• The Korean Journal of Physiology
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• v.21 no.2
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• pp.259-272
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• 1987

This was study carried out to investigate the effect of calcium on spontaneous contraction and electrical activity induced by ethanol in gastric smooth muscle. After peeling off the mucous membrane from the isolated whole stomach of 102 cats, two kinds of small muscle preparations $(2.0{\times}0.2\;cm)$, one longitudinal and the other circular, were excised from the fundus, the corpus and the antrum portion of each whole stomach specimen. The isometric contraction of the small muscle preparation was measured in a cylinder-shaped chamber filled with Krebs-Ringer-dextrose solution (pH 7.4, temperature $36{\pm}0.5^{\circ}C$) bubbling with 5% $CO_2$ in $O_2$. A large muscle preparation $(5.0{\times}1.2\;cm)$ was excised from the anterior wall of the corpus-antrum portion of the same specimen in 72 of 102 cats. The gastric electrical activity (slow wave and spike potential) was monopolarly recorded by four capillary electrodes (Ag-AgCl), of which two were placed on the corpus and two on the antrum, in a muscle chamber filled with the same solution as described above. Changes in the amplitude of the contraction, frequency of the gastric slow wave and the production of the spike potential were observed after adding ethanol and/or under the treatments with verapamil, $CaCl_2$ and Ca-free Krebs-Ringer-dextrose solution. The results were as follows: 1) After adding ethanol, the spontaneous phasic contraction of the corpus was reduced dose-dependently (0.125-2.0%), which was totally abolished by higher concentrations (2.0-8.0%) of ethanol. 2) The corporal phasic contraction was also completely abolished by verapamil $(3{\times}10^{-5}\;M)$ or Ca-free Krebs-Ringer-dextrose solution. The contraction was increased by $CaCl_2\;(1.8{\times}10^{-3}\;M)$, but the inhibitory effect of ethanol on the contraction persisted even under the treatment with $CaCl_2$. 3) At higher concentrations, ethanol caused tonic contraction of both preparations from the fundus, the corpus and the antrum in a dose-dependent manner. The tonic contraction of the fundus produced by ethanol was not influenced by $CaCl_2$ or verapamil, whereas the tonic contraction was not produced by ethanol in tile Ca-free solution. 4) Frequency of gastric slow wave was decreased dose-dependently by the addition of ethanol (0.25-1.0%), and tile slow wave was not produced by higher concentration of ethanol (2.0%). 5) The frequency of slow wave was significantly reduced by verapamil only and the inhibitory influence of ethanol on the slow wave frequency was reinforced by verapamil. 6) The treatment of $CaCl_2$ increased significantly the slow wave frequency, and attenuated the inhibitory effect of ethanol on the frequency. It is therefore suggested that ethanol regulates the phasic contraction and the production of slow wave by interfering with the transport of calcium in the stomach muscle of the cat.

• The Korean Journal of Physiology
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• v.9 no.1
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• pp.13-22
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• 1975

