Abstract

We determined the effect of acute extracellular fluid volume changes on saline flow through 4 gut segments (ileocolonic, ileal, ileocolonic sphincter and proximal colon), perfused at constant pressure in anesthetized dogs. Two different experimental protocols were used: hypervolemia (iv saline infusion, 0.9% NaCl, 20 ml/min, volume up to 5% body weight) and controlled hemorrhage (up to a 50% drop in mean arterial pressure). Mean ileocolonic flow (N = 6) was gradually and significantly decreased during the expansion (17.1%, P < 0.05) and expanded (44.9%, P < 0.05) periods while mean ileal flow (N = 7) was significantly decreased only during the expanded period (38%, P < 0.05). Mean colonic flow (N = 7) was decreased during expansion (12%, P < 0.05) but returned to control levels during the expanded period. Mean ileocolonic sphincter flow (N = 6) was not significantly modified. Mean ileocolonic flow (N = 10) was also decreased after hemorrhage (retracted period) by 17% (P < 0.05), but saline flow was not modified in the other separate circuits (N = 6, 5 and 4 for ileal, ileocolonic sphincter and colonic groups, respectively). The expansion effect was blocked by atropine (0.5 mg/kg, i.v.) both on the ileocolonic (N = 6) and ileal (N = 5) circuits. Acute extracellular fluid volume retraction and expansion increased the lower gastrointestinal resistances to saline flow. These effects, which could physiologically decrease the liquid volume being supplied to the colon, are possible mechanisms activated to acutely balance liquid volume deficit and excess.

Highlights

  • The luminal fluid in the gastrointestinal (GI) tract is in dynamic equilibrium with the extracellular fluid (ECF) volume [1]

  • Mean arterial pressure (MAP) was not significantly modified while Central venous pressure (CVP) levels increased at the beginning of expansion (1% body weight), remaining stable at least during the first 20 min of the expanded period (P

  • We have previously demonstrated that acute volume expansion increases gastroduodenal resistance to saline flow in rats and dogs, while hypovolemia due to hemorrhage decreases it [4,5]

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Summary

Introduction

The luminal fluid in the gastrointestinal (GI) tract is in dynamic equilibrium with the extracellular fluid (ECF) volume [1]. ECF volume expansion by intravenous infusion of saline decreases both gastric and jejunal compliance while hemorrhage increases it [6,7] These observations suggest that the GI tract, at least in its upper portions, behaves like a regulatory liquid reservoir capable of adjusting its volumetric, absorptive and secretory capacities to cope with organic needs, i.e., accommodating and absorbing more liquid volume after hemorrhage and, contrarily, becoming less receptive to liquid volume distension and less absorptive after acute hypervolemia. This evidence is supported by the functional interaction between motor changes and absorption; increased tone reduces absorption while decreased tone stimulates salt and water absorption [8]

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