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Departments of 1 Geriatric Dentistry and 2 Pharmacology, School of Dentistry, Tohoku University, 4-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The effects of different types of stress (water bathing, cold, restraint, and prolonged walking) on histidine decarboxylase (HDC) activity in masseter, quadriceps femoris, and pectoralis superficial muscles, and in the stomach were examined in mice. All of these stresses elevated gastric HDC activity. Although water bathing, in which muscle activity was slight, was sufficiently stressful to produce gastric hemorrhage and to increase gastric HDC activity, it produced no detectable elevation of HDC activity in any of the muscles examined. The other stresses all elevated HDC activity in all three muscles. We devised two methods of restraint, one accompanied by mastication and the other not. The former elevated HDC activity in the masseter muscle, but the latter did not. These results suggest that 1) HDC activity in the stomach is an index of responses to stress, 2) the elevation of HDC activity in skeletal muscles during stress is induced partly or wholly by muscle activity and/or muscle tension, and 3) stress itself does not always induce an elevation of HDC activity in skeletal muscles.
histamine; masseter muscle; mastication; temporomandibular disorders
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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MUSCLE FATIGUE due to unaccustomed hard and/or prolonged physical exercise may lead to both pain and stiffness in skeletal muscles. However, the underlying molecular mechanisms have not been established. The pain and stiffness in craniofacial muscles seen in temporomandibular disorders (TMD) are also typical symptoms that are thought to be due to muscle fatigue resulting from abnormal masticatory exercise (such as bruxism) or from improper occlusion.
As to the relationship between stress and muscle fatigue, many studies have been carried out on TMD. With regard to the etiology of TMD, Haber et al. (14) presented the hypothesis that psychological stress or a stress-related emotional response might have a primary role in its development. This stress model hypothesizes that excessive psychological stress induces masticatory muscle hyperactivity that is expressed as abnormal muscle activities such as teeth clenching and/or grinding (or bruxism), causing eventual pain in muscle and joint, joint noise, and limitation of jaw motion. This model suggests that such stress is a common underlying etiological factor for TMD. Clenching and grinding easily damages masticatory muscles (6, 27), and healing of damaged joints is slow (17). Therefore, the stress model leads us to the idea that short-term psychological stress might induce muscular pain, whereas chronic stress would be associated with combined muscle and joint pain or just joint pain. Although this stress model has not been supported by some other investigators (18-20), the importance of psychological stress as an etiological agent has been repeatedly emphasized with regard to the development of muscular pain both in TMD (13, 15, 21, 23) and in shoulder and neck pain (28).
Histamine, a classical and important mediator of inflammation, produces pain as well as dilatation of precapillary arterioles and enhanced capillary permeability (2, 3, 12). It is pooled in large quantities in mast cells in the tissues and in basophils in the blood (2, 12), and there is an increase in blood histamine during hard physical exercise (7). Histamine is supposed to be released from mast cells during muscle damage, and it may then induce pain and/or vasodilatation in the muscle itself (22). However, muscular pain occurs in most cases some time after exercise, and there is no evidence that such a histamine release from mast cells or basophils occurs in the postexercise period.
Recently, we demonstrated that in mice brief electrical stimulation of skeletal muscles and prolonged walking both induce within the active muscles a prolonged elevation of the activity of histidine decarboxylase (HDC), the enzyme that forms histamine (11, 29). The histamine newly formed by the induced HDC is released without being stored and has been suggested to play roles in the regulation of the microcirculation (24, 25) and in anabolic processes during rapid cell growth (16). We also found that training of mice diminishes the elevation of muscle HDC activity in the quadriceps femoris muscles induced by walking (11). Moreover, an antagonist of H1 receptors has been shown to improve or tend to improve some symptoms in patients with TMD (29). Having considered these findings, we proposed the hypothesis that the histamine newly formed through the induction of HDC is involved in mediating the muscular fatigue that occurs after exercise and/or during the development of TMD (11, 29).
