Acute experimental colitis decreases colonic circular smooth muscle contractility in rats

Abstract

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.

The endogenous cannabinoid system protects against colonic inflammation

“…Contractility of smooth muscle to cholinergic or tachykinergic stimuli is increased in the early stages and decreased in the later stages of inflammation (38,39), and contractility following electrical neuronal stimulation in the inflamed gut is increased (40). The electrophysiological changes in the distal colon, as used in this study, show increased smooth muscular excitability, leading to the occurrence of spontaneous spiking activity.…”

Alterations of Colonic Contractility in an Interleukin-10 Knockout Mouse Model of Inflammatory Bowel Disease

“…14 Although many studies have been conducted to investigate digestive tract motility using various animal models, [15][16][17][18][19][20][21][22][23][24] few studies have been conducted using IL-10 −/− mice. Accordingly, this study was conducted to investigate changes in colonic contractility in IL-10 −/− mice and the possible mechanisms of these changes.…”

Protective and Therapeutic Effects of Polygonum cognatum Meissn Aqueous Extract in Experimental Colitis

“…Ulcerative colitis (UC) is a chronic inflammatory bowel disease that causes ongoing inflammation and ulcers in the innermost layers of the colon and rectum (1). Although the etiology and pathophysiology of UC is not known with certainty, inflammatory mediators, such as cytokines and eicosanoids, and excessive production of reactive oxygen species (ROS) by the inflamed mucosa have been proposed to contribute significantly to the development of tissue injury (2).…”

“…An acetic acid-induced colitis model is one of them. This model causes a mild acute mucosal inflammation in the distal colon of rats (1). The acetic acidinduced colitis model is an experimental model that has shown morphological similarities to human UC (3).…”