PubMed Health⌕ Search

Biomedical subjects

A A Santos

Publications and source records attributed to A A Santos.

At least 19 recordsLinked to original sources

Variations in gastric compliance induced by acute blood volume changes in anesthetized rats.

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% (P<0.05). Hypovolemic rats (N = 12) were bled up to 10 ml/kg, a procedure that increased GV values by 15.8% (P<0.05). In the restored group (N = 12), shed blood replacement brought GV values back to basal levels in bled animals (P>0.05). MAP and CVP values increased (P<0.05) after hypervolemia but decreased (P<0.05) with hypovolemia. In conclusion, blood volume level modulates gastric compliance, turning the stomach into an adjustable reservoir, which could be part of the homeostatic process to balance blood volume.

Analysis of Variance↗

Improved methods for examination of Toxoplasma gondii cytoskeleton at ultrastructural level.

To evaluate an improved method for identifying the presence of the structural elements of the cytoskeleton of Toxoplasma gondii and their influence on invasion of the parasite in host cells, copper grids coated with plastic film were used for adhesion of whole parasites. Tachyzoites were incubated with 0.5% Triton X-100 in PHEM buffer containing protease inhibitors, post-fixed in 1% glutaraldehyde, stained with uranyl acetate and submitted to critical point drying. In order to analyze the presence of the structural elements of the cytoskeleton, immunolocalization was carried out using colloidal gold. Invasion of the parasite was examined on cell culture after treatment of tachyzoites with cytochalasin B (CB). In order to observe this effect, an immunocytochemical assay using alkaline phosphatase was carried out. A very well conserved extraction of the cytoskeleton elements of T. gondii, such as conoid and microtubules, as well as the rhoptries, was observed. By immunolocalization with colloidal gold, it was possible to detect the actin in its globular form. In the assay of invasion of the parasite on the host cell, after treatment of the T. gondii tachyzoites with CB, the invasion process was totally inhibited.

Actins↗

Mast cell types and cell-to-cell interactions in lymph nodes of the opossum Didelphis albiventris.

Previous light-microscopic studies have shown a unique population of mast cells in lymphatic sinuses of lymph nodes located in the head, neck, axillary fossa and inguinal region of the opossum. In the present work, scanning and transmission electron-microscopic studies in the opossum mandibular and superficial axillary lymph nodes have strengthened the differences between connective-tissue mast cells (CTMC) and the lymphatic-sinus mast cells (LSMC). Further, close appositions of mast cells to other cells were described. At the nodal capsule, CTMC contacted fibroblast and granulocytes. In the lymphatic sinuses a few CTMC contacted LSMC, macrophages and reticular cells. The LSMC contacted macrophages, reticular cells and other LSMC. A few LSMC could be located in the medullary cord in close contact with plasma cells or other lymphoid cells, keeping the same ultrastructural features of those found in the lymphatic sinuses. An important new finding was provided by light-microscopic studies in nine abdominal lymph nodes. Most of them (para-aortic, common iliac, cardial, cecocolic and those of the body and tail of the pancreas) displayed numerous LSMC with the same distribution and histological features described herein. However, the mesenteric, pyloric and head-of-pancreas lymph nodes were virtually devoid of LSMC. Instead, their mast cells occurred mainly at the medullary cords and were very similar to the CTMC. Ultrastructural studies at the mesenteric lymph nodes confirmed the CTMC character of the mast cells located at both medullary cords and sinuses, and disclosed interactions with macrophages and lymphoid cells.

Animals↗

Inhibition of gastric emptying and intestinal transit in anesthetized rats by a Tityus serrulatus scorpion toxin.

The effects of a fraction (T1) of Tityus serrulatus scorpion venom prepared by gel filtration on gastric emptying and small intestinal transit were investigated in male Wistar rats. Fasted animals were anesthetized with urethane, submitted to tracheal intubation and right jugular vein cannulation. Scorpion toxin (250 microg/kg) or saline was injected iv and 1 h later a bolus of saline (1.0 ml/100 g) labeled with 99m technetium-phytate (10 MBq) was administered by gavage. After 15 min, animals were sacrificed and the radioactivity remaining in the stomach was determined. Intestinal transit was evaluated by instillation of a technetium-labeled saline bolus (1.0 ml) through a cannula previously implanted in the duodenum. After 60 min, the progression of the marker throughout 7 consecutive gut segments was estimated by the geometric center method. Gastric retention of the liquid test meal in rats injected with scorpion toxin (median: 88%; range: 52-95%) was significantly higher (P<0.02) than in controls (54%; 21-76%), an effect which was not modified by gastric secretion blockade with ranitidine. The progression of the isotope marker throughout the small intestine was significantly slower (P<0.05) in rats treated with toxin (1.2; 1.0-2.5) than in control animals (2.3; 1.0-3.2). Inhibition of both gastric emptying and intestinal transit in rats injected with scorpion toxin suggests an increased resistance to aboral flow, which might be caused by abnormal neurotransmitter release or by the local effects of venom on smooth muscle cells.