In the present study, we examined whether psychological stress with or without muscle activity would induce HDC activity in skeletal muscles in mice. In this study, to assess the systemic effect of stress, we made a comparative examination of the levels of HDC activity not only in various skeletal muscles but also in the stomach. Although the relationship has not been firmly established, gastric HDC activity seems to be potentially useful as an index of biochemical responses to stressful stimuli, because gastric HDC activity has been shown in rats to be increased in response to stresses such as water bathing, restraint, or restraint combined with exposure to cold (1, 4, 26). In the present study, we also looked for signs of hemorrhage in the stomach for much the same reason.
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Animals
BALB/c mice were bred at the animal facility of our university and used as a normal strain in the present study. The mice (male) used for the present experiments were 6-7 wk old (23-25 g body wt). They were kept under standard conditions [12:12-h light-dark cycle (0700-1900 and 1900-0700) at a controlled temperature (23 ± 1°C)] for 7-10 days, and given standard food pellets (LabMR Stock; Nihon Nosan, Yokohama, Japan) and water ad libitum. All experiments complied with the Guidelines for Care and Use of Laboratory Animals issued by Tohoku University.Stress Experiments
At 0900 on the morning of the day of the experiments, all mice were moved to cages with new wood-chip bedding and kept for 5 h without food but with free access to water. Each stress was imposed on mice for 4 h from 1400 to 1800 at room temperature (23 ± 1°C) as will be described. In each experiment, control mice were kept in the cages without food or water for the same 4-h period.Water bathing. Water (25°C) was poured into a colorless transparent plastic beaker (diameter 9 cm, height 12 cm) to a depth of 4 cm. Wire netting (5-mm mesh) was placed on the bottom of the beaker to provide a secure footing. Each mouse was put into one of these beakers and kept there for 4 h at room temperature (23 ± 1°C).
Prolonged walking. Forced walking for 4 h was imposed on mice at room temperature (23 ± 1°C) as described previously (11). Briefly, mice were put into a cylindrical cage (37 cm diameter, 37 cm width), the wall of which was made of stainless steel rods (2 mm diameter, 1 cm apart). The cage was turned around a horizontal axis at 5.2 rpm by an electric motor, giving a walking speed of 6 m/min.
For the first 1-2 h of the experiment, most mice followed the rotation of the cage by clinging to the steel rods with forefeet and hindfeet or by hanging rather than by walking. Some mice even spent this period jumping from higher positions to lower positions. There was also falling from the hanging position. However, the number of falls was very small, and bruising was very rare, at least under the conditions used in this study. In our experience, the number of falls increases when walking is prolonged for >6 h, when experiments are carried out at a higher room temperature (26-28°C), or when the animals used are aged with a heavy body weight. Whenever we observed falling or signs of distress (e.g., vocalization, unsuccessful attempts to walk at the required speed), we immediately removed the mouse from the cage and excluded it from the experiments.Exposure to cold. Four mice were put into an aluminum cage (width 16 cm, length 30 cm, height 11 cm) with new wood-chip bedding and kept at 7°C for 4 h without food or water.
Restraint.
The device we used to prevent mice from carrying on their usual
activities is shown in Fig. 1. Each mouse
was put into a gray plastic cylinder (2.5 cm internal diameter, 10 cm
length), the front end of which had been partially closed with a
colorless transparent plastic strip (7 cm length, 1.5 cm width, and 1.0 mm thickness). This strip was inserted across the cylinder through two
slots near the end (see Fig. 1a). It should be noted that two apertures (about 5 mm maximum width) remain in the front end of the
cylinder when the strip is in place (above and below the strip). After
each mouse had been placed in the cylinder from the back end, the back
end was closed with tape. Interestingly, although the mouse can move
back and forth in the cylinder, it usually bites the plastic strip
throughout the whole experimental period (4 h; Fig. 1b).
