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F H Rola

Publications and source records attributed to F H Rola.

At least 19 recordsLinked to original sources
PubMed2001

Neural mechanisms involved in the delay of gastric emptying and gastrointestinal transit of liquid after thoracic spinal cord transection in awake rats.

Spinal cord transection (SCT) delays gastric emptying (GE), and intestinal and gastrointestinal (GI) transit of liquid in awake rats. This study evaluates the neural mechanisms involved in this phenomenon. Male Wistar rats (N = 147) were fasted for 16 h and had the left jugular vein cannulated followed by laminectomy or laminectomy + complete SCT between T4 and T5 vertebrae. The next day, a test meal (1.5 ml of a phenol red solution, 0.5 mg/ml in 5% glucose) was administered by gavage feeding and 10 min later cervical dislocation was performed. Dye recovery in the stomach, and proximal, mid and distal small intestine was determined by spectrophotometry. SCT inhibited GE and GI transit since it increased gastric recovery by 71.3% and decreased mid small intestine recovery by 100% (P < 0.05). Subdiaphragmatic vagotomy, celiac ganglionectomy + section of the splanchnic nerves, i.v. hexamethonium (20 mg/kg) or yohimbine (3 mg/kg) prevented the development of the SCT effect on GE and GI transit. Pretreatment with i.v. naloxone (2 mg/kg), L-NAME (3 mg/kg) or propranolol (2 mg/kg) was ineffective. Bilateral adrenalectomy or guanethidine (10 mg/kg) increased the magnitude of the GE inhibition, while i.v. prazosin (1 mg/kg) or atropine (0.5 mg/kg) decreased the magnitude but did not abolish the GE inhibition. In summary, the inhibition of GI motility observed 1 day after thoracic SCT in awake rats seems to involve vagal and possibly splanchnic pathways.

Animals↗
PubMed2001

Gastric emptying and gastrointestinal transit of liquid throughout the first month after thoracic spinal cord transection in awake rats.

Spinal cord transection (SCT) inhibits gastrointestinal motility in awake rats. We studied the gastric emptying (GE) and gastrointestinal transit of liquid throughout the first month after thoracic SCT. Male Wistar rats (N = 66) were submitted to laminectomy followed or not by complete SCT between T4 and T5 vertebrae. Phenol red recovery in the stomach, proximal, mid-and distal small intestine was determined 1, 7, 10, 15, and 30 days thereafter. Gastric recovery increased by 51.2 and 38.9% and mid-intestinal recovery decreased by 45.5 and 66.6% at one and seven days after SCT (P < 0.05). Proximal small intestine recovery increased by 45.9% 10 days after SCT but no inhibition of gastrointestinal motility was observed thereafter. Stool output significantly decreased in the first seven days after SCT (P < 0.05). In summary, gastrointestinal motility in awake rats is inhibited throughout the first 10 days after thoracic SCT but not thereafter.

Animals↗
PubMed1999

Complete cervical or thoracic spinal cord transections delay gastric emptying and gastrointestinal transit of liquid in awake rats.

STUDY DESIGN: To determine the changes on gastric emptying and gastrointestinal transit of liquid throughout the first week after spinal cord transection (SCT) in rats. METHODS: Male Wistar rats (n=121) were fasted for 16 h and a complete SCT or laminectomy was performed between C7 and T1 (cervical group) or between T4 and T5 (thoracic group). Dye recovery in the stomach, proximal, mid and distal small intestine was determined 30 min, 6 h, 1, 3 or 7 days after surgery. The test meal (1.5 ml of a phenol red solution, 0.5 mg/ml in 5% glucose) was intragastrically administered and the animals sacrificed by cervical dislocation 10 min later. RESULTS: Cervical SCT increased dye recovery in the stomach (P<0.05) by 70.1, 78.7, 34.2, 41.3 and 50.9% while it decreased recovery in the mid small intestine (P<0.05) by 87.1, 85.1, 74.8, 59.5 and 80.1%, respectively 30 min, 6 h, 1, 3 and 7 days after SCT. Thoracic SCT increased gastric recovery (P<0.05) by 43.5, 67.6, 51.2, 75.4 and 38. 9% while it decreased recovery in the mid small intestine (P<0.05) by 100, 100, 45.6, 100 and 66.6%, respectively 30 min, 6 h, 1, 3 and 7 days after SCT. A separate group was submitted to laminectomy+bilateral sciatic nerve transection (paraplegic sham). Gastric emptying and gastrointestinal transit were not inhibited in this group. CONCLUSION: In summary, gastric emptying and gastrointestinal transit of liquid are inhibited throughout the first week after high SCT in awake rats.