Animals↗

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↗

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↗

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↗

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↗

Use of growth hormone for postoperative respiratory failure.

BACKGROUND: The authors examined the efficacy of human growth hormone (HGH) in patients dependent on mechanical ventilation who were being weaned from the respirator. METHODS: A total of 53 patients were chosen by the primary surgical team in consultation with the critical care service to undergo HGH therapy. These patients had been receiving standard ICU support and had failed standard ventilator weaning protocols. As such, they were treated with HGH in an attempt to increase respiratory muscle strength and facilitate weaning from mechanical ventilation. RESULTS: General demographic information was recorded. Patients suffered from a high incidence of co-morbid conditions and infectious complications. The average duration of HGH therapy was 38 days, and 81% of the previously unweanable patients were eventually weaned from mechanical ventilation with an overall survival of 76%. Mortality as predicted by APACHE II Scores was significantly less than actual mortality (24% actual mortality vs. 42% predicted mortality, P < 0.05). CONCLUSIONS: This phase I study presents clinical evidence supporting the safety and efficacy of HGH in promoting respiratory independence in a selected group of surgical ICU patients. Randomized, blinded, controlled trials now seem warranted.

Aged↗

The systemic inflammatory response: perspective of human endotoxemia.

Improvements in detection of cytokines and other intermediary substances has allowed a new wave of investigations to determine the role that endotoxin plays in initiating these mediators. We have reviewed all studies of endotoxin administration (Escherichia coli, Lot EC-5, 4 ng/kg) to healthy humans in an effort to collate the currently available data that describes mediator elaboration and therapy directed against them. More than 60 studies included descriptions of the effects of administering endotoxin alone and with pretreatments, such as antiendotoxin molecules (n = 8), mediator receptor antagonist (n = 9), antimediator therapy (n = 5), and anti-inflammatory agents (n = 49), which were given in an attempt to modify the inflammatory response. Endpoints that were monitored included vital signs and symptoms, leukocyte and platelet patterns, alterations in coagulation, hormonal secretion, plasma enzyme activities, plasma cytokine and anticytokine concentrations, plasma metabolic substrates, and ex vivo mononuclear cell responses. Analysis of investigations of human endotoxemia with and without pretreatments suggests that such trials a) are safe, b) are unable to achieve the success of small animal studies using pretreatments of endotoxemia, and c) have results similar to antimediator therapy administered recently to patients with Gram-negative bacteremia. Establishment of endotoxemia in humans may provide a valuable screening method to determine which antimediator treatments should be submitted to carefully constructed clinical trials.

Body Temperature↗

Hypercalcemia associated with the use of human growth hormone in an adult surgical intensive care unit.

BACKGROUND: The anabolic properties of human growth hormone (HGH) may prove beneficial in critically ill surgical patients. Potential effects of hypercalcemia with HGH therapy have not been addressed for adult patients in the intensive care unit. METHODS: We performed a retrospective review of the past 100 patients treated with HGH in a surgical intensive care unit. Laboratory data, including serum calcium levels, were recorded at baseline and during HGH therapy. Additionally, calcium levels in 27 burn patients receiving HGH were compared with calcium levels in a well-matched group of 27 burn patients not receiving HGH. The incidence and severity of hypercalcemia were recorded, with attention to contributing factors and overall outcome. RESULTS: There was a statistically significant increase in the mean +/- SD serum calcium level with the institution of HGH therapy (2.50 +/- 0.20 mmol/L [10.0 +/- 0.8 mg/dL] before HGH vs 2.74 +/- 0.27 mmol/L [11.0 +/- 1.1 mg/dL] during HGH, P < .05). Before HGH, 14% of the patients had hypercalcemia, defined as a calcium level greater than 2.74 mmol/L (11.0 mg/dL). During HGH, 43% of the patients developed hypercalcemia. Before HGH, no patient exhibited severe hypercalcemia, defined as a calcium level greater than 3.12 mmol/L (12.5 mg/dL). However, during HGH, 10% of the patients developed severe hypercalcemia. Elevations in serum calcium levels were correlated with the duration of HGH therapy and renal dysfunction. Burn patients receiving HGH exhibited significantly higher mean +/- SD calcium levels than controls (2.87 +/- 0.32 mmol/L [11.5 +/- 1.3 mg/dL] vs 2.50 +/- 0.17 mmol/L [10.0 +/- 0.7 mg/dL], P < .001). Studies performed in selected patients demonstrated that alterations in parathyroid function, vitamin D metabolism, and thyroid function did not appear to contribute to this effect. CONCLUSION: Prolonged HGH therapy in critically ill surgical patients may result in severe hypercalcemia, particularly in patients with altered renal function. Possible mechanisms for HGH-induced hypercalcemia include increased intestinal absorption and decreased urinary excretion. Outcome was not adversely affected by this biochemical alteration, but careful monitoring of calcium levels should be undertaken in this population receiving HGH.

