Massive intestinal resection depresses circular smooth muscle contractility in the rat

1995 ◽  
Vol 73 (10) ◽  
pp. 1443-1450 ◽  
Author(s):  
Beth C. Chin ◽  
Daimen T. M. Tan ◽  
R. Brent Scott
Keyword(s):  
Smooth Muscle ◽  
Contractile Activity ◽  
Intestinal Resection ◽  
Circular Muscle ◽  
Intestinal Transit ◽  
Sham Operation ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Phasic Activity ◽  
Circular Smooth Muscle

To determine whether functional changes in in vitro contractility and in vivo gastrointestinal transit accompany the adaptive structural changes seen in jejunal circular muscle after massive intestinal resection, rats were subjected to either surgical resection of 75% of the mid-jejunoileum or a sham operation. Basal stress in response to stretch was similar for both groups on postoperative days 10, 20, 30, and 40. By day 10 after surgery, tissues from resected rats exhibited a significant reduction in bethanechol-stimulated tonic stress and in frequency of phasic contractions. The amplitude of spontaneous phasic activity was significantly increased; however, following cholinergic stimulation, the magnitude of the increase in the amplitude of phasic activity was significantly reduced. Experiments with tetrodotoxin (10−6 M) indicated a myogenic origin to the reduction in bethanechol-stimulated tonic stress and the reduced frequency and altered amplitude of phasic contractile activity in resected animals. The tonic stress developed in response to depolarization with KCl did not differ significantly between sham-operated and resected rats. Transit studies showed no change in the rate of gastric emptying after resection but did reveal a significant reduction in the velocity of intestinal transit. Thus, following massive intestinal resection the bethanechol-stimulated tonic stress response and phasic contractile activity of circular smooth muscle are significantly reduced, concomitant with altered intestinal transit. The reduction in contractility in the resected animals may be due to an alteration at the level of the smooth muscle receptor and (or) its signal transduction pathway.Key words: short gut, intestinal circular smooth muscle, contractility, adaptation.

Smooth Muscle Contractility after Intestinal Resection

1996 ◽  
Vol 60 (2) ◽  
pp. 379-384 ◽  
Author(s):  
J.S. Thompson ◽  
E.M.M. Quigley ◽  
D. Lassiter ◽  
T.E. Adrian
Keyword(s):  
Smooth Muscle ◽  
Intestinal Resection ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility

scholarly journals Smooth muscle contractility causes the gut to grow anisotropically

2019 ◽  
Vol 16 (159) ◽  
pp. 20190484 ◽  
Author(s):  
Diana Khalipina ◽  
Yusuke Kaga ◽  
Nicolas Dacher ◽  
Nicolas R. Chevalier
Keyword(s):  
Smooth Muscle ◽  
Squeezing Effect ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Circular Smooth Muscle ◽  
Growth Defects ◽  
Mechanical Deformations ◽  
Set Up ◽  
Innovative Culture

The intestine is the most anisotropically shaped organ, but, when grown in culture, embryonic intestinal stem cells form star- or sphere-shaped organoids. Here, we present evidence that spontaneous tonic and phasic contractions of the circular smooth muscle of the embryonic gut cause short-timescale elongation of the organ by a purely mechanical, self-squeezing effect. We present an innovative culture set-up to achieve embryonic gut growth in culture and demonstrate by three different methods (embryological, pharmacological and microsurgical) that gut elongational growth is compromised when smooth muscle contractions are inhibited. We conclude that the cumulated short-term mechanical deformations induced by circular smooth muscle lead to long-term anisotropic growth of the gut, thus demonstrating a self-consistent way by which the function of this organ (peristalsis) directs its shape (morphogenesis). Our model correctly predicts that longitudinal smooth muscle differentiation later in embryogenesis slows down elongation, and that several mice models with defective gut smooth muscle contractility also exhibit gut growth defects. We lay out a comprehensive scheme of forces acting on the gut during embryogenesis and of their role in the morphogenesis of this organ. This knowledge will help design efficient in vitro organ growth protocols and handle gut growth pathologies such as short bowel syndrome.

Progressive alterations in circular smooth muscle contractility in TNBS-induced colitis in rats

1999 ◽  
Vol 11 (5) ◽  
pp. 347-356 ◽  
Author(s):  
Hosseini ◽  
Goldhill ◽  
Bossone ◽  
Pineiro-Carrero ◽  
Shea-Donohue
Keyword(s):  
Smooth Muscle ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility ◽  
Circular Smooth Muscle

scholarly journals Ranolazine inhibits voltage-gated mechanosensitive sodium channels in human colon circular smooth muscle cells

2015 ◽  
Vol 309 (6) ◽  
pp. G506-G512 ◽  
Author(s):  
Leila Neshatian ◽  
Peter R. Strege ◽  
Poong-Lyul Rhee ◽  
Robert E. Kraichely ◽  
Amelia Mazzone ◽  
...  
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Circular Muscle ◽  
Muscle Cells ◽  
Human Colon ◽  
Smooth Muscle Contractility ◽  
Western Blots ◽  
Voltage Gated ◽  
Circular Smooth Muscle