From the study of movements of $Ca^{++}$ in frog cardiac muscle, Niedergerke (1963) postulated that $Ca^{++}$ necessary for the cardiac contraction is stored in a specific pool. Langer et al (1967) and DeCaro (1967) also found a close relationship between the change of $Ca^{++}$ flux kinetics and the change of contractile force. According to the studies of several investigators, Ca II (Bailey and Dressel 1968) or phase I and II (Langer 1965, Langer et al 1967, 1971) in the $Ca^{++}$ washout curve was associated with cardiac contractility. This investigation was aimed to elucidate the anatomical region of the contractile active $Ca^{++}$ pool. At the same time, it was assumed in this study that $Ca^{++}$ in the sarcoplasmic reticulumn represents one of the major intracellular $Ca^{++}$ pool and cardiac contractility was also dependent on the intracellular $Ca^{++}$ concentration. Consequently, this experiment was performed at different temperatures to activate to activate inhibit the deactivating process of activated $Ca^{++}$ in the intracellular space to see if changes in the contractility decay curve existed at different temperatures. The isolated hearts of rabbits and turtles (Amyda maackii) were attached to the perfusion apparatus according to the method employed by Bailey and Dressel (1968). The isolated hearts were initally perfused with a full Ringer solution containing 2 mg/ml of inulin for 1 hr, and then $Ca^{++}$ and inulin-free Ringer solution was perfused while the isometric tension was recorded and a serial sample of perfusion fluid dripping from the cardiac apex was collected for 10 sec throughout experimental period. The above procedure was performed at $23^{\circ}C$, $30^{\circ}C$ and $38^{\circ}C$ on the rabbit heart and $10{\sim}13^{\circ}C$, $10^{\circ}C$, $25^{\circ}C$, $30^{\circ}C$ and $35^{\circ}C$ on the turtle heart. After determination of $Ca^{++}$ and inulin concentration of the samples, the $Ca^{++}$, inulin washout curve and the contractile tensin decay curve were analysed according to the method of Riggs (1963). The results were summarized as follows; 1. In the rabbit heart, there are 2 inulin compartments, 3 $Ca^{++}$ compartments and sing1e exponential decay of contractile tension. In the turtle heart, there are $1{\sim}2$ inulin compartments, $1{\sim}2$ $Ca^{++}$ compartments and $1{\sim}2$ phases of contractile tension decay. The fact that the inulin space was divided into 3 compartments in the washout curve in these hearts indicates the presence of heterogeneity in cardiac perfusion, i.e., overfused and underperfused area. 2. Ca I a9d Ca II in these hearts were found to have $Ca^{++}$ in the ECF compartments because their half times in the washout curves were far smaller than those of the inulin washout curves in the rabbit heart and similar to those of the inulin washout curves in the turtle heart. Ca III in the rabbit heart may have originated from the intracellular $Ca^{++}$ store. But no Ca III in the turtle heart was found. This may be due to the fact that the iutracellular $Ca^{++}$ pool in the turtle heart was too small to detect using this experimental procedure since sarcoplasmic reticulumn in the turtle heart is poorly developed. 3. In the rabbit heart, there were no chages in the half time of Ca I, Ca II, inulin I and inulin II at different temperatures, but the half time of Ca III was significantly prolonged at lower temperatures, and the half time of the contractile tension decay tended to be prolonged at lower temperatures but this was not significant. In the turtle heart, there were no changes in the half time of Ca I, Ca II, inulin 1, inulin II and phase I of the contractile tension decay at different temperatures, but the half time of phase II of the contractile tension decay was significantly prolonged at lower temperatures. This finding indicates that intracellu!ar $Ca^{++}$ in these hearts was also responsible particulary for maintaining the cardiac contractility at the lower temperatures. 4. The half times of contractile tension decay were shorter than those of Ca II in the $Ca^{++}$ washout curves in both animal hearts. According to the above results it was shown that $Ca^{++}$ in ECF is primarily and $Ca^{++}$ in the intracellular space is partially associated with the cardic contractility.

• Journal of Chest Surgery
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• v.43 no.4
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• pp.345-355
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• 2010

Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.

• Journal of the Korean Arthroscopy Society
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• v.12 no.1
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• pp.18-23
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• 2008

Purpose: The purpose of this study is to evaluate the clinical results of the function and stability of ACL reconstruction using the flexible reamer. Materials and Methods: We reviewed 98 patients who taken ACL reconstruction using the flexible reamer from March, 1999 to May, 2004. And the follow-up period was more than 12 months in all cases. We used the subjective tests including Lysholm knee score and 2000 International Knee Documentation Committee(IKDC) subjective knee score, and the objective tests such as anterior drawer test, Lachman test, pivot shift test, and KT-2000 arthrometer to evaluate the clinical results. Results: In the range of motion of the affected knee, the extension deficit more than 5 degree was 8 cases preoperatively and 1 case postoperatively. The flexion deficit more than 5 degree was 12 cases preoperatively and 2 cases postoperatively. The mean Lysholm knee score was 61.3 point(${\pm}3.5$ SD) preoperatively and 87.7 point(${\pm}2.0$ SD) postoperatively. The mean 2000 International Knee Documentation Committee(IKDC) subjective knee score was 49 point(${\pm}3.3$ SD) preoperatively and 84 point (${\pm}2.2$ SD) postoperatively. 93 cases were more than grade II in Lachman test preoperatively and 5 cases postoperatively. 71 cases were more than grade II in pivot shift test preoperatively but 89 cases were negative postoperatively. The mean maximal manual difference by KT-2000 arthrometer was 6.8 mm(${\pm}1.9$ SD) preoperatively and 1.8 mm(${\pm}0.8$ SD) postoperatively. Conclusion: ACL reconstruction using the flexible reamer achieved the ideal isometric point of femur and anatomic graft placement, so we could obtain good results, especially in rotational stability.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.588-596
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• 2009

Background: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. Material and Method: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the $O_2$ in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or $CN^-$. Result: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the $K^+$ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the $Ca^{2+}$ influx. Conclusion: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing $[[Ca^{2+}]_i$.

