The length-tension relationship was not affected by lidocaine, suggesting the same mechanical condition of the muscle-tendon complex with and without lidocaine. Accordingly, the reduction in the reflex cardiovascular responses results from blunted muscle afferent signals. Although muscle afferent fibers passing through the myotendinous junction cannot be excluded from the lidocaine experiments, the mechanoreceptors in most part of the Achilles tendon are unlikely to contribute to the reflex cardiovascular responses as mentioned in the previous paragraph. Because the myotendinous junction is arranged in series with extrafusal fibers, the mechanoreceptors near the myotendinous junction are advantageous for monitoring tension development and more sensitive to a change in tension development like a Golgi tendon organ. As a candidate, free nerve endings of group III afferent fibers found in the tendon at the myotendinous junction and in the capsule of Golgi tendon organs (2, 4, 30, 32) are at least partly considered. However, because the injection of lidocaine could not abolish the cardiovascular responses during passive stretch, it cannot be denied that the mechanoreceptors eliciting the exercise pressor reflex might be located at the head of the triceps surae muscle and in the muscle belly.
It is of interest that, even after local injection of lidocaine into the myotendinous junction, HR and MAP increased at the initial period of passive stretch as shown in Fig. 5, implying that intramuscular mechanosensitive thin fiber afferents may play a partial role in evoking the initial increases in HR and MAP. Because the cardiovascular responses appeared only at the initial brief period and did not last throughout passive stretch, the mechanoreceptors should respond to a change in muscle length and/or velocity rather than tension development. The local application of lidocaine into the myotendinous junction may distinguish the reflex cardiovascular responses that correspond to a mechanical event of the changes in muscle length and/or velocity from those that correspond to a mechanical event of tension development. The former cardiovascular responses appear to be small and short-lasting, whereas the latter cardiovascular responses appear to be greater and sustained throughout passive stretch. This is in favor of the previous finding that the discharge of mechanosensitive group III and IV afferents showed a variety of responses during passive mechanical stretch of skeletal muscle (11, 14); discharge of some group III afferents was rapidly adapting at the onset of passive stretch, and other group III and IV afferents had a sustained type of discharge.
Limitations
Some limitations are involved in this study. First, the triceps surae muscle might be stretched beyond the physiological rage. To investigate this, the triceps surae muscle was maximally lengthened by manual stretch of a hindlimb in three anesthetized rats. When the knee joint was extended by 55° from the normal posture and the ankle joint was dorsiflexed by 5° during manual stretch, the increase in length of the triceps surae muscle was 5 ± 1 mm. Therefore, the 1,000-g-tension stretch in the present study might be beyond the physiological range of the muscle length and might activate not only mechanoreceptors but also nociceptors. However, because 500- and 750-g-tension stretch did not exceed the physiological limit of the muscle length, they were capable of stimulating muscle mechanosensitive afferents alone. All muscle interventions used in this study influenced the reflex cardiovascular responses during 750-g-tension stretch as well as 1,000-g-tension stretch. Therefore, our major findings can be predominantly explained by stimulating mechanosensitive afferents. Second, mechanosensitive receptor near the myotendinous junction may be sensitive to passive stretch, but not to muscle contraction, because Hayes et al. (11) reported that tendon stretch stimulated a different population of group III mechanosensitive afferents than did static contraction. Mense and Meyer (25) reported that one-half of static contraction-sensitive afferents did not respond to passive stretch. However, because we found in a preliminary experiment that local injection of lidocaine into the myotendinous junction blunted the reflex responses in HR and MAP during evoked static contraction of the triceps surae muscle as well as passive stretch (unpublished observation), it is speculated that the mechanosensitive receptors that are localized near the myotendinous junction respond not only to passive stretch but also to muscle contraction. Third, it cannot be neglected that intravenous or intra-arterial injection of gadolinium might affect mechanosensitive receptors in other tissues except for skeletal muscle. To examine this possibility, we performed some experiments to inject gadolinium intra-arterially with occluding the venous side of the hindlimb circulation as previously reported (10, 29). Indeed, the reflex responses in HR and MAP during passive stretch were similarly reduced by gadolinium irrespective of venous occlusion, suggesting that gadolinium predominantly influenced the mechanosensitive receptors in skeletal muscle, but not in other tissues. Finally, gadolinium may influence mechanoreceptors existing in skeletal muscle cells as well as mechanoreceptors on the afferent nerve endings, because the mechanoreceptors in skeletal muscle cells may contribute to a release of metabolites and thereby elicit a pressor reflex (17). If gadolinium can block the mechanoreceptors in skeletal muscle cells, a blunted release of metabolites may lead to an attenuated response of group IV muscle afferents, many of which are metabolically sensitive. However, gadolinium had no effect on the responses of group IV muscle afferents to either static contraction or to intraarterial-injection of capsaicin (10). Therefore, it is unlikely that gadolinium can influence a release of metabolites from skeletal muscle during passive stretch if any.
It is concluded that, although free nerve endings of muscle thin fiber afferents seems to be present in every tissue of skeletal muscle, the mechanosensitive receptors responsible for the reflex cardiovascular responses may at least partly locate close to the myotendinous junction, to monitor tension development during muscular activity.
|
GRANTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
ACKNOWLEDGMENTS |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
|
FOOTNOTES |
|---|
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
|
REFERENCES |
|---|
|
TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSACKNOWLEDGMENTSREFERENCES |
|---|
This article has been cited by other articles:
|
|
 |
|
  K. Matsukawa and T. Nakamoto Muscle mechanosensitive reflex is suppressed in the conscious condition: effect of anesthesia J Appl Physiol, January 1, 2008; 104(1): 82 - 87. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