However, if the tail of the mouse is fastened to the back end of the
cylinder by tape, the mouse cannot reach the strip and therefore cannot
bite it. Using these two methods, we could examine the effect of
restraint with or without mastication on HDC activity in the masseter
muscle. In this study, these methods are called "restraint with
mastication" [R(+)M] and "restraint without mastication"
[R(
)M], respectively. These experiments were also carried out at
room temperature (23 ± 1°C).
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Assessment of Masseter Muscle Activity
As described previously, a mouse placed in a narrow cylinder usually bites the plastic strip inserted across the cylinder throughout the whole experimental period. In so doing, it chews away part of the strip (Fig. 1). Therefore, to make a rough assessment of the amount of movement or activity in the masseter muscle (i.e., mastication), we weighed the plastic strips before and after R(+)M.Assay of HDC Activity
For the assay of HDC activity mice were decapitated, and the masseter, quadriceps femoris, and pectoralis superficial muscles were removed and stored at80°C until assayed. The whole stomach was
removed and opened with scissors, washed in ice-cold saline in a glass
tube, blotted on a filter paper, and stored at 80°C. HDC activity
was assayed with our previously published method (8) with
a slight modification (9, 10). Briefly, each tissue sample
(<250 mg) was put into a cooled Teflon tube with phosphorylated
cellulose (50-100 mg) and 2.5 ml of ice-cold 0.02 M phosphate
buffer (pH 6.2) containing pyridoxal 5'-phosphate (20 µM) and
dithiothreitol (200 µM) and then homogenized with an Ultra Turrax
homogenizer (Janke and Kunkel). The supernatant obtained after
centrifugation of the homogenate (10,000 g for 15 min at
4°C) was used as the enzyme solution. The histamine in the tissues
was bound to the phosphorylated cellulose and was removed almost
completely from the enzyme solution by centrifugation. Reaction mixture
(1 ml) containing the enzyme solution was incubated at 37°C for
14 h with histidine (1 mM). After the enzyme reaction had been
terminated by adding 2 ml of 0.5 M HClO4, the histamine formed during the incubation was separated by chromatography on a small
phosphorylated cellulose column and quantified fluorometrically (8). HDC activity was expressed as nanomoles of histamine
formed during a 1-h period of incubation by the enzyme contained in
1 g (wet weight) of each tissue
(nmol · h
1 · g1).
Observation of Gastric Injury
Methods do exist for quantifying gastric lesions in rats, including measurement of the necrotic area after fixation in Formalin solution. However, we could not use this method, because Formalin denatures enzyme proteins and because we needed to freeze the stomach rapidly after its removal for the assay of HDC activity. Therefore, we counted the number of red spots on the gastric mucosa (4) through a magnifying glass when each stomach was put into a glass tube to be washed with cold saline (see Assay of HDC Activity). Any hemorrhagic gastric lesion present was quantified as follows: none, 0 red spots; slight, 1-3 red spots; medium, 4-6 red spots; and strong, >7 red spots.Data Analysis
Experimental values are given as means ± SD. The statistical significance of the difference between two means was evaluated with Student's unpaired t-test, and P < 0.05 was considered significant.| |
RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Water Bathing and Prolonged Walking
Under the conditions we used for water bathing, each mouse remained for 4 h in an almost stationary standing posture with forefeet on the side of the beaker and the hindfeet on the wire netting at the bottom. On the other hand, the mice in the revolving cage were forced to walk, cling, and/or hang by the forefeet and hindfeet from the rods forming the wall of the cage without rest. Although the prolonged walking induced a marked elevation of HDC activity in all the skeletal muscles tested, the water bathing did not (Fig. 2). Water bathing and prolonged walking each produced an elevation of HDC activity in the stomach. In addition, these stresses resulted in strong hemorrhagic lesions in the stomach of all four mice in each group. It should be noted that the stomach contains a considerable HDC activity even without these stresses (Fig. 2).
