Yersinia enterocolitica enteritis affects rabbit intestinal longitudinal smooth muscle function

1992 ◽  
Vol 262 (2) ◽  
pp. G278-G284 ◽  
Author(s):  
R. B. Scott ◽  
D. T. Tan
Keyword(s):  
Smooth Muscle ◽  
Weight Gain ◽  
Food Intake ◽  
Yersinia Enterocolitica ◽  
Biomechanical Properties ◽  
Isometric Tension ◽  
Infected Group ◽  
Tension Development ◽  
Longitudinal Smooth Muscle ◽  
Tension Curves

To determine whether Yersinia enterocolitica (YE) enteritis has an effect on the biomechanical properties of intestinal smooth muscle, New Zealand White rabbits (600-900 g) were divided into an infected group (n = 9) and sham-infected animals fed ad libitum (n = 9), or pair fed with the infected group (n = 9). Animals were inoculated with 10(10) organisms of YE in 10 ml NaHCO3 (infected group) or 10 ml NaHCO3 (sham-infected control and pair-fed groups) at time 0. Daily food intake, weight gain, and YE excretion were noted. Six days later animals were killed and longitudinal smooth muscle strips prepared from proximal (P), medial (M), and distal (D) segments of intestine in each treatment group. Isometric tension was recorded in tissue baths perfused with oxygenated Krebs solution and 10(-6) M tetrodotoxin. Basal and active (the response to 10(-5) M carbachol) length-tension curves were generated. Then, with the muscle strips stretched to their optimum length for tension development, the dose response to carbachol and to graded depolarization with KCl was determined. Infected animals had a significantly reduced food intake and weight gain compared with controls. The development of basal tension with stretch was not significantly different in infected compared with control or pair-fed tissues from the same site.(ABSTRACT TRUNCATED AT 250 WORDS)

Intestinal motility during acute Yersinia enterocolitica enteritis in rabbits

1989 ◽  
Vol 67 (6) ◽  
pp. 553-560 ◽  
Author(s):  
R. B. Scott ◽  
D. G. Gall ◽  
S. C. Diamant
Keyword(s):  
Weight Gain ◽  
Food Intake ◽  
Motor Activity ◽  
Yersinia Enterocolitica ◽  
Phase Iii ◽  
Intestinal Lumen ◽  
Fecal Excretion ◽  
Cycle Period ◽  
Motility Index ◽  
And Control

To determine if Yersinia enterocolitica (YE) enteritis is associated with an alteration of intestinal myoelectric and motor activity, and with an increased rate of aboral transit, New Zealand white rabbits (500–900 g) were surgically prepared with ileal bipolar electrodes and a manometry catheter adjacent to the distal electrode. One week later animals were inoculated with 1010 organisms of YE in 10 mL NaHCO3 (infected group) or 10 mL NaHCO3 (sham-infected pair-fed and control groups). Daily food intake, weight gain, YE excretion, and stool pattern were noted. Intestinal myoelectric and motor activity over a 6- to 8- h period before and 3, 6, and 14 days after inoculation was compared in infected (I), pair-fed (PF), and control (C) groups. Intestinal transit was evaluated in I and C animals on days 3 and 6 after inoculation by measuring the distribution in the intestinal lumen of 51Cr 20 min after it was instilled directly into the jejunum. Infected animals exhibited diarrhea, fecal excretion of YE, and significantly decreased food intake, weight gain, and survival (11.4 ± 0.6 days). Infection was associated with a significant (p < 0.05) decrease in both the cycle period of the migrating myoelectric complex (MMC) and the total number of single, paired, and (or) clustered contractions per MMC, and a significant (p < 0.001) increase in duration of phase III of the MMC. There was no change in intestinal slow wave frequency (19 cycles/min), motility index per MMC, or the percentage of contractions that propagated in an orad (7%) or aboral (69%) direction or that appeared stationary (25%). The changes in myoelectric and motor activity were specific for YE infection (not related to decreased food intake and weight gain) and were associated with a significantly increased rate of aboral transit. Thus, the inflammatory enteritis induced by YE is associated with alterations of intestinal myoelectric and motor activity, and an increased rate of aboral transit.Key words: Yersinia enterocolitica, infection, intestine, motility, transit.

