Distension In Dogs Research Articles

Reliability and interobserver variability of a grading system of ventricular distension in dogs

Reliability and interobserver variability of a grading system of ventricular distension in dogs

Electrical neuromodulation at acupoint ST36 normalizes impaired colonic motility induced by rectal distension in dogs.

Electroacupuncture (EA) has been shown to improve impaired gastric motility and slow waves in both humans and animals. However, its effects on colonic motility have rarely been investigated. The aim of this study was to investigate the effects and underlying mechanisms of EA on impaired colonic motility induced by rectal distension (RD)in dogs. Colon contractions and transit were measured in various sessions with and without EA in hound dogs chronically placed with a colonic cannula. Colonic contractile activity was assessed by motility index (MI). Autonomic functions were determined by the spectral analysis of the heart rate variability derived from the electrocardiogram. It was found 1) RD suppressed colonic motility by 40.5% (10.8 ± 0.9 with RD vs. 6.4 ± 0.8 at baseline, P < 0.002). EA at ST36 normalized colonic contractions suppressed by RD (12.9 ± 2.8, P < 0.002 vs. RD and P = 0.1 vs. control). 2) Administration of atropine blocked the ameliorating effect of EA on colon motility. 3) RD also delayed colonic transit (65.0 ± 2.0% with RD vs. 86.0 ± 1.9% without RD, P < 0.001) that was restored with EA (84.0 ± 1.9%, P = 0.178 vs. control). 4) EA increased vagal activity suppressed by RD (0.37 ± 0.07 with RD + EA vs. 0.09 ± 0.03 with RD without EA, P < 0.001). In conclusion, RD inhibits colonic contractions and delays colonic transit in dogs; EA at ST36 restores the RD-induced impairment in both colonic contraction and transit by enhancing vagal activity and mediated via the cholinergic pathway.

The participation of the nitrergic pathway in increased rate of transitory relaxation of lower esophageal sphincter induced by rectal distension in dogs.

The rectal distension in dogs increases the rate of transitory lower esophageal sphincter relaxation considered the main factor causing gastroesophageal reflux. The aim of this study was evaluate the participation of the nitrergic pathway in the increased transitory lower esophageal sphincter relaxation rate induced by rectal distension in anesthetized dogs. Male mongrel dogs (n = 21), weighing 10-15 kg, were fasted for 12 hours, with water ad libitum. Thereafter, they were anesthetized (ketamine 10 mg.Kg-1 + xylazine 20 mg.Kg-1), so as to carry out the esophageal motility evaluation protocol during 120 min. After a 30-minute basal period, the animals were randomly intravenous treated whith: saline solution 0.15M (1ml.Kg-1), L-NAME (3 mg.Kg-1), L-NAME (3 mg.Kg-1) + L-Arginine (200 mg.Kg-1), glibenclamide (1 mg.Kg-1) or methylene blue (3 mg.Kg-1). Forty-five min after these pre-treatments, the rectum was distended (rectal distension, 5 mL.Kg-1) or not (control) with a latex balloon, with changes in the esophageal motility recorded over 45 min. Data were analyzed using ANOVA followed by Student Newman-Keuls test. In comparison to the respective control group, rectal distension induces an increase in transitory lower esophageal sphincter relaxation. Pre-treatment with L-NAME or methylene blue prevents (P<0.05) this phenomenon, which is reversible by L-Arginine plus L-NAME. However, pretreating with glibenclamide failed to abolish this process. Therefore, these experiments suggested, that rectal distension increases transitory lower esophageal sphincter relaxation in dogs via through nitrergic pathways.

Electroacupuncture improves impaired gastric motility and slow waves induced by rectal distension in dogs

Rectal distension (RD) is known to induce upper gastrointestinal (GI) symptoms. The aim of this study was to investigate the effects and underlying mechanisms of RD on gastric slow waves (GSW) and motor activity and furthermore to investigate the effects and mechanisms of electroacupuncture (EA) on GSW and motor activity. Eight female hound dogs chronically implanted with gastric serosal electrodes and a gastric fistula were studied in six separate sessions. Antral motility, GSW, heart rate variability, and rectal pressure were evaluated for the above purposes. 1) RD at a volume of 120 ml suppressed antral motility significantly. Guanethidine blocked the inhibitory effect of RD. EA at ST36 was able to restore the suppressed antral contractions induced by RD (16.6+/-1.7 vs. 8.0+/-1.4, P<0.001). Naloxone partially blocked the effect of EA on antral contractions. 2) RD reduced the percentage of normal GSW from 98.8+/-0.8% at baseline to 76.1+/-8.6% (P<0.05) that was increased to 91.8+/-3.0% with EA. The effects of EA on the GSW were nullified by the presence of naloxone. 3) EA did not show any significant effect on rectal pressure, suggesting that the ameliorating effects of EA on RD-induced impaired gastric motility were not due to a decrease in rectal pressure. 4) EA increased the vagal activity suppressed by RD. In conclusion, RD inhibits postprandial gastric motility and impairs GSW in dogs, and the inhibitory effects are mediated via the adrenergic pathways. EA at ST36 is able to restore the RD-induced impaired GSW and motor activities, possibly by enhancing vagal activity, and is partially mediated via the opioid pathway. EA may have therapeutic potential for functional gastrointestinal disorders.

