A videomicroscopic method was used to quantitatively analyze villous motility in the dog small intestine. The frequency and duration of villous contractions (retractions) were measured in the duodenum, midjejunum, and distal ileum under controlled conditions. A pronounced gradient of villous motility was evident along the bowel. The duodenum exhibited the highest frequency (7.3 +/- 0.1/min) and longest duration (2.6 +/- 0.1 s) of contraction; the jejunum exhibited an intermediate frequency and duration of contraction (4.0 +/- 0.1/min, 2.1 +/- 0.1 s), and the lowest values were measured in the ileum (2.0 +/- 0.1/min and 1.8 +/- 0.1 s). In contrast to the retraction movements, the frequency of pendular villous movements (whipping, swaying movements without shortening) was highest in the jejunum and lowest in the duodenum. The frequency and duration of villous contractions (retractions) remained relatively constant over a 2-h observation period. Reducing mucosal surface temperature from 38 to 30 degrees C caused the frequency of contraction to fall by 33% and the duration to increase by 106%. Varying the suffusate pH within the physiological range of 5.0-7.4 produced no significant effects on jejunal villous motility. Suffusion with glucose (140 and 280 mM) failed to alter villous motility. However, amino acid (15 and 30 mM) and fatty acid (10 mM) solutions significantly increased contraction frequency by 30-50% and 90%, respectively. The videomicroscopic method provides useful quantitative information, which should extend current knowledge regarding the regulation and physiological importance of villous motility.
Collateral blood flow and the pressures and resistances determining that flow were measured between two adjacent segments of canine jejunum following acute occlusion of the arterial branch perfusing one of the segments (the "recipient" segment). Collateral flow was approximately 55% of control flow in the recipient segment. This flow was provided by an equal increment in arterial flow to the nonischemic ("donor") segment, such that pressures, resistances, and flows in the donor segment were not affected. Virtually all of the total collateral flow was derived from precapillary channels and was therefore available to the capillary bed of the recipient segment. Collateral flow was adequate to maintain the recipient segment in a nonischemic state, as indicated by the absence of a reactive hyperemia following release of the arterial occlusion. Selective occlusions of intramural or extramural collateral channels indicate that about two-thirds of the total collateral flow is derived from the extramural (marginal) vessels, while the remainder is supplied by intramural collaterals. For the most part collateral flow between adjacent segments is determined simply by the pressure gradient between connecting collateral channels.
The intramural distribution of blood flow in the gastrointestinal tract was measured in shamoperated control and portal vein-stenosed rats. Total organ blood flow, measured via the radioactive microsphere technique, was elevated in the esophagus (66%), stomach (102%), duodenum (42%), jejunum (52%), ileum (54%), and colon (79%) of portal-hypertensive rats. Histological evaluation of carbonized nonradioactive 15-microns microspheres allowed for fractionation of blood flow within the wall (mucosa, submucosa, and muscularis externa) of each organ. The microsphere distribution pattern indicates that intramural blood flow distribution in all organs was not dramatically affected by chronic portal hypertension. These findings further define the characteristics of the factors responsible for the gastrointestinal hyperemia produced by chronic portal hypertension.
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