Stiffness of active smooth muscle during forced elongation

1987 ◽  
Vol 253 (3) ◽  
pp. C484-C493 ◽  
Author(s):  
R. A. Meiss
Keyword(s):  
Smooth Muscle ◽  
Phase Angle ◽  
Muscle Length ◽  
Isometric Tension ◽  
Microcomputer System ◽  
Tension Development ◽  
Stretch Rate ◽  
Angle Data ◽  
Cross Bridges ◽  
System Phase

The stiffness of isometrically contracting mesotubarium superius and ovarian ligament smooth muscle from estrous female rabbits was measured continuously by using sinusoidal length perturbations (at 80 Hz, less than 15 microns peak to peak). Muscles were stimulated with alternating current fields, and all records were digitized using a microcomputer system. Phase-angle data were used to resolve computed stiffness into elastic and viscous components. Stiffness measurements were continued during long ramp-type stretches (up to 25% of muscle length) delivered as soon as force was maximal. To use the period of isometric tension development as a standard for comparison, the expected stiffness was computed during the long stretch. Stiffness was reduced in approximate proportion to the ramp stretch rate, and the reduction was confined largely to the elastic component. Cooling the muscle increased the stiffness deviation at a given stretch rate. It is proposed that the long stretch detaches cross bridges that can reattach to new sites as myofilaments shear past one another. At higher shearing speeds, less time is available for reattachment and stiffness is further reduced.

An abnormal rate of actin myosin cross-bridge cycling in colonic smooth muscle associated with experimental colitis

1992 ◽  
Vol 262 (5) ◽  
pp. G921-G926 ◽  
Author(s):  
Y. N. Xie ◽  
W. T. Gerthoffer ◽  
S. N. Reddy ◽  
F. Cominelli ◽  
V. E. Eysselein ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Maximum Velocity ◽  
Experimental Colitis ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Mucosal Inflammation ◽  
Control Group ◽  
Tension Development ◽  
Abnormal Rate ◽  
Mlc Phosphorylation

Previous studies showed that colonic smooth muscle develops less contractile force to neurohumoral stimulation when associated with mucosal inflammation. This study evaluated 1) the Ca2+ dependence for colonic smooth muscle contraction, 2) the maximum velocity of muscle shortening (Vmax), and 3) changes in 20-kDa myosin light-chain (MLC) phosphorylation in distal circular colonic muscle from healthy rabbits and from rabbits with experimental colitis, induced by Formalin and immune complexes. The isometric tension of unskinned muscle stimulated with bethanechol or KCl was less (P less than 0.05) in animals with colitis compared with the control group. In saponin-skinned muscle, the amplitude of the maximal tension at [Ca2+] of 3 x 10(-7) M was decreased (P less than 0.05) in colitis animals (4.3 +/- 0.9 x 10(4) N/m2, n = 7) compared with healthy animals (10.5 +/- 2.4 x 10(4) N/m2, n = 6). However, the ED50 for Ca2+ stimulation was similar (P greater than 0.05) in both groups. When MLC was thiophosphorylated with ATP gamma S, the tension development was decreased in colitis (2.1 +/- 0.3 x 10(4) N/m2, n = 5; P less than 0.01) compared with normals (5.0 +/- 1.4 x 10(4) N/m2, n = 5). In healthy animals, phosphorylation of 20-kDa MLC increased rapidly to 51.2 +/- 3.1% within 15 s after stimulation and subsequently declined to 19.0 +/- 2.1% at 5 min. Vmax was maximal (0.14 Lo/s) 13 s after stimulation and declined before maximal active isometric stress. In colitis animals, the 20-kDa MLC phosphorylation (P less than 0.05) and the Vmax (P less than 0.01) were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanical alterations in sensitized canine saphenous vein