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Cold Stress and Restraint
Throughout the period of exposure to cold (4 h), the mice remained huddled together with only occasional movements. Nevertheless, HDC activity was enhanced or tended to be enhanced in all skeletal muscles tested as well as in the stomach (Fig. 3), the elevation in the masseter muscle being very clear. As mentioned in MATERIALS AND METHODS, in the experiment involving restraint stress with mastication, each mouse started to bite the plastic strip soon after being shut in the narrow cylinder (Fig. 1b), and this behavior continued almost all the time the experiment lasted. In this experiment, the mouse can move back and forth in the cylinder and can move his forelimbs so as to grip the plastic strip (Fig. 1b). HDC activity in all the skeletal muscles tested increased in these mice, and the increased levels tended to be greater than those induced by cold stress, although in the stomach the elevation of HDC activity was similar in magnitude to that induced by cold stress. During cold stress, the incidence of hemorrhage in the stomach was one out of four mice (slight), but there was no such hemorrhage in the R(+)M group.
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Effect of Mastication on HDC Activity in Restrained Mice
As mentioned in MATERIALS AND METHODS when the tail of the mouse was fastened to the back end of the cylinder by tape, the mouse could not bite the plastic strip. Therefore, by comparing data from the two restraint experiments, we could assess the effect of mastication on HDC activity in the masseter muscle. As shown in Fig. 4, HDC activity did not increase at all in the masseter muscle of the R()M mice (i.e., without mastication).
It also should be noted that the elevation of HDC activity was slight in the superficial pectoralis muscle of the R()M mice, although HDC
activities in the quadriceps femoris muscle and stomach increased to
levels similar to those seen in the R(+)M mice. In this experiment, a
slight hemorrhage in the stomach was observed in one mouse in the R(+)M
group.
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Relationship Between Mastication and HDC Activity
As mentioned previously in the R(+)M experiment, the mouse chews the plastic strips and thus the weight of the strip decreases (Fig. 5). In fact, every mouse bit the plastic strip during the whole experimental time (6 h), and HDC activity in the masseter muscle increased with the mastication time (Fig. 5).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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In the present study we found that different types of stress or exercise produce different effects on HDC activity in skeletal muscles in mice, even though mice all showed an elevated HDC activity in the stomach.
Prolonged walking (which includes clinging and/or hanging by forefeet and hindfeet), restraint (with or without mastication), exposure to cold, and water bathing all elevated HDC activity in the stomach. In addition, prolonged walking and water bathing produced a high incidence of strong hemorrhage in the stomach. Although both the incidence and severity were lower, hemorrhage also was seen in response to cold stress and R(+)M. The HDC activity induced in the stomach was highest following prolonged walking, whereas the responses induced by the other stresses were weaker and similar to each other. To judge from these results, it seems unlikely that the level of HDC activity in the stomach itself determines the degree of hemorrhage (if any). However, these results suggest that all the conditions we tested in the present study are stressful for mice.
During water bathing the mice made no apparent movements, and there was no detectable elevation of HDC activity in any of the muscles tested. Although each mouse remained standing throughout the experimental period, the buoyancy effect presumably reduced the weight burden imposed on the hindlimbs. On the other hand, during the cold stress small movements were made. Despite the small size of these movements, there was a significant elevation of HDC activity in the masseter muscle and quadriceps femoris muscle and there was a tendency toward an increase in the superficial pectoralis muscle. Possibly, this may have been related to shivering, which was indeed observed in these mice. During R(+)M, the mouse could move back and forth, although with some difficulty. The HDC activities induced in these mice were higher or showed a tendency to be higher than those induced in the mice exposed to cold. These results led us to think that there might be an intimate relationship between the level of HDC activity and the amount of muscle activity or muscle tension.