Animals↗
PubMed1999

Neural mechanisms involved in the delay of gastric emptying of liquid elicited by acute blood volume expansion in awake rats.

We have previously reported that acute blood volume expansion in awake rats delays the gastric emptying of a liquid meal, using the phenol red method. In this study we attempted to investigate the neural mechanisms involved in this phenomenon. Blood volume expansion, due to Ringer-bicarbonate infusion up to a volume equivalent to 5% of body weight, decreased the gastric emptying of a liquid meal by half (38.2 +/- 1.8 vs 18.7 +/- 3.2%, P < 0.05). The blood volume expansion effect on gastric emptying of liquid was prevented by separate pretreatments, consisting of subdiaphragmatic vagotomy or i.v. injection of hexamethonium (20 mg kg-1) or yohimbine (3 mg kg-1). Intravenous injection of atropine (0.5 mg kg-1), guanethidine (10 mg kg-1), L-NAME (3 mg kg-1), prazosin (1 mg kg-1) or propranolol (2 mg kg-1) did not prevent the blood volume expansion effect on gastric emptying. Bilateral adrenalectomy or coeliac ganglionectomy were also ineffective. The results indicate that blood volume expansion decreases gastric emptying of liquid through vagal-dependent pathways, sensitive to hexamethonium and yohimbine. Evidence for the participation of the peripheral sympathetic nervous system was not found.

Animals↗
PubMed1998

Effect of pyloroplasty and fundectomy on the delay of gastric emptying and gastrointestinal transit of liquid elicited by acute blood volume expansion in awake rats.

We evaluated the effects of fundectomy and pyloroplasty on the delay of gastric emptying (GE) and gastrointestinal (GI) transit of liquid due to blood volume (BV) expansion in awake rats. Male Wistar rats (N = 76, 180-250 g) were first submitted to fundectomy (N = 26), Heinecke-Mikulicz pyloroplasty (N = 25) or SHAM laparotomy (N = 25). After 6 days, the left external jugular vein was cannulated and the animals were fasted for 24 h with water ad libitum. The test meal was administered intragastrically (1.5 ml of a phenol red solution, 0.5 mg/ml in 5% glucose) to normovolemic control animals and to animals submitted to BV expansion (Ringer-bicarbonate, i.v. infusion, 1 ml/min, volume up to 5% body weight). BV expansion decreased GE and GI transit rates in SHAM laparotomized animals by 52 and 35.9% (P < 0.05). Fundectomy increased GE and GI transit rates by 61.1 and 67.7% (P < 0.05) and prevented the effect of expansion on GE but not on GI transit (13.9% reduction, P < 0.05). Pyloroplasty also increased GE and GI transit rates by 33.9 and 44.8% (P < 0.05) but did not prevent the effect of expansion on GE or GI transit (50.7 and 21.1% reduction, P < 0.05). Subdiaphragmatic vagotomy blocked the effect of expansion on GE and GI transit in both SHAM laparotomized animals and animals submitted to pyloroplasty. In conclusion 1) the proximal stomach is involved in the GE delay due to BV expansion but is not essential for the establishment of a delay in GI transit, which suggests the activation of intestinal resistances, 2) pyloric modulation was not apparent, and 3) vagal pathways are involved.

Animals↗
PubMed1998

Acute blood volume expansion delays the gastrointestinal transit of a charcoal meal in awake rats.

The present study evaluates the effect of blood volume expansion on the gastrointestinal transit of a charcoal 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 i.v. 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 < 0.05), but no effect was observed after 1 or 2% body weight expansion. The effect of blood volume expansion (up to 5% body weight) on gastrointestinal transit lasted for at least 60 min (P < 0.05). Mean arterial pressure increased transiently and central venous pressure increased and hematocrit decreased (P < 0.05). Subdiaphragmatic vagotomy and yohimbine (3 mg/kg) prevented the delay caused by expansion on gastrointestinal transit, while atropine (0.5 mg/kg), L-NAME (2 mg/kg), hexamethonium (10 mg/kg), prazosin (1 mg/kg) or propranolol (2 mg/kg) were ineffective. These data show that blood volume expansion delays the gastrointestinal transit of a charcoal meal and that vagal and yohimbine-sensitive pathways appear to be involved in this phenomenon. The delay in gastrointestinal transit observed here, taken together with the modifications of gastrointestinal permeability to salt and water reported by others, may be part of the mechanisms involved in liquid excess management.