• Journal of Chest Surgery
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• v.31 no.9
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• pp.884-892
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• 1998

Background: The gastroepiploic artery is not only an alternative graft but also may be considered an important primary graft for coronary revascularization. However, the long-term patency of the gastroepiploic arterial graft is yet to be determined and the incidence of perioperative spasm and long-term patency of a coronary graft may be affected by the properties of the graft response to certain vasoactive substances. The reactivity of the gastroepiploic artery to vasoactive substances has not been studied extensively and the results of the studies are contradictory. Material and Method: This study was designed to test the reactivity of human gastroepiploic artery to four constrictors and four relaxants. The middle sections of the human gastroepiploic arteries were collected from the patients undergoing gastrectomy and the arterial rings with intact endothelium were suspended in organ baths for isometric tension recording. Result: Epinephrine, norepinephrine, and potassium chloride induced the maximum constriction to higher forces (7.0$\pm$1.1g, 6.6$\pm$0.9g, and 6.5$\pm$1.1g) than 5-hydroxytryptamine did (3.8$\pm$1.7g, p<0.05). Nitroprusside and histamine induced almost full relaxation in the gastroepiploic arteries preconstricted with norepinephrine. There was no significant difference between two relaxants regarding maximum relaxation force. Acetylcholine induced the maximum relaxation to weaker force when compared with nitroprusside and histamine (p<0.05), and isoproterenol was the weakest of the relaxants (p<0.05 compared with acetylcholine). Conclusion: The gastroepiploic artery has a strong capacity of endothelium-dependent relaxation which could have an important influence on long-term patency. The gastroepiploic artery exhibits a potent contractility to catecholamines and the enhanced contractility may facilitate vasospasm in the presence of high circulating levels of catecholamines. Nitroprusside, a potent relaxant in gastroepiploic artery, might be beneficial for the treatment of gastroepiploic arterial graft spasm. The gastroepiploic arterial graft with intact endothelium may respond weakly to beta-adrenoceptor agonist and 5-hydroxytryptamine.

• Journal of Chest Surgery
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• v.23 no.3
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• pp.452-464
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• 1990

It is well known that extracellular Calcium plays a very important role in several steps of smooth muscle excitability and contractility, and there have been many concerns about factors influencing the distribution of extracellular Ca++ and the Ca++ flux through the cell membrane of the smooth muscle. Based on the assumption that Mg++ may also play an important role in the excitation and contraction processes of the smooth muscle by taking part in affecting Ca++ distribution and flux, many researches are being performed about the exact role of Mg++, especially in the vascular smooth muscle. But yet the effect of Mg++ in the smooth muscle activity is not clarified, and moreover the mechanism of Mg++ action is almost completely unknown. Present study attempted to clarify the effect of Mg++ on the excitability and contractility in the multiunit and unitary smooth muscle, and the mechanism concerned in it. The preparations used were the guinea-pig aortic strip as the experimental material of the multiunit smooth muscle and the rat uterine strip as the one of the unitary smooth muscle. The tissues were isolated from the sacrificed animal and were prepared for recording the isometric contraction. The effects of Mg++ and Ca++ were examined on the electrically driven or spontaneous contraction of the preparations. And the effects of these ions were also studied on the K+ or norepinephrine contracture. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% 02 and kept at 35oC. The results obtained were as follows: 1] Mg++ suppressed the phasic contraction induced by electrical field stimulation dose-dependently in the guinea-pig aortic strip, while the high concentration of Ca++ never recovered the decreased tension. These phenomena were not changed by the a - or b - adrenergic blocker. 2]Mg++ played the suppressing effect on the low concentration [20 and 40 mM] of K+-contracture in the aortic muscle, but the effect was not shown in the case of 100mM K+-contracture. 3] Mg++ also suppressed the contracture induced by norepinephrine in the aortic preparation. And the effect of Mg++ was most prominent in the contracture by the lowest [10 mM] concentration of norepinephrine. 4] In both the spontaneous and electrically driven contractions of the uterine strip, Mg++ decreased the amplitude of peak tension, and by the high concentration of Ca++ the amplitude of tension was recovered unlike the aortic muscle. 5] The frequency of the uterine spontaneous contraction increased as the [Ca++] / [Mg++] ratio increased up to 2, but the frequency decreased above this level. 6] Mg++ decreased the tension of the low[20 and 40mM] K+-contracture in the uterine smooth muscle, but the effect did not appear in the 100mM K+-contracture. From the above results, the following conclusion could be made. 1] Mg++ seems to suppress the contractility directly by acting on the smooth muscle itself, besides through the indirect action on the nerve terminal, in both the aortic and uterine smooth muscles. 2] The fact that the depressant effect of Mg++ on the K+-contracture is in inverse proportion to an increase of K+ concentration appears resulted from the extent of the opening state of the Ca++ channel. 3] Mg++ may play a depressant role on both the potential dependent and the receptor-operated Ca++ channels. 4] The relationship between the actions of Mg++ and Ca++ seems to be competitive in uterine muscle and non-competitive in aortic strip.