1990 ◽  
Vol 69 (1) ◽  
pp. 171-178 ◽  
Author(s):  
Z. Wang ◽  
C. Y. Seow ◽  
W. Kepron ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Saphenous Vein ◽  
Specific Antigen ◽  
Isometric Tension ◽  
Antigen Challenge ◽  
Pollen Extract ◽  
Shortening Velocity ◽  
Tension Development ◽  
Cycling Rate ◽  
Cross Bridge

Because it is likely that antigen sensitization is not restricted to airway smooth muscle but probably involves all tissues in the animal, we decided to test the hypothesis that saphenous vein from pollen extract-sensitized dogs is sensitized and is, in addition, mechanically altered. To this end, we studied responses to specific antigen challenge and length-tension and force-velocity relationships in sensitized (SSV) and control saphenous veins (CSV). The antigen challenge revealed that the venous smooth muscle was strongly sensitized and developed a Schultz-Dale response, the two main mediators of which were histamine and norepinephrine. Length-tension relationship studies showed that whereas there is no difference in maximum isometric tension development between SSV and CSV [93.95 +/- 7.34 and 87.86 +/- 4.00 (SE) mN/mm2, respectively], SSV exhibited a significantly greater maximum isotonic shortening capacity of 0.613 +/- 0.009 optional length (lo) vs. 0.578 +/- 0.012 lo for CSV. Unloaded shortening velocity (Vo), which reflects the cross-bridge cycling rate, was determined at different times after the onset of electrical stimulation. Maximum Vo was attained early (5 s) in the contraction; a 15% decline in Vo was observed at the plateau of the contraction (15 s). At 5 s, Vo of SSV (0.316 +/- 0.019 lo/s) was significantly higher than that of CSV (0.269 +/- 0.018 lo/s), although Vos were same at 15 (0.249 +/- 0.021 lo/s for SSV and 0.237 +/- 0.019 lo/s for CSV). The increase in shortening likely results from th e increase in the early cross-bridge cycling rate because our studies show that the bulk of shortening occurs in the first 5 s.(ABSTRACT TRUNCATED AT 250 WORDS)

Force–velocity relationships in hypertensive arterial smooth muscle

1985 ◽  
Vol 63 (6) ◽  
pp. 669-674 ◽  
Author(s):  
C. S. Packer ◽  
N. L. Stephens
Keyword(s):  
Smooth Muscle ◽  
Spontaneously Hypertensive Rat ◽  
Peripheral Resistance ◽  
Muscle Length ◽  
Maximum Velocity ◽  
Isometric Tension ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Force Velocity ◽  
Wistar Kyoto

Increased total peripheral resistance is the cardinal haemodynamic disorder in essential hypertension. This could be secondary to alterations in the mechanical properties of vascular smooth muscle. Adequate study has not been made of the force–velocity (F–V) relationship in hypertensive arterial smooth muscle. Increased shortening in arterial smooth muscle would result in greater narrowing of arteries. The objectives of this investigation were to see if there is (i) increased shortening or increased maximum change in muscle length (ΔLmax where L stands for muscle length), (ii) an increased maximum velocity of shortening (Vmax) measured in lo per second where lo is the optimal muscle length for tension development, and (iii) a difference in maximum isometric tension (Po) developed in spontaneously hypertensive rat (SHR; N = 6) compared with normotensive Wistar Kyoto rat (WKY; N = 5) caudal artery strips. An electromagnetic muscle lever was employed in recording force–velocity data. Analysis of these data revealed the following: (a) the SHR mean Po of 6.21 ± 1.01 N/cm2 was not different from the mean WKY Po of 6.97 ± 1.64 N/cm2 (p > 0.05); (b) the SHR preparations showed greater shortening for all loads imposed; (c) the SHR Vmax of 0.016 lo/s was greater than the WKY Vmax of 0.013 lo/s (p < 0.05). This study provides evidence that while hypertensive arterial smooth muscle is not able to produce more force than normotensive arterial smooth muscle, it is capable of faster and greater shortening. The latter could result in increased narrowing of hypertensive arteries and increased blood pressure.

scholarly journals Rate-limiting steps in the tension development of freeze-glycerinated vascular smooth muscle.