Animals↗
PubMed1998

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 (180-200 g) 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% 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% body weight, or 3) retraction (N = 22) by controlled bleeding (1.5 ml/100 g). Gastric emptying of liquid was inhibited by 19-51.2% (P < 0.05) after blood volume expansion (volumes of 1, 2, 3 or 5% body weight). Blood volume expansion produced a sustained increase in central venous pressure while mean arterial pressure was transiently increased during expansion (P < 0.05). Blood volume retraction increased gastric emptying by 28.5-49.9% (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.

Animals↗
PubMed1998

Decreased gastric emptying and gastrointestinal and intestinal transits of liquid after complete spinal cord transection in awake rats.

We studied the effect of complete spinal cord transection (SCT) on gastric emptying (GE) and on gastrointestinal (GI) and intestinal transits of liquid in awake rats using the phenol red method. Male Wistar rats (N = 65) weighing 180-200 g were fasted for 24 h and complete SCT was performed between C7 and T1 vertebrae after a careful midline dorsal incision. GE and GI and intestinal transits were measured 15 min, 6 h or 24 h after recovery from anesthesia. A test meal (0.5 mg/ml phenol red in 5% glucose solution) was administered intragastrically (1.5 ml) and the animals were sacrificed by an i.v. thiopental overdose 10 min later to evaluate GE and GI transit. For intestinal transit measurements, 1 ml of the test meal was administered into the proximal duodenum through a cannula inserted into a gastric fistula. GE was inhibited (P < 0.05) by 34.3, 23.4 and 22.7%, respectively, at 15 min, 6 h and 24 h after SCT. GI transit was inhibited (P < 0.05) by 42.5, 19.8 and 18.4%, respectively, at 15 min, 6 h and 24 h after SCT. Intestinal transit was also inhibited (P < 0.05) by 48.8, 47.2 and 40.1%, respectively, at 15 min, 6 h and 24 h after SCT. Mean arterial pressure was significantly decreased (P < 0.05) by 48.5, 46.8 and 41.5%, respectively, at 15 min, 6 h and 24 h after SCT. In summary, our report describes a decreased GE and GI and intestinal transits in awake rats within the first 24 h after high SCT.

Animals↗
PubMed1997

Acute extracellular fluid volume changes increase ileocolonic resistance 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% 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.

Anesthesia↗
PubMed1997

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). 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 < 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.

Animals↗
PubMed1991

Acute volaemic changes modify the gastroduodenal resistance to the flow of saline in anaesthetized dogs.

The effect of acute and sequential volaemic changes on the gastroduodenal flow of saline was assessed in 23 anaesthetized dogs following two different experimental protocols. Hypervolaemia, by i.v. infusion of saline, induced a gradual decrease on gastroduodenal flow which amounted to 76% below control values (P less than 0.001) when volaemic expansion attained 5% of body weight. This effect was volume dependent (17% increase on gastroduodenal flow per volume of infused saline equivalent to 0.5% of body weight, P less than 0.001), lasted for at least 90 minutes after infusion was completed and was also obtained by expanding previously bled animals. Hypovolaemia due to bleeding was followed by an increase on gastroduodenal flow of about 88% above control values (P less than 0.05) when haemorrhage was equal to 3% of body weight. This effect was also volume dependent (23% increase on gastroduodenal flow per volume of blood shed equivalent to a 0.5% of body weight, P less than 0.01) and was reversed after blood volume was restored. These modifications in the resistance of the gastroduodenal segment to the flow of liquid due to acute volaemic changes suggest that the extracellular fluid volume modulates the contractile activity of the gastroduodenal portion of the gut possibly to set a gastroduodenal handling of liquid adequate to cope with volaemic imbalances.

