scholarly journals EFFECTS OF SUBCELLULAR FRACTIONS OF THE DOG SMALL INTESTINAL SMOOTH MUSCLE ON ACETYLCHOLLNE-INDUCED CONTRACTION OF GLYCEROL EXTRACTED SKELETAL MUSCLE

1970 ◽  
Vol 20 (3) ◽  
pp. 448-450 ◽  
Author(s):  
KEIJIRO TAKAGI ◽  
MASAATSU UCHIDA
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Subcellular Fractions ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Role of stat6 in hypercontractility of murine small intestinal smooth muscle induced by nematode infection

2001 ◽  
Vol 120 (5) ◽  
pp. A534-A534
Author(s):  
A ZHAO ◽  
D MULLOY ◽  
J URBANJR ◽  
W GAUSE ◽  
T SHEADONOHUE
Keyword(s):  
Smooth Muscle ◽  
Nematode Infection ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Electrical activity of small intestinal smooth muscle and its temperature dependence

1975 ◽  
Vol 229 (5) ◽  
pp. 1268-1276 ◽  
Author(s):  
TY El-Sharkawy ◽  
EE Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Activity ◽  
Temperature Dependence ◽  
Intestinal Smooth Muscle ◽  
Plateau Phase ◽  
Control Activity ◽  
Electrical Control ◽  
Electrical Control Activity ◽  
Small Intestinal

Some important features of the intracellularly recorded electrical control activity of rabbit jejunal smooth muscle and its temperature dependence are reported in this study. This activity consisted of repetitive 18-mV depolarizations (control potentials (CP) or slow waves), which at 37degreesC lasted 2 s and had a frequency of 18/min and arose from a membrane potential of --55 mV. In some cells periods between CP's exhibited "diastolic" progressive depolarizations (intercontrol-potential depolarization), which may be the trigger of the CP in driving cells. While CP was usually monophasic, some cells persistently exhibited a notch early in the plateau phase. We suggest that CP consists of two components, an "initial depolarization" and a "secondary depolarization," which are usually fused together to give a monophasic potential. Cooling reduced CP frequency and prolonged its duration and caused more cells to show notching. While amplitude and rate of CP initial depolarization had low Q10's, duration and rates of onset and offset of the secondary depolarization had higher Q10's. Thus, the process responsible for secondary depolarization is more sensitive to temperature thant that underlying initial depolarization of the CP.

scholarly journals Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ziqi Lin ◽  
Chenlong Zhang ◽  
Xiaoxin Zhang ◽  
Na Shi ◽  
Yongjian Wen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intestinal Motility ◽  
Contractile Function ◽  
Specific Inhibitor ◽  
Intestinal Smooth Muscle ◽  
Fatty Acid Binding ◽  
Treatment Groups ◽  
Necrotising Pancreatitis ◽  
Acute Necrotising Pancreatitis ◽  
Small Intestinal

Protein kinase C-potentiated inhibitor protein of 17 kDa (CPI-17), a specific inhibitor of myosin light-chain phosphatase (MLCP) regulated by proinflammatory cytokines, is central for calcium sensitisation. We investigated the effects of chaiqin chengqi decoction (CQCQD) on the CPI-17/MLCP pathway in the small intestinal smooth muscle cells (SMCs) and strips (SMS) in an AP model. Necrotising AP was induced in rats by intraperitoneal injections (IPI) of L-ornithine (3.0 g/kg, pH 7.0; hourly × 2) at 1 hour apart; controls received saline. In treatment groups, carbachol (CCh; 60 μg/kg, IPI) or CQCQD (20 g/kg; 2-hourly × 3, intragastric) was administered. The necrotising AP model was associated with systemic inflammation (serum IL-1β and TNF-α) and worsened jejunum histopathology and motility (serum vasoactive intestinal peptide and intestinal fatty acid-binding protein) as the disease progressed. There was decreased intracellular calcium concentration ([Ca2+]i) SMCs. Contractile function of isolated SMCs was reduced and associated with down-regulated expression of key mRNAs and proteins of the CPI-17/MLCP pathway as well as increased IL-1β and TNF-α. CQCQD and CCh significantly reversed these changes and the disease severity. These data suggest that CQCQD can improve intestinal motility by modulating the CPI-17/MLCP pathway in small intestinal smooth muscle during AP.

Role of stat6 in hypercontractility of murine small intestinal smooth muscle induced by nematode infection

2001 ◽  
Vol 120 (5) ◽  
pp. A534 ◽  
Author(s):  
Aiping Zhao ◽  
Daniel P. Mulloy ◽  
Joseph F. Urban ◽  
William C. Gause ◽  
Terez Shea-Donohue
Keyword(s):  
Smooth Muscle ◽  
Nematode Infection ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

scholarly journals Effect of piperine on arecoline induced contraction of isolated small intestinal smooth muscle from rabbits

2019 ◽  
Vol 27 (1) ◽  
pp. 20-28
Author(s):  
Zhong-Quan Chen ◽  
Chun-Ru Fu ◽  
Feng-Qin Fu ◽  
Ying Chen ◽  
Chang-Wen Fu ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Structural and functional characteristics of muscle from diabetic rodent small intestine

1990 ◽  
Vol 258 (5) ◽  
pp. G690-G698 ◽  
Author(s):  
T. V. Nowak ◽  
B. Harrington ◽  
J. P. Weisbruch ◽  
J. H. Kalbfleisch
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Surface Area ◽  
Muscle Mass ◽  
Insulin Treatment ◽  
Intestinal Smooth Muscle ◽  
Unit Surface Area ◽  
Unit Surface ◽  
Small Intestinal ◽  
Mucosal Mass

After 30 days of streptozotocin-induced diabetes, the small intestine from untreated diabetic, insulin-treated diabetic, and nondiabetic rodents was excised in toto and measured. Despite a net loss in body weight, the diabetic animals showed a near twofold increase in small intestinal weight. This was characterized by a 148% increase in mucosal mass as well as a 39% increase in intestinal smooth muscle mass (P less than 0.05, respectively). The diabetic intestine was significantly longer and had a greater diameter and surface area. Diabetes significantly increased mucosal mass per unit surface area but produced an insignificant decrease in smooth muscle mass per unit surface area. Insulin treatment of the diabetic animals prevented the increase in total mucosal mass and mucosal mass per unit surface area. Insulin treatment also prevented the increase in smooth muscle mass, but reduced smooth muscle mass per unit surface area to a level significantly less than that found in nondiabetic intestine. In vitro dose-response studies of circular and longitudinal small intestinal muscle from the diabetic animals showed normal tension development and sensitivity to both bethanechol chloride and physostigmine. These observations show that the diabetic state produces alterations in not only mucosal but also smooth muscle mass in the small intestine. However, despite these morphological changes, diabetic intestinal smooth muscle retains its sensitivity to cholinergic stimulation and its capacity for tension generation.

Contractions of cat small intestinal smooth muscle in calcium-free solution

Nature ◽  
1979 ◽  
Vol 281 (5732) ◽  
pp. 582-583 ◽  
Author(s):  
Allen W. Mangel ◽  
D. O. Nelson ◽  
John A. Connor ◽  
C. Ladd Prosser
Keyword(s):  
Smooth Muscle ◽  
Intestinal Smooth Muscle ◽  
Free Solution ◽  
Small Intestinal
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