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The impact of acute volume imbalances on gastric volume (GV) was studied in anesthetized rats (250-300 g). After cervical and femoral vessel cannulation, a balloon catheter was positioned in the proximal stomach. The opposite end of the catheter was connected to a barostat with an electronic sensor coupled to a plethysmometer. A standard ionic solution was used to fill the balloon (about 3.0 ml) and the communicating vessel system, and to raise the reservoir liquid level 4 cm above the animals' xiphoid appendix. Due to constant barostat pressure, GV values were considered to represent the gastric compliance index. All animals were monitored for 90 min. After a basal interval, they were randomly assigned to normovolemic, hypervolemic, hypovolemic or restored protocols. Data were compared by ANOVA followed by Bonferroni's test. Mean arterial pressure (MAP), central venous pressure (CVP) and GV values did not change in normovolemic animals (N = 5). Hypervolemic animals (N = 12) were transfused at 0.5 ml/min with a suspension of red blood cells in Ringer-lactate solution with albumin (12.5 ml/kg), which reduced GV values by 11.3% (P0.05). MAP and CVP values increased (P

The present study evaluates the effect of blood volume expansion on the gastrointestinal transit of a charchoal meal (2.5 ml of an aqueous suspension consisting of 5% charcoal and 5% gum arabic) in awake male Wistar rats (200-270 g). On the day before the experiments, the rats were anesthetized with ether, submitted to left jugular vein cannulation and fasted with water ad libitum until 2 h before the gastrointestinal transit measurement. Blood volume expansion by iv infusion of 1 ml/min Ringer bicarbonate in volumes of 3, 4 or 5% body weight delayed gastrointestinal transit at 10 min after test meal administration by 21.3-26.7% (P

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

Context: The understanding of pulmonary hypertension has been focused on binomial model for injuries and dysfunctions of endothelial and muscular vascular layer. However, recent studies have shown that the vascular adventitia and myofibroblast may act as biological processing center and critical regulator of vascular remodeling. Our aim is to investigate the role of myofibroblast activation in adventitial pulmonary remodeling. Design: Wister male rats were sacrificed 21 days after treatment with monocrotaline (MCT; n = 5) compared to controls (CTR; n = 5). Right ventricular pressure; H&E and picrosirius red staining; immunohistochemistry for IL-17-related markers; and in situ immunofluorescence for SMA and collagen types I and V, electron microscopy, and fibronexus morphometry were performed. Results: The right ventricular pressure and right cardiac hypertrophy index were significantly higher in the MCT group than the CTR group (P < .05). By morphometry, adventitial thickness to Conclusions: SMA expression and fibronexus, an ultrastructural feature and gold standard for myofibroblast, indicate that myofibroblastic activation is turned on in adventitial pulmonary remodeling, which induces collagen V overexpression, an immunogenic collagen, in a Th-17-related environmental manner., A. T. Fabro (1); L. Perdona (1); A. L. Santos (1); A. A. Santos (1); H. R. Crunivel (1); J. R. Machado (1); R. A. Oliveira (2); A. P. P. [...]

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). Steady-state 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% body weight) significantly (P