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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 ST36 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at ST36. (b), (c), and (d) displayed the facilitatory effects of EAS at ST36 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; *P < 0.05, **P < 0.01, versus background activities).
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fig1: Gastric motility in response to EAS at ST36 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at ST36. (b), (c), and (d) displayed the facilitatory effects of EAS at ST36 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; *P < 0.05, **P < 0.01, versus background activities).

Mentions: EAS at ST36 induced facilitatory effects which were related to the intensities. Figure 1(a) showed typical responses of gastric motility following EAS with various intensities for 60 s. Figures 1(b) and 1(c) summarized the responses obtained from all 9 tested rats. It should be noted that when the stimulation was less than 1 mA, there was no significant response of gastric motility (amplitude changes: 0.5 mA: 2.4 ± 1.1%, 1 mA: 4.7 ± 2.4%, P > 0.05) (integral changes: 0.5 mA: 7.8 ± 2.8%, 1 mA: 12.7 ± 5.8%, P > 0.05). However, 3 mA, 5 mA, 7 mA, and 9 mA EAS at ST36 elicited a significant enhancement on the amplitude and integral of gastric contraction compared with the background activities (amplitude changes: 3 mA: 37.9 ± 5.8%, 5 mA: 43.7 ± 3.7%, 7 mA: 52.3 ± 4.4%, 9 mA: 53.1 ± 5.4%, P < 0.01, P < 0.001) (integral changes: 3 mA: 47.2 ± 3.2%, 5 mA: 55.2 ± 5.3%, 7 mA: 64.9 ± 5.6%, 9 mA: 64.3 ± 6.2%, P < 0.001). The facilitation of EAS at ST36 appeared from a low intensity with an EC50 value of approximately 2.3 mA for amplitude (Figure 1(b)) and 2.1 mA for integral (Figure 1(c)), which means that EAS with 2.1–2.3 mA can obtain 50% of the maximum facilitatory effect. For the intensity of EAS above 5 mA, the response efficiency did not increase correspondingly as intensities increasing, which indicated that the effects may hit a “plateau region” when the stimulating intensity reached to a certain level.


"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 ST36 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at ST36. (b), (c), and (d) displayed the facilitatory effects of EAS at ST36 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; *P < 0.05, **P < 0.01, versus background activities).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3713365&req=5

fig1: Gastric motility in response to EAS at ST36 with different intensities in rats. (a) Representative examples of the alterations of gastric contraction wave induced by different intensities of EAS at ST36. (b), (c), and (d) displayed the facilitatory effects of EAS at ST36 on the amplitude, integral, and frequency of gastric motility, respectively (n = 9; *P < 0.05, **P < 0.01, versus background activities).
Mentions: EAS at ST36 induced facilitatory effects which were related to the intensities. Figure 1(a) showed typical responses of gastric motility following EAS with various intensities for 60 s. Figures 1(b) and 1(c) summarized the responses obtained from all 9 tested rats. It should be noted that when the stimulation was less than 1 mA, there was no significant response of gastric motility (amplitude changes: 0.5 mA: 2.4 ± 1.1%, 1 mA: 4.7 ± 2.4%, P > 0.05) (integral changes: 0.5 mA: 7.8 ± 2.8%, 1 mA: 12.7 ± 5.8%, P > 0.05). However, 3 mA, 5 mA, 7 mA, and 9 mA EAS at ST36 elicited a significant enhancement on the amplitude and integral of gastric contraction compared with the background activities (amplitude changes: 3 mA: 37.9 ± 5.8%, 5 mA: 43.7 ± 3.7%, 7 mA: 52.3 ± 4.4%, 9 mA: 53.1 ± 5.4%, P < 0.01, P < 0.001) (integral changes: 3 mA: 47.2 ± 3.2%, 5 mA: 55.2 ± 5.3%, 7 mA: 64.9 ± 5.6%, 9 mA: 64.3 ± 6.2%, P < 0.001). The facilitation of EAS at ST36 appeared from a low intensity with an EC50 value of approximately 2.3 mA for amplitude (Figure 1(b)) and 2.1 mA for integral (Figure 1(c)), which means that EAS with 2.1–2.3 mA can obtain 50% of the maximum facilitatory effect. For the intensity of EAS above 5 mA, the response efficiency did not increase correspondingly as intensities increasing, which indicated that the effects may hit a “plateau region” when the stimulating intensity reached to a certain level.

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