Variations in gastric emptying of liquid elicited by acute blood volume changes in awake rats

We have observed that acute blood volume expansion increases the gastroduodenal resistance to the flow of liquid in anesthetized dogs, while retraction decreases it (Santos et al. (1991) Acta Physiologica Scandinavica, 143:261-269). This study evaluates the effect of blood volume expansion and retraction on the gastric emptying of liquid in awake rats using a modification of the technique of Scarpignato (1980) (Archives Internationales de Pharmacodynamie et de Therapie, 246:286-294). Male Wistar rats (180-220g( were fasted for 16 h with water ad libitum and 1.5 ml of the test meal (0.5 mg/ml phenol red solution in 5 percent glucose) was delivered to the stomach immediately after random submission to one of the following protocols: 1) normovolemic control (N=22), 2) expansion (N=72) by intravenous infusion (1 ml/min) of Ringer-bicarbonate solution, volumes of 1,2,3 or 5 percent body weight, or 3) retraction (N-22) by controlled bleeding (1.5 ml/100g). Gastric emptying of liquid was inhibited by 19-51.2 percent (P<0.05) after blood volume expansion (volumes of 1,2,3 or 5 percent body weight). Blood volume expansion produced a sustained increase in central venous pressure while mean arterial presure was transiently increased during expansion (P<0.05). Blood volume retraction increased gastric emptying by 28.5-49.9 percent (P<0.05) and decreased central venous pressure and mean arterial pressure (P<0.05). Infusion of the shed blood 10 min after bleeding reversed the effect of retraction on gastric emptying. These findings suggest that gastric emptying of liquid is subject to modulation by the blood volume.

Gastroduodenal resistance and neural mechanisms involved in saline flow decrease elicited by acute blood volume expansion in anesthetized rats

We have previously demonstrated that blood volume (BV) expansion decreases saline flow through the gastroduodenal (GD) segment in anesthetized rats (Xavier-Neto J, dos Santos AA & Rola FH (1990) Gut, 31: 1006-1010). The present study attempts to identify the site(s) of resistance and neural mechanisms involved in this phenomenon. Male Wistar rats (N = 97,200-300 g) were surgically manipulated to create four gut circuits: GD, gastric, pyloric and duodenal. These circuits were perfused under barostatically controlled pressure (4 cmH2O). Steadysate changes in flow were taken to reflect modifications in circuit resistances during three periods of time: normovolemic control (20 min), expansion (10-15 min), and expanded (30 min). Perfusion flow rates did not change in normovolemic control animals over a period of 60 min. BV expansion (Ringer bicarbonate, 1 ml/min up to 5 percent body weight) significantly (p<0.05) reduced perfusion flow in the GD (10.3 + 0.5 to 7.6 + 0.6 ml/min), pyloric (9.0 + 0.6 to 5.6 + 1.2 ml/min) and duodenal (10.8 + 0.4 to 9.0 + 0.6 ml/min) circuits, but not in the gastric circuit (11.9 + 0.4 to 10.4 + 0.6 ml/min). Prazosin (1 mg/kg) and yohimbine (3 mg/kg) prevented the expansion effect on the duodenal but not on the pyloric circuit. Bilateral cervical vagotomy prevented the expansion effect on the pylorus during the expansion but not during the expanded period and had no effect on the duodenum. Atropine (0.5 mg/kg), hexamethonium (10 mg/kg) and propranolol (2 mg/kg) were ineffective on both circuits. These results indicate that 1) BV expansion increases the GD resistance to liquid flow, 2) pylorus and duodenum are important sites of resistance, and 3) yohimbine and prazosin prevented the increase in duodenal resistance and vagotomy prevented it partially in the pylorus.

Acute extracellular fluid volume changes increase ileocolonic resistancce to saline flow in anesthetized dogs

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 per cent NaCl, 20 ml/min, volume up to 5 per cent body weight) and controlled hemorrhage (up to a 50 per cent drop in mean arterial pressure). Mean ileocolonic flow (N = 6) was gradually and significantly decreased during the expansion (17.1 per cent P<0.05) and expanded (44.9 per cent, P<0.05) periods while mean ileal flow (N = 7) was significantly decreased only during the expanded period (38 per cent, P<0.05). Mean colonic flow (N = 7) was decreased during expansion (12 per cent, P<0.05) but returned to control levels during the expanded period. Mean ileocolonic sphincter flow (N = 6) was not significantly modified. Mean ielocolonic flow (n = 10) was also decreased after hemorhage (retracted period) by 17 per cent (P<0.05), but saline flow was not modified in the other separate circuitis (N = 6,5 and 4 for ileal, ileocolonic sphincter and colonic groups, respectively). The expansion effect was blocked by atropine (0.5 mg/kg, iv) 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.