Human jejunum smooth muscle cells (SMCs) and interstitial cells of Cajal (ICCs) express the SCN5A-encoded voltage-gated, mechanosensitive sodium channel NaV1.5. NaV1.5 contributes to small bowel excitability, and NaV1.5 inhibitor ranolazine produces constipation by an unknown mechanism. We aimed to determine the presence and molecular identity of Na+ current in the human colon smooth muscle and to examine the effects of ranolazine on Na+ current, mechanosensitivity, and smooth muscle contractility. Inward currents were recorded by whole cell voltage clamp from freshly dissociated human colon SMCs at rest and with shear stress. SCN5A mRNA and NaV1.5 protein were examined by RT-PCR and Western blots, respectively. Ascending human colon strip contractility was examined in a muscle bath preparation. SCN5A mRNA and NaV1.5 protein were identified in human colon circular muscle. Freshly dissociated human colon SMCs had Na+ currents (−1.36 ± 0.36 pA/pF), shear stress increased Na+ peaks by 17.8 ± 1.8% and accelerated the time to peak activation by 0.7 ± 0.3 ms. Ranolazine (50 μM) blocked peak Na+ current by 43.2 ± 9.3% and inhibited shear sensitivity by 25.2 ± 3.2%. In human ascending colon strips, ranolazine decreased resting tension (31%), reduced the frequency of spontaneous events (68%), and decreased the response to smooth muscle electrical field stimulation (61%). In conclusion, SCN5A-encoded NaV1.5 is found in human colonic circular smooth muscle. Ranolazine blocks both peak amplitude and mechanosensitivity of Na+ current in human colon SMCs and decreases contractility of human colon muscle strips. Our data provide a likely mechanistic explanation for constipation induced by ranolazine.

scholarly journals Downregulation of Gαq-11protein expression in guinea pig antral and colonic circular muscle during pregnancy

1999 ◽  
Vol 276 (4) ◽  
pp. G895-G900 ◽  
Author(s):  
Qian Chen ◽  
Zuo-Liang Xiao ◽  
Piero Biancani ◽  
Jose Behar
Keyword(s):  
Smooth Muscle ◽  
G Proteins ◽  
Guinea Pigs ◽  
Muscle Relaxation ◽  
Circular Muscle ◽  
Enzymatic Digestion ◽  
Inhibitory Effect ◽  
Smooth Muscle Contractility ◽  
Circular Smooth Muscle ◽  
Gtpγs Binding

Pregnancy has an inhibitory effect on motility of the gastrointestinal tract. The present study was designed to examine the mechanisms responsible for antral and colonic hypomotility in pregnant guinea pigs. Circular smooth muscle cells from the antrum and left colon were isolated by enzymatic digestion with collagenase from pregnant and nonpregnant guinea pigs. Contractile responses to agonists were expressed as percent shortening from resting cell length. The function of G proteins in antral and colonic circular smooth muscle was assessed by [35S]guanosine 5′- O-(3-thiotriphosphate) (GTPγS) binding induced by CCK-8 and G protein quantitation. The contraction of antral and colonic circular smooth muscle from pregnant guinea pigs was reduced in response to CCK-8 and to GTPγS but was normal in response to KCl andd- myo-inositol 1,4,5-trisphosphate compared with nonpregnant animals. The stimulation of [35S]GTPγS binding to Gαq-11induced by 1 μM CCK-8 was significantly lower in antral and colonic circular smooth muscle from pregnant guinea pigs than that in controls. Furthermore, Western blot analysis showed a decreased Gαq-11and an increased Gsα protein content in both tissues during pregnancy. It is concluded that pregnancy appears to impair gastrointestinal circular smooth muscle contractility by downregulating G proteins such as Gαq-11protein, which mediates muscle contraction, and upregulating Gsα protein, which mediates muscle relaxation.

scholarly journals Acute experimental colitis decreases colonic circular smooth muscle contractility in rats

1997 ◽  
Vol 273 (4) ◽  
pp. G928-G936 ◽  
Author(s):  
Brian S. Myers ◽  
John S. Martin ◽  
Daniel T. Dempsey ◽  
Henry P. Parkman ◽  
Rebecca M. Thomas ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intracellular Calcium ◽  
Calcium Influx ◽  
Circular Muscle ◽  
Inhibitory Effect ◽  
Calcium Handling ◽  
Extracellular Potassium ◽  
Smooth Muscle Contractility ◽  
Circular Smooth Muscle ◽  
Lesion Severity

Distal colitis decreases the contractility of the underlying circular smooth muscle. We examined how time after injury and lesion severity contribute to the decreased contractility and how colitis alters the calcium-handling properties of the affected muscle. Distal colitis was induced in rats by intrarectal administration of 4% acetic acid. Contractile responses to acetylcholine, increased extracellular potassium, and the G protein activator NaF were determined for circular muscle strips from sham control and colitic rats at days 1, 2, 3, 7, and 14 postenemas. Acetylcholine stimulation of tissues from day 3colitic rats was performed in a zero calcium buffer, in the presence of nifedipine, and after depletion of intracellular stores of calcium. The colitis was graded macroscopically as mild, moderate, or severe. Regardless of agonist, maximal decrease in force developed 2 to 3 days posttreatment, followed by a gradual return to control by day 14. The inhibitory effect of colitis on contractility increased with increasing severity of inflammation. Limiting extracellular calcium influx had a greater inhibitory effect on tissues from colitic rats; intracellular calcium depletion had a greater inhibitory effect on tissues from control animals. The data suggest that both lesion severity and time after injury affect the contractile response of circular smooth muscle from the inflamed distal colon. Impaired utilization of intracellular calcium may contribute to the decreased contractility.

Sign in / Sign up

Export Citation Format

Share Document