In the present study we found that throughout R(+)M, each and every
mouse, excitedly or eagerly and almost without respite, continued to
bite, grip, or pull the strip; this behavior may represent an attempt
to escape from the restraint. In these mice, the HDC elevation in the
masseter muscle was much higher than in control mice. In contrast, in
mice restrained without mastication, such an increase in HDC activity
was not detected in the masseter muscle. The elevation of HDC activity
in the superficial pectoralis muscle was also higher in R(+)M mice than
in R()M mice. As shown in Fig. 5, HDC activity in the masseter muscle
increased in parallel with the cumulative amount of masticatory
activity (as indicated by the change in the weight of the plastic
strips). These results strongly support the idea that HDC activity
levels induced in skeletal muscles during stress with exercise mainly
reflect the strength of the muscle activity or tension and/or the
amount of time for which the contractions occur.
In our R(+)M experiment the mice used their masseter muscles voluntarily, i.e., no artificial stimulation was imposed on the muscle. We believe that this experimental system provides us with a singularly useful method for examining the relationship among stress, muscle activity, and the biochemical events accompanying muscle fatigue. We are now using this method to examine how drugs acting on the central nervous system (including psychotropic agents) might affect HDC activity in the masseter muscle and its masticatory behavior.
Interestingly, prolonged walking (and/or hanging by the feet) induced the highest level of HDC activity not only in the quadriceps femoris and superficial pectoralis muscles but also in the masseter muscle (Figs. 2 and 3). The muscular activities of the quadriceps femoris and pectoralis superficial muscles in this experiment were unequivocally the most vigorous among the experiments in the present study. As shown in our previous studies (11, 29), prolonged walking results in an elevation of HDC activity even in the liver, lung, spleen, and bone marrow. A number of cytokines have been suggested as causative factors in the muscular injury that can be induced by exercise (5). We found that small doses of interleukin-1 (IL-1) can elevate HDC activity in all the above tissues (11, 29), and we detected IL-1-like substances in muscle tissues by means of an immunostaining technique (11). This being the case, the elevation of HDC activity in the masseter muscle during prolonged walking might have been induced by cytokines, including IL-1. It is also likely that a degree of muscle tension in the masseter muscle during the prolonged walking (from clenching the teeth, although we could not detect it by eye) might also be involved in the induction of HDC activity.
As mentioned previously, water bathing produced a stomach hemorrhage in all the mice, indicating that this is a potent stress for the mouse. Thus this experiment presumably involved potent psychological or emotional effects. Nevertheless, there was no detectable elevation of HDC activity in any of the muscles tested, including the masseter muscle. On this basis, it seems likely that psychological stress itself does not necessarily induce an elevation of HDC activity in skeletal muscles.
In conclusion, our results suggest that 1) elevation of HDC activity in the stomach may be an index of responses to various types of stress, 2) the elevation of HDC activity in skeletal muscles may be partly or wholly induced by muscle activity and/or tension, and 3) psychological stress itself does not necessarily induce an elevation of HDC activity in skeletal muscles.
Perspectives
Our findings in the present study and those reported previously (11, 29) are consistent with our hypothesis that an elevation of HDC activity is involved in inducing fatigue in skeletal muscles. The newly formed histamine in skeletal muscles [possibly generated within vascular endothelial cells as suggested previously (11)] may contribute to the production of muscle pain. Moreover, the dual effects of histamine on the blood vessels [a constrictor effect on the larger vessels and a dilator effect on the finer vessels (12)] might contribute to the ensuing stiffness. Direct electrical stimulation induces an elevation of HDC activity in skeletal muscles even in mast cell-deficient mice (11, 29), and we tentatively suggest that the histamine newly formed as a result of an elevation of HDC activity should be referred to as "neo-histamine" to distinguish it from mast cell histamine. On the basis of our findings, we speculate that the induction of HDC activity in response to muscle activity could be considered part of the animal's self-defense repertoire. The neo-histamine, by enhancing capillary permeability and causing arteriolar vasodilatation, may contribute to increases in the supply of O2 and nutrients and the removal of CO2 and other waste products, and may thus aid the recovery from fatigue. It may also stimulate sensory nerve endings, producing pain and so deterring the individual from engaging in further exercise.| |
ACKNOWLEDGEMENTS |
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We are grateful to Dr. Robert Timms for useful discussion and editing the manuscript.
