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"Intensity-response" effects of electroacupuncture on gastric motility and its underlying peripheral neural mechanism.

Su YS, He W, Wang C, Shi H, Zhao YF, Xin JJ, Wang XY, Shang HY, Hu L, Jing XH, Zhu B - Evid Based Complement Alternat Med (2013)

Bottom Line: The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA.The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility.TRPV1 receptor was involved in the regulation of gastric motility of EAS.

View Article: PubMed Central - PubMed

Affiliation: Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie, Dongzhimennei, Beijing 100700, China.

ABSTRACT
The aim of this study was to explore the "intensity-response" relationship between EAS and the effect of gastric motility of rats and its underlying peripheral neural mechanism by employing ASIC3 knockout (ASIC3-/-), TRPV1 knockout (TRPV1-/-), and C57BL/6 mice. For adult male Sprague-Dawley (n = 18) rats, the intensities of EAS were 0.5, 1, 3, 5, 7, and 9 mA, respectively. For mice (n = 8 in each group), only 1 mA was used, by which C fiber of the mice can be activated. Gastric antrum motility was measured by intrapyloric balloon. Gastric motility was facilitated by EAS at ST36 and inhibited by EAS at CV12. The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA. In comparison with C57BL/6 mice, the facilitatory effect of ST36 and inhibitive effect of CV12 in ASIC3-/- mice decreased, but the difference was not statistically significant (P > 0.05). However, these effects in TRPV1-/- mice decreased significantly (P < 0.001). The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility. TRPV1 receptor was involved in the regulation of gastric motility of EAS.

No MeSH data available.


Related in: MedlinePlus

Gastric motility in response to EAS at CV12 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at CV12. (b), (c), and (d) displayed the inhibitory effects of EAS at CV12 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; ***P < 0.001 versus background activities).
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fig2: Gastric motility in response to EAS at CV12 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at CV12. (b), (c), and (d) displayed the inhibitory effects of EAS at CV12 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; ***P < 0.001 versus background activities).

Mentions: EAS at CV12 induced inhibitory effects which were also related to the intensities. Figure 2(a) showed typical responses of gastric motility following EAS with different intensities for 60 s, and Figures 2(b) and 2(c) summarized the responses obtained from all 9 tested rats. EAS with all the intensities at CV12 induced significant inhibition effects on the amplitudes and integrals of gastric contraction (amplitude: 0.5 mA: −11.1 ± 2.7%, P < 0.05; 1 mA: −18.8 ± 3.2%, 3 mA: −42.0 ± 5.5%, 5 mA: −56.7 ± 10%, 7 mA: −56.3 ± 10%, and 9 mA: −57.3 ± 7.2%, P < 0.01) (integral: 0.5 mA: −17.0 ± 3.2%, P < 0.01; 1 mA: −34.0 ± 2.3%, 3 mA: −50.1 ± 3%, 5 mA: −64.4 ± 3.2%, 7 mA: −64.0 ± 3.7%, and 9 mA: −63.4 ± 2.5%, P < 0.001). The inhibition of EAS at CV12 appeared from a low intensity (0.5 mA), with IC50 value of approximately 2.8 mA for both amplitude and integral (Figure 2(b)). This means that EAS with 2.8 mA can obtain 50% of the maximum inhibitory effect. When the intensity reached to 5 mA, the response efficiency did not increase correspondingly. The “plateau region” also appeared in the CV12 which induced the inhibitory effects.


"Intensity-response" effects of electroacupuncture on gastric motility and its underlying peripheral neural mechanism.

Su YS, He W, Wang C, Shi H, Zhao YF, Xin JJ, Wang XY, Shang HY, Hu L, Jing XH, Zhu B - Evid Based Complement Alternat Med (2013)

Gastric motility in response to EAS at CV12 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at CV12. (b), (c), and (d) displayed the inhibitory effects of EAS at CV12 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; ***P < 0.001 versus background activities).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3713365&req=5

fig2: Gastric motility in response to EAS at CV12 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at CV12. (b), (c), and (d) displayed the inhibitory effects of EAS at CV12 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; ***P < 0.001 versus background activities).
Mentions: EAS at CV12 induced inhibitory effects which were also related to the intensities. Figure 2(a) showed typical responses of gastric motility following EAS with different intensities for 60 s, and Figures 2(b) and 2(c) summarized the responses obtained from all 9 tested rats. EAS with all the intensities at CV12 induced significant inhibition effects on the amplitudes and integrals of gastric contraction (amplitude: 0.5 mA: −11.1 ± 2.7%, P < 0.05; 1 mA: −18.8 ± 3.2%, 3 mA: −42.0 ± 5.5%, 5 mA: −56.7 ± 10%, 7 mA: −56.3 ± 10%, and 9 mA: −57.3 ± 7.2%, P < 0.01) (integral: 0.5 mA: −17.0 ± 3.2%, P < 0.01; 1 mA: −34.0 ± 2.3%, 3 mA: −50.1 ± 3%, 5 mA: −64.4 ± 3.2%, 7 mA: −64.0 ± 3.7%, and 9 mA: −63.4 ± 2.5%, P < 0.001). The inhibition of EAS at CV12 appeared from a low intensity (0.5 mA), with IC50 value of approximately 2.8 mA for both amplitude and integral (Figure 2(b)). This means that EAS with 2.8 mA can obtain 50% of the maximum inhibitory effect. When the intensity reached to 5 mA, the response efficiency did not increase correspondingly. The “plateau region” also appeared in the CV12 which induced the inhibitory effects.

Bottom Line: The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA.The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility.TRPV1 receptor was involved in the regulation of gastric motility of EAS.

View Article: PubMed Central - PubMed

Affiliation: Institute of Acupuncture and Moxibustion, China Academy of Chinese Medical Sciences, 16 Nanxiaojie, Dongzhimennei, Beijing 100700, China.

ABSTRACT
The aim of this study was to explore the "intensity-response" relationship between EAS and the effect of gastric motility of rats and its underlying peripheral neural mechanism by employing ASIC3 knockout (ASIC3-/-), TRPV1 knockout (TRPV1-/-), and C57BL/6 mice. For adult male Sprague-Dawley (n = 18) rats, the intensities of EAS were 0.5, 1, 3, 5, 7, and 9 mA, respectively. For mice (n = 8 in each group), only 1 mA was used, by which C fiber of the mice can be activated. Gastric antrum motility was measured by intrapyloric balloon. Gastric motility was facilitated by EAS at ST36 and inhibited by EAS at CV12. The half maximal facilitation intensity of EAS at ST36 was 2.1-2.3 mA, and the half maximal inhibitory intensity of EAS at CV12 was 2.8 mA. In comparison with C57BL/6 mice, the facilitatory effect of ST36 and inhibitive effect of CV12 in ASIC3-/- mice decreased, but the difference was not statistically significant (P > 0.05). However, these effects in TRPV1-/- mice decreased significantly (P < 0.001). The results indicated that there existed an "intensity-response" relationship between EAS and the effect of gastric motility. TRPV1 receptor was involved in the regulation of gastric motility of EAS.

No MeSH data available.


Related in: MedlinePlus