Intestinal electrical stimulation improves delayed gastric emptying and vomiting induced by duodenal distension in dogs

The aim of this study was to investigate the effects of short-pulse intestinal electrical stimulation (IES) on duodenal distention-induced delayed gastric emptying and vomiting in dogs and its possible mechanisms. The study was performed in 12 dogs with jejunal electrodes and a duodenal cannula in three separate experiments to investigate the effects of IES on duodenal distension (DD)-induced delayed gastric emptying and discomfort signs, vagal efferent activity, and jejunal tone. We found that: (i) IES significantly accelerated gastric emptying of liquid delayed by distension (18.05 +/- 4.06%vs. 7.18 +/- 1.99%, P = 0.036 at 60 min). (ii) IES significantly reduced vomiting and discomfort/pain induced by distension. The average signs score was 15.33 +/- 1.37 during distension which decreased to 6.50 +/- 0.91 (P = 0.0002) with IES. (iii) IES did not change vagal afferent activity, which was assessed by the spectral analysis of the heart rate variability. (iv) IES decreased jejunal tone. In conclusion, IES with parameters commonly used in gastric electrical stimulation for nausea and vomiting associated with gastroparesis improves DD-induced delayed gastric emptying and prevents DD-induced vomiting and discomfort signs. Further studies are warranted to investigate the therapeutic potential of IES for gastrointestinal symptoms associated with disturbances in motility and sensory function in small intestine.

Impairment of gastric and jejunal myoelectrical activity during rectal distension in dogs.

It is known that distension of the rectum induces gastric hypomotility and delays gastric emptying. Its effect on gastrointestinal myoelectrical activity has not been well studied, however. The aim of this study was to investigate the effects of rectal distension on gastrointestinal myoelectrical activity in dogs. Six hound dogs implanted with electrodes on the serosa of the stomach and proximal jejunum were studied. The protocol consisted of a 30-min baseline recording and another 30-min recording during rectal distension. Gastric myoelectrical activity was severely impaired by rectal distension. The dominant power was significantly decreased from -2.79 +/- 0.52 dB at baseline to -4.84 +/- 1.26 dB during distension (P < 0.05). The percentage of normal 4-6 cycles per minute gastric slow waves was reduced from 95.08 +/- 1.11% to 83.63 +/- 4.00% (P < 0.02), and the percentage of tachygastria was increased during distension (0.33 +/- 0.19% vs 6.03 +/- 1.27%, P < 0.02). The instability coefficient of the dominant frequency was significantly increased (0.134 +/- 0.012 vs 0.326 +/- 0.074, P < 0.05). The percentage of slow wave coupling was reduced from 93.99 +/- 0.76% to 73.43 +/- 2.07% (P < 0.00003). In the small bowel, only the instability coefficient of dominant frequency showed a significant increase during distension. Other parameters were not affected by rectal distension. We conclude that rectal distension severely impairs gastric myoelectrical activity. The induced gastric dysrhythmia and reduced slow wave amplitude and coupling may be the underlying pathophysiology of gastric hypomotility and delayed gastric emptying observed during rectal distension.

Central modulation of rectal distension-induced blood pressure changes by alosetron, a 5-HT3 receptor antagonist.

Irritable bowel syndrome (IBS) represents one of the most common gastrointestinal-related diagnoses. Although the precise etiologic basis of IBS is not known, a common presenting symptom is abdominal pain or discomfort that is thought to develop, at least in part, from a heightened awareness of visceral nociceptive input. Agents capable of reducing this heightened visceral nociception would, therefore, have utility in the treatment of IBS. In this study we evaluated the effects of intravenous and intracerebroventricular administration of a 5-HT3 receptor antagonist, alosetron, on blood pressure changes associated with rectal distension in anesthetized and awake dogs. This vasoactive reflex serves as a model for visceral nociception. For intracerebroventricular studies, the cerebroventricular guides were placed over the lateral ventricle. In anesthetized studies, blood pressure was measured by femoral artery cannulation. In awake studies, blood pressure was monitored by noninvasive measurement. A rectal balloon was placed in the rectum of each dog and maintained throughout the experiments. Each dose of alosetron was given to the dogs as an intravenous or intracerebroventricular bolus, and every 30 min the rectal balloon was inflated and blood pressure responses observed. In both anesthetized and awake dogs alosetron produced a significant inhibition of the vasoactive reflex. In particular, alosetron showed high potency when administered intracerebroventricularly. Alosetron, administered either centrally or peripherally, appears to modulate the visceral nociceptive effect of rectal distension in dogs.

Renal effects of left atrial distension in dogs with chronic congestive heart failure

The renal response to left atrial balloon inflation in normal dogs was compared with that in dogs with chronic congestive heart failure (CHF). CHF was induced by the production of an aortocaval fistula below the level of the renal arteries. CHF dogs showed elevated left ventricular end-diastolic pressure, enlarged hearts, a depression of myocardial contractility, pulmonary edema, ascites, and peripheral edema. They also showed significant decreases in urine flow, creatinine clearance, para-aminohippurate clearance, sodium and potassium excretion, fractional sodium excretion, osmolar clearance, arterial blood pressure, and heart rate. Balloon distension of the left atrium evoked a significant increase in urine flow and free-water clearance in the normal group. The reflex nature of this response was indicated by its blockade after bilateral cervical vagotomy. In contrast, the CHF group did not exhibit significant changes in urine flow or free-water clearance during balloon inflation. Plasma antidiuretic hormone (ADH) was significantly elevated in the CHF group; however, balloon distension reduced plasma ADH in both groups of dogs. Plasma renin activity was significantly elevated in the CHF dogs and was not changed by balloon distension in either group of dogs. It is concluded that animals with high-output CHF do not exhibit the atrial-diuretic reflex in spite of their ability to reduce ADH levels by atrial distension.