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FOOTNOTES |
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This work was supported by a grant-in-aid for Scientific Research from the Ministry of Education of Japan (No. 11877335 and 10470412) and a grant from Taisho Pharmaceutical (Ohmiya, Japan).
Address for reprint requests and other correspondence: Y. Endo, Dept. of Pharmacology, School of Dentistry, Tohoku Univ., 4-1 Aoba-ku, Seiryo-machi, Sendai 980-8575, Japan (E-mail: endo{at}pharmac.dent.tohoku.ac.jp).
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.
Received 15 November 1999; accepted in final form 29 June 2000.
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REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Asahara, M,
Mushiaki S,
Shimad S,
Fukui H,
Kinoshita Y,
Kawanami C,
Watanabe T,
Tanaka S,
Ichikawa A,
Uchiyama Y,
Narushima Y,
Takasawa S,
Okamoto H,
Tohyama M,
and
Chiba T.
Reg gene expression is increased in rat gastric enterochromaffin-like cells following water immersion stress.
Gastroenterology
111:
45-55,
1996[Web of Science][Medline].
2.
Beaven, MA.
Histamine: its role in physiological and pathological processes.
In: Monographs in Allergy, edited by Dukor P,
Kallós P,
Trnka Z,
Waksman BH,
and de Weck AL.. Basel: Karger, 1978, vol. 13, p. 1-113.
3.
Beer, JD,
Maltoff SM,
and
Rocklin RE.
The influence of histamine on immune and inflammatory responses.
Adv Immunol
35:
209-268,
1983.
4.
Bouclier, M,
Jung MJ,
and
Gerhart F.
Histamine receptor blockade (H2) vs. inhibition of histamine synthesis in stress ulceration in rats.
Eur J Pharmacol
90:
129-132,
1983[Web of Science][Medline].
5.
Cannon, JG,
and
Pierre BAS
Cytokines in exertion-induced skeletal muscle injury.
Mol Cell Biochem
179:
159-167,
1998[Web of Science][Medline].
6.
Christensen, LV.
Facial pain and internal pressure of masseter muscle in experimental bruxism in man.
Arch Oral Biol
16:
1021-1031,
1971[Web of Science][Medline].
7.
Dunér, H,
and
Pernow B.
Histamine and leukocytes in blood during muscular work.
Scand J Clin Lab Invest
10:
394-396,
1958[Web of Science][Medline].
8.
Endo, Y.
A simple method for the determination of polyamines and histamine and its application to the assay of ornithine decarboxylase and histidine decarboxylase activities.
Methods Enzymol
94:
42-47,
1983[Web of Science][Medline].
9.
Endo, Y,
Kikuchi T,
Nakamura M,
and
Shinoda H.
Determination of histamine and polyamines in calcified tissues of mice: contribution of mast cells and histidine decarboxylase to the amount of histamine in the bone.
Calcif Tissue Int
51:
67-71,
1992[Web of Science][Medline].
10.
Endo, Y,
Nakamura M,
Nitta Y,
and
Kumagai K.
Effect of macrophage depletion on the induction of histidine decarboxylase by lipopolysaccharide, interleukin-1 and tumor necrosis factor.
Br J Pharmacol
114:
187-193,
1995[Web of Science][Medline].
11.
Endo, Y,
Tabata T,
Kuroda H,
Tadano T,
Matsushima K,
and
Watanabe M.
Induction of histidine decarboxylase in skeletal muscle in mice by electrical stimulation, prolonged walking and interleukin-1.
J Physiol (Lond)
509:
587-598,
1998
12.
Garrison, JC.
