{"title":"马骨盆屈曲的体外电活动。","authors":"C Fintl, G T Pearson, I G Mayhew, N P H Hudson","doi":"10.1111/j.2042-3306.2011.00396.x","DOIUrl":null,"url":null,"abstract":"<p><strong>Reasons for performing study: </strong>The generation and maintenance of intestinal motility patterns involve the complex interactions of several components including the gastrointestinal pacemaker cells (interstitial cells of Cajal, ICC). Central to ICC function is the generation of rhythmic pacemaker currents, namely slow waves, which represent the rate limiting step for intestinal smooth muscle contractions. Currently, intracellular slow wave activity has not been demonstrated in the equine colon.</p><p><strong>Objectives: </strong>To characterise the in vitro myoelectrical activity of the equine pelvic flexure using intracellular recording techniques.</p><p><strong>Methods: </strong>Intestinal samples were collected immediately following euthanasia from 14 normal horses. One millimetre thick tissue sections were pinned and superfused with warmed, oxygenated Krebs solution. Intracellular recordings were made from smooth muscle cells close to the submucosal border of the circular muscle layer. The L-type Ca(2+) channel blocker nifedipine was added to the superfusion fluid in 9 experiments while the Na(+) channel blocker tetrodotoxin was added to the superfusion fluid in 4 experiments. The data were recorded and stored using an acquisition system and a software package used to analyse the recordings.</p><p><strong>Results: </strong>In 10 of the 14 horses, electrical events consistent with slow wave patterns were recorded from individual smooth muscle cells. Surprisingly, adding nifedipine to the superfusion fluid abolished all electrical activity. In contrast, tetrodotoxin had no apparent effect on the electrical activity.</p><p><strong>Conclusions: </strong>Assuming that the electrical events were slow waves, the blockade by nifedipine suggests significant and potentially important differences in the ionic mechanisms responsible for slow waves in the different regions of the equine intestinal tract, which deserve further evaluation.</p>","PeriodicalId":11801,"journal":{"name":"Equine veterinary journal. Supplement","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2011-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.2042-3306.2011.00396.x","citationCount":"2","resultStr":"{\"title\":\"In vitro electrical activity of the equine pelvic flexure.\",\"authors\":\"C Fintl, G T Pearson, I G Mayhew, N P H Hudson\",\"doi\":\"10.1111/j.2042-3306.2011.00396.x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Reasons for performing study: </strong>The generation and maintenance of intestinal motility patterns involve the complex interactions of several components including the gastrointestinal pacemaker cells (interstitial cells of Cajal, ICC). Central to ICC function is the generation of rhythmic pacemaker currents, namely slow waves, which represent the rate limiting step for intestinal smooth muscle contractions. Currently, intracellular slow wave activity has not been demonstrated in the equine colon.</p><p><strong>Objectives: </strong>To characterise the in vitro myoelectrical activity of the equine pelvic flexure using intracellular recording techniques.</p><p><strong>Methods: </strong>Intestinal samples were collected immediately following euthanasia from 14 normal horses. One millimetre thick tissue sections were pinned and superfused with warmed, oxygenated Krebs solution. Intracellular recordings were made from smooth muscle cells close to the submucosal border of the circular muscle layer. The L-type Ca(2+) channel blocker nifedipine was added to the superfusion fluid in 9 experiments while the Na(+) channel blocker tetrodotoxin was added to the superfusion fluid in 4 experiments. The data were recorded and stored using an acquisition system and a software package used to analyse the recordings.</p><p><strong>Results: </strong>In 10 of the 14 horses, electrical events consistent with slow wave patterns were recorded from individual smooth muscle cells. Surprisingly, adding nifedipine to the superfusion fluid abolished all electrical activity. In contrast, tetrodotoxin had no apparent effect on the electrical activity.</p><p><strong>Conclusions: </strong>Assuming that the electrical events were slow waves, the blockade by nifedipine suggests significant and potentially important differences in the ionic mechanisms responsible for slow waves in the different regions of the equine intestinal tract, which deserve further evaluation.</p>\",\"PeriodicalId\":11801,\"journal\":{\"name\":\"Equine veterinary journal. 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In vitro electrical activity of the equine pelvic flexure.
Reasons for performing study: The generation and maintenance of intestinal motility patterns involve the complex interactions of several components including the gastrointestinal pacemaker cells (interstitial cells of Cajal, ICC). Central to ICC function is the generation of rhythmic pacemaker currents, namely slow waves, which represent the rate limiting step for intestinal smooth muscle contractions. Currently, intracellular slow wave activity has not been demonstrated in the equine colon.
Objectives: To characterise the in vitro myoelectrical activity of the equine pelvic flexure using intracellular recording techniques.
Methods: Intestinal samples were collected immediately following euthanasia from 14 normal horses. One millimetre thick tissue sections were pinned and superfused with warmed, oxygenated Krebs solution. Intracellular recordings were made from smooth muscle cells close to the submucosal border of the circular muscle layer. The L-type Ca(2+) channel blocker nifedipine was added to the superfusion fluid in 9 experiments while the Na(+) channel blocker tetrodotoxin was added to the superfusion fluid in 4 experiments. The data were recorded and stored using an acquisition system and a software package used to analyse the recordings.
Results: In 10 of the 14 horses, electrical events consistent with slow wave patterns were recorded from individual smooth muscle cells. Surprisingly, adding nifedipine to the superfusion fluid abolished all electrical activity. In contrast, tetrodotoxin had no apparent effect on the electrical activity.
Conclusions: Assuming that the electrical events were slow waves, the blockade by nifedipine suggests significant and potentially important differences in the ionic mechanisms responsible for slow waves in the different regions of the equine intestinal tract, which deserve further evaluation.