• Journal of the Korean Arthroscopy Society
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• v.8 no.2
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• pp.75-81
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• 2004

Purpose: Recent development and advances in arthroscopic surgical techniques for Anterior Cruciate Ligament(ACL) reconstruction have led to the ideal location for the etric point from 10 o'clock (in right knee) and 13:30 (in left knee) to 10:30 (in right knee) and 14 o'clock (in left knee) in the frontal plane. This study was performed to compare operative methods and the radiologic results of femoral tunnels made through the tibial tunnel(trans-tibial approach) and the anteromedial portal. Material and Methods: From January 2003 to May 2004, one-hundred reconstructions of anterior cruciate ligament were performed. Group I (femoral tunnel through tibial tunnel) was composed of 50 cases and group ll (femoral tunnel through anteromedial portal) was consisted of 50 cases. The study was performed to compare the radiographic results of femoral tunnels made through the tibial tunnel and the anteromedial portal and operative methods. Results: In operative methods at Group II, femoral tunnel was made more easily at isometric point than Group I, a good visual field was achived because 100$^{\circ}$ flxion of knee, they can be reduced risk of posterior cortical breakage and tunnel-graft mismatching and decreased divergence of femoral interference screw in radiology (P<0.05). The angle between femoral tunnel and longitudinal axis of ACL wae increased at Group ll. Conclusion: Aanteromedial portal technique was more useful in ACL reconstruction for femoral tunnel toward 10 o'clock to10:30(in right) or 1:30 to 2 o'clock(in left).

• Journal of Chest Surgery
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• v.37 no.3
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• pp.210-219
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• 2004

Extracellular $K^{+}$ concentration ([ $K^{+}$]$_{0}$ ) can be increased within several mM by the efflux of intracellular $K^{+}$. To investigate the effect of an increase in [ $K^{+}$]$_{0}$ on vascular contractility, we attempted to examine whether extracellular $K^{+}$ might modulate vascular contractility, endothelium-dependent relaxation (EDR) and intracellular $Ca^2$$^{+}$ concentration ([C $a^2$$^{+}$]$_{i}$ ) in endothelial cells (EC). We observed isometric contractions in rabbit carotid, superior mesenteric, basilar arteries and movse aorta. [C $a^2$$^{+}$]$_{i}$ was recorded by microfluorimeter using Fura-2/AM in EC. No change in contractility was recorded by the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM in conduit artery such as rabbit carotid artery. whereas resistant vessels, such as basilar and branches of superior mesenteric arteries (SMA), were relaxed by the increase. In basilar artery, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 1 to 3 mM was bigger than that by the increase from 6 to 12 mM. In contrast, in branches of SMA, the relaxation by the increase in [ $K^{+}$]$_{0}$ to from 6 to 12 mM is bigger than that by the increase from 1 to 3 mM. $Ba^2$$^{+}$ (30 $\mu$M) did not inhibit the relaxation by the increase in [ $K^{+}$]$_{0}$ from 1 to 3 mM but did inhibit the relaxation by the increase from 6 to 12 mM. In the mouse aorta without the endothelium or treated with $N^{G}$_nitro-L-arginine (30 $\mu$M), nitric oxide synthesis blocker, the increase in [ $K^{+}$]$_{0}$ from 6 to 12 mM did not change the magnitude of contraction induced either norepinephrine or prostaglandin $F_2$$_{\alpha}$. The increase in [ $K^{+}$]$_{0}$ up to 12 mM did not induce contraction of mouse aorta but the increase more than 12 mM induced contraction. In the mouse aorta, EDR was completely inhibited on increasing [ $K^{+}$]$_{0}$ from 6 to 12 mM. In cultured mouse aorta EC, [C $a^2$$^{+}$]$_{i}$ , was increased by acetylcholine or ATP application and the increased [C $a^2$$^{+}$]$_{i}$ , was reduced by the increase in [ $K^{+}$]$_{0}$ reversibly and concentration-dependently. In human umbilical vein EC, similar effect of extracellular $K^{+}$ was observed. Ouabain, a N $a^{+}$ - $K^{+}$ pump blocker, and N $i^2$$^{+}$, a N $a^{+}$ - $Ca^2$$^{+}$ exchanger blocker, reversed the inhibitory effect of extracellular $K^{+}$. In resistant arteries, the increase in [ $K^{+}$]$_{0}$ relaxes vascular smooth muscle and the underlying mechanisms differ according to the kinds of the arteries; $Ba^2$$^{+}$-insensitive mechanism in basilar artery and $Ba^2$$^{+}$ -sensitive one in branches of SMA. It also inhibits [C $a^2$$^{+}$]$_{i}$ , increase in EC and thereby EDR. The initial mechanism of the inhibition may be due to the activation of N $a^{+}$ - $K^{+}$pump. activation of N $a^{+}$ - $K^{+}$pump.p.p.p.