1982 ◽  
Vol 79 (3) ◽  
pp. 437-452 ◽  
Author(s):  
J W Peterson
Keyword(s):  
Smooth Muscle ◽  
Protein Content ◽  
Time Course ◽  
Isometric Tension ◽  
Native Protein ◽  
Arterial Smooth Muscle ◽  
Tension Development ◽  
Rate Limiting Step ◽  
Limiting Step ◽  
Rate Limiting

A method for "skinning" arterial smooth muscle is presented which yields isometric tension development typically 60-80% of maximum physiological tension in the presence of micromolar Ca++ and millimolar Mg-ATP, while retaining essentially the native protein content. Using the methods of "CA jump," the time-course of Ca++-activated tension development in the skinned artery can be made identical to, but not faster than, the rate of tension development in the intact artery. In the skinned artery, activating free [Ca++] does not substantially alter the rate at which tension development approaches the final steady tension attained at that free [Ca++] (less than 25% decline in speed for a 10-fold decrease in [Ca++]). These observations are taken to mean that the rate-limiting step in isometric tension development in arterial smooth muscle does not depend directly on Ca++.

Role of cADPR in sodium nitroprusside-induced opossum esophageal longitudinal smooth muscle contraction

2007 ◽  
Vol 292 (6) ◽  
pp. G1543-G1548 ◽  
Author(s):  
R. K. Campbell ◽  
R. W. Wells ◽  
D. V. Miller ◽  
W. G. Paterson
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Sodium Nitroprusside ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Circular Smooth Muscle ◽  
Longitudinal Smooth Muscle ◽  
Second Messenger Pathways ◽  
Opposing Effects

Nitric oxide (NO) relaxes most smooth muscle, including the circular smooth muscle (CSM) of the esophagus, whereas in the adjacent longitudinal smooth muscle (LSM), it causes contraction. The second messenger pathways responsible for this NO-induced LSM contraction are unclear, given that these opposing effects of NO are both cGMP dependent. In intestinal LSM, but not CSM, cADP ribose (cADPR)-dependent pathways participate in Ca2+ mobilization and muscle contraction; whether similar differences exist in the esophagus is unknown. The purpose of this study was to determine whether cADPR plays a role in the NO-mediated contraction of opossum esophageal LSM. Standard isometric tension recordings were performed using both LSM and CSM strips from opossum distal esophagus that were hung in 10-ml tissue baths perfused with oxygenated Krebs solution. cADPR produced concentration-dependent contraction of LSM strips with an EC50 of 1 nM and peak contraction of 57 ± 18% of the 60 mM KCl-induced contraction. cADPR had no effect on CSM strips at concentrations up to 10−6 M. The EC50 of cADPR caused contraction (18 ± 2% from initial resting length) of isolated LSM cells. Sodium nitroprusside (SNP; 300 μM) induced contraction of LSM strips that averaged 67 ± 5% of the KCl response. cADPR antagonists 8-bromo-cADPR and 8-amino-cADPR, as well as ryanodine receptor antagonists ryanodine and tetracaine, significantly inhibited the SNP-induced contraction. In conclusion, in the opossum esophagus, 1) cADPR induces contraction of LSM, but not CSM, and 2) NO-induced contraction of LSM appears to involve a cADPR-dependent pathway.

Sign in / Sign up

Export Citation Format

Share Document