Animals↗
PubMed1990

Acute hypervolaemia increases gastroduodenal resistance to the flow of liquid in the rat.

The effect of volume expansion of extracellular fluid on gastroduodenal resistance to the flow of isotonic saline was assessed in three groups of rats using intravenous infusions of isotonic, isotonic-isoncotic, and isotonic-isoncotic-isohaemic solutions. The gastroduodenal segment of 29 male Wistar rats was barostatically perfused at a constant pressure gradient of 4 cm H2O and changes in flow (ml/minute) were taken as a reflection of changes in gastroduodenal resistance. Isotonic expansion led to a 33% drop in gastroduodenal flow compared with the normovolaemic period in the same animals (p less than 0.01). Extracellular fluid expansion with isotonic-isoncotic and isotonic-isoncotic-isohaemic solutions was associated with reductions in gastroduodenal flow of 29% (p less than 0.05) and 31% (p less than 0.01) respectively. The increase in gastroduodenal resistance is due to hypervolaemia per se and not to haemodilution, decreases in plasma oncotic pressure, or electrolyte imbalance. The effect of hypervolaemia on gastroduodenal resistance, which was reversed by small haemorrhages (0.5-1.0 ml per 100 g body weight), may be due to changes in tonus or phasic motor activity, or both, and may be part of the homeostatic processes that help the organism minimise liquid volume excess.

Animals↗
PubMed1989

Effects of acute volemic changes on jejunal compliance in dogs.

1. Jejunal compliance (delta V/delta P) was calculated from the intraluminal pressures measured in anesthetized dogs in an in situ upper jejunal pouch (40-50-ml capacity) with intraluminal volumes of 10, 20, 30, 40 and 50 ml of isotonic saline. 2. Measurements were made in the same animal during and after acute and sequential alterations of the extracellular fluid (ECF) volume obtained by: a) acute intravenous (iv) infusion of isotonic saline, b) acute hemorrhage, and c) iv reinfusion of isotonic saline. 3. Expansion of the ECF volume caused a significant, reversible downward shift of the compliance curve, i.e., the jejunal pouch became less receptive to liquid distension. After saline infusion was discontinued, compliance gradually returned to control levels. 4. Acute loss of a substantial volume of blood after ECF expansion gradually shifted the compliance curve upwards to levels significantly different from control, indicating that retraction of the ECF volume made the jejunal pouch more receptive to liquid distension. 5. Reinfusion of bled animals with saline rather than autologous blood also induced a significant decrease in jejunal compliance to below control levels. 6. The jejunal pouch behaved as a suitable preparation for monitoring in vivo modifications of compliance induced by acute changes in ECF volume, especially when it was nearly "half-full" (i.e., filled with 20 ml), suggesting a critical relationship between the volume capacity of the pouch and its fluid content. 7. These results suggest that the modulation of the jejunal portion of small intestine compliance is involved in the processes that balance the ECF volume during acute life-threatening situations such as accidental hyperhydration or hemorrhage.

Adaptation, Physiological↗
PubMed1988

Acute changes in extracellular fluid volume modify the antroduodenal flow of saline in dogs: a possible physiological role.

The antroduodenal (AD) flow of saline was measured in anesthetized dogs following two different protocols of acute changes in extracellular fluid (ECF) volume. ECF expansion by iv infusion of saline before or after hemorrhage decreased the AD flow; conversely, hemorrhage before or after expansion increased flow. These alternating modifications in the AD flow are independent of the sequence of volemic changes and may constitute part of the homeostatic responses of the gut to confront life-threatening situations such as accidental hyperhydration or hemorrhage.

Animals↗
PubMed1972

Adenosine triphosphatase associated with adenosine triphosphate-dependent deoxyribonuclease (recB-recC enzyme-E. coli-ATP to phosphodiester hydrolysis ratio-DNA-dependent ATPase activity).

An ATPase activity that is completely dependent on DNA is associated with the ATP-dependent DNase (recB-recC enzyme) purified from Escherichia coli. There is a strong correlation between the ATPase and the DNase activities under various assay conditions. With E. coli DNA as substrate, 8-9 molecules of ATP are hydrolyzed to ADP and inorganic phosphate for every phosphodiester bond hydrolyzed by the DNase. The possible functional relationship of the ATPase and DNase activities is discussed.

Acrylamides↗