• The Korean Journal of Physiology
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• v.8 no.2
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• pp.1-17
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• 1974

This experiment was designed to explore the specific functional interrelations between the vestibular semicircular canals and the extraocular muscles which may disclose the neural organization, connecting the vestibular canals and each ocular motor nuclei in the brain system, for vestibuloocular reflex mechanism. In urethane anesthetized rabbits, a fine wire insulated except the cut cross section of its tip was inserted into the canals closely to the ampullary receptor organs through the minute holes provided on the osseous canal wall for monopolar stimulation of each canal nerve. All extraocular muscles of both eyes were ligated and cut at their insertio, and the isometric tension and EMG responses of the extraocular muscles to the vestibular canal nerve stimulation were recorded by means of a physiographic recorder. Upon stimulation of the semicircular canal nerve, direction if the eye movement was also observed. The experimental results were as follows. 1) Single canal nerve stimulation with high frequency square waves (240 cps, 0. 1 msec) caused excitation of three extraocular muscles and inhibition of remaining three muscles in the bilateral eyes; stimulation of any canal nerve of a unilateral labyrinth caused excitation (contraction) of the superior rectus, superior oblique and medial rectus muscles and inhibition (relaxation) of the inferior rectus, inferior oblique and lateral rectos muscles in the ipsilateral eye, and it caused the opposite events in the contralateral eye. 2) By the overlapped stimulation of triple canal nerves of a unilateral labyrinth, unidirectional (excitatory or inhibitory) summation of the individual canal effects on a given extraocular muscles was demonstrated, and this indicates that three different canals of a unilateral vestibular system exert similar effect on a given extraocular muscles. 3) Based on the above experimental evidences, a simple rule by which one can define the vestibular excitatory and inhibitory input sources to all the extraocular muscles is proposed; the superior rectus, superior oblique and medial rectus muscles receive excitatory impulses from the ipsilateral vestibular canals, and the inferior rectus, inferior oblique and lateral rectus muscles from the contralateral canals; the opposite relationship applies for vestibular inhibitory impulses to the extraocular muscles. 4) According to the specific direction of the eye movements induced by the individual canal nerve stimulation, an extraocutar muscle exerting major role (a muscle of primary contraction) and two muscles of synergistic contraction could be differentiated in both eyes. 5) When these experimental results were compared to the well known observations of Cohen et al. (1964) made in the cats, extraocular muscles of primary contraction were the same but those of synergistic contraction were partially different. Moreover, the oblique muscle responses to each canal nerve excitation appeared to be all identical. However, the responnes of horizontal (medial and lateral) and vertical (superior and inferior) rectus muscles showed considerable differences. By critical analysis of these data, the author was able to locate theoretical contradictions in the observations of Cohen et al. but not in the author's results. 6) An attempt was also made to compare the functional observation of this experiment to the morphological findings of Carpenter and his associates obtained by degeneration experiments in the monkeys, and it was able to find some significant coincidence between there two works of different approach. In summary, the author has demonstrated that the well known observations of Cohen et al. on the vestibulo-ocular interrelation contain important experimental errors which can he proved by theoretical evaluation and substantiated by a series of experiments. Based on such experimental evidences, a new rule is proposed to define the interrelation between the vestibular canals and the extraocular muscles.