Histamine, bradykinin, 5-hydroxytryptamine, and their antagonists.
In: Goodman and Gilman's The Pharmacological Basis of Therapeutics (8th Ed.), edited by Gilman AG,
Rall TW,
Nies AS,
and Taylor P.. New York: Pergamon, 1990, p. 575-599.
13.
Grzesiak, RC.
Psychologic considerations in temporomandibular dysfunction. A biopsychosocial view of symptom formation.
Dent Clin North Am
35:
209-226,
1991[Medline].
14.
Haber, JD,
Moss RA,
Kuczmierczk RA,
and
Garrett JC.
Assessment and treatment of stress in myofascial pain-dysfunction syndrome: a model for analysis.
J Oral Rehabil
10:
187-196,
1983[Web of Science][Medline].
15.
Jones, DA,
Rollman GB,
and
Brooke RI.
The cortisol response to psychological stress in temporomandibular dysfunction.
Pain
72:
171-182,
1997[Web of Science][Medline].
16.
Kahlson, G,
and
Rosengren E.
New approaches to the physiology of histamine.
Physiol Rev
48:
155-196,
1968
17.
Kreutziger, KL,
and
Mahan PE.
Temporomandibular degenerative joint disease.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod
40:
165-182,
1975.
18.
Lundeen, TF,
George MW,
and
Sturdevant JR.
Stress in patients with pain in the muscles of mastication and temporomandibular joints.
J Oral Rehabil
15:
631-637,
1988[Web of Science][Medline].
19.
Lundeen, TF,
Levitt SR,
and
McKinney MW.
Evaluation of temporomandibular joint disorders by clinician ratings.
J Prosthet Dent
59:
202-211,
1988[Web of Science][Medline].
20.
Lundeen, TF,
Sturdevant JR,
and
George JM.
Stress as a factor in muscle and temporomandibular joint pain.
J Oral Rehabil
14:
447-456,
1987[Web of Science][Medline].
21.
Marbach, JJ,
and
Lipton JA.
Biopsychosocial factor of the temporomandibular pain dysfunction syndrome.
Dent Clin North Am
31:
473-486,
1987[Web of Science][Medline].
22.
Morganroth, ML,
Young EW,
and
Sparks HV.
Prostaglandin and histaminergic mediation of prolonged vasodilatation after exercise.
Am J Physiol Heart Circ Physiol
233:
H27-H33,
1977.
23.
Rudy, TE,
Turk DC,
Zaki HS,
and
Curtin HD.
An empirical taxometric alternative to traditional classification of temporomandibular disorders.
Pain
36:
311-320,
1989[Web of Science][Medline].
24.
Schayer, RW.
Histamine and microcirculation.
Life Sci
15:
391-401,
1974[Web of Science][Medline].
25.
Schayer, RW.
Metabolism and excretion of histamine.
In: Handbook of Experimental Pharmacology XVIII, edited by Rocha e Silva M.. Berlin: Springer-Verlag, 1978, pt. 2, p. 109-129.
26.
Schwartz, JC,
Cohen Y,
and
Valette G.
Histidine decarboxylase gastrique et ulcerés experimentau chez le rat.
Biochem Pharmacol
15:
2122-2124,
1966[Web of Science][Medline].
27.
Scott, DS,
and
Lundeen TF.
Myofascial pain involving the masticatory muscle: an experimental model.
Pain
8:
207-215,
1980[Web of Science][Medline].
28.
Vasseljen, V, Jr,
and
Westgaard RH.
Can stress-related shoulder and neck pain develop independently of muscle activity?
Pain
64:
221-230,
1996[Web of Science][Medline].
29.
Watanabe, M,
Tabata T,
Huh JI,
Inai T,
Tsuboi A,
Sasaki K,
and
Endo Y.
Possible involvement of histamine in muscular fatigue in temporomandibular disorders: animal and human studies.
J Dent Res
78:
769-775,
1999
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