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 decre ases saline flow through the gastroduodenal (GD) segment in anesthetiz ed rats (Xavier-Neto J, dos Santos AA & Rola FH (1990) Gut, 31: 1006-1 010). 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 circ uits: GD, gastric, pyloric and duodenal. These circuits were perfused under barostatically controlled pressure (4 cmH(2)O). Steady-state cha nges in flow were taken to reflect modifications in circuit resistance s during three periods of time: normovolemic control (20 min), expansi on (10-15 min), and expanded (30 min). Perfusion flow rates did not ch ange in normovolemic control animals over a period of 60 min. BV expan sion (Ringer bicarbonate, 1 ml/min up to 5% 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 (1 0.8 +/- 0.4 to 9.0 +/- 0.6 ml/min) circuits, but not in the gastric ci rcuit (11.9 +/- 0.4 to 10.4 +/- 0.6 ml/min). Prazosin (1 mg/kg) and yo himbine (3 mg/kg) prevented the expansion effect on the duodenal but n ot on the pyloric circuit. Bilateral cervical vagotomy prevented the e xpansion effect on the pylorus during the expansion but not during the expanded period and had no effect on the duodenum. Atropine (0.5 mg/k g), hexamethonium (10 mg/kg) and propranolol (2 mg/kg) were ineffectiv e on both circuits. These results indicate that 1) EV expansion increa ses the GD resistance to liquid flow, 2) pylorus and duodenum are impo rtant sites of resistance, and 3) yohimbine and prazosin prevented the increase in duodenal resistance and vagotomy prevented it partially i n the pylorus.