Adult↗

Tropical pyomyositis presenting in the upper extremity.

Tropical pyomyositis is a staphylococcal infection, usually of a single large muscle, most commonly seen in young men in tropical regions. The following presents a case of tropical pyomyositis in a 62-year-old man that affected all four extremities, including the muscles of the forearms. Computed tomography was a useful guide for directing surgical explorations. To decrease the degree of disability from the multiple operative sites, we successfully used limited longitudinal incisions and conservative débridements.

Arm↗

Are events after endotoxemia related to circulating phospholipase A2?

OBJECTIVE: The authors sought to determine whether the signs and symptoms of endotoxemia were related to the endotoxin-stimulated increase in circulating phospholipase A2 (PLA2) activity. BACKGROUND: Because hypotension and pulmonary injury have been associated with elevated PLA2 activity in septic shock and PLA2 levels are reduced with the administration of glucocorticoids, the PLA2 response to endotoxin was investigated in volunteers pretreated with and without hydrocortisone. METHODS: Carefully screened human subjects were studied under four conditions: (1) saline, (2) hydrocortisone, (3) endotoxin, and (4) hydrocortisone administration before endotoxin exposure. Pulse rate, blood pressure, temperature, and symptoms of endotoxemia were serially measured. Plasma for tumor necrosis factor concentrations and PLA2 activity was obtained. RESULTS: After lipopolysaccharide, pulse rate and tumor necrosis factor concentrations rose at 1 to 2 hours; temperature increased maximally at 4 hours. PLA2 activity reached peak levels at 24 hours. With hydrocortisone pretreatment, a 50% reduction in the concentrations of tumor necrosis factor and PLA2 occurred. Significant correlations between other variables and PLA2 activity were not observed. The enzyme identified by monoclonal antibody was the secreted nonpancreatic PLA2 (SNP-PLA2). CONCLUSIONS: The results of this study suggest that elevations in circulating SNP-PLA2 activity and systemic events associated with intravenous endotoxin administration are unrelated.

Adult↗

Does the route of feeding modify the inflammatory response?

OBJECTIVE: The authors compared the responses to endotoxin in enterally and parenterally fed human volunteers. BACKGROUND: Recent investigations have reported that the response to endotoxin in humans is greater in individuals who receive parenteral nutrition rather than enteral feeding. It was proposed that this difference was related to gut barrier dysfunction during intravenous nutrition. To evaluate this hypothesis, the authors analyzed the responses of human subjects to an intravenously administered bolus of endotoxin after enteral or parenteral nutrition. METHODS: Fifteen randomly selected healthy volunteers were studied during two separate investigations; ten studies were performed in ten subjects who received enteral nutrition, and nine studies were carried out in five additional subjects who received parenteral nutrition. After 2 days of enteral feedings or 7 days of parenteral feedings, endotoxin was administered by intravenous injection; temperature, symptom score, and duration then were measured serially. Blood samples were obtained for leukocyte and platelet count, and plasma concentrations of corticotrophin, cortisol, epinephrine, norepinephrine, tumor necrosis factor, and interleukin-6. Mononuclear cell response to phytohemagglutinin was determined at 0, 4, and 24 hours. RESULTS: In the parenteral group, a diminished response was observed in platelet count and plasma interleukin-6 levels compared with volunteers who received enteral nutrition. The duration of symptoms tended to be reduced in the parenterally fed group, although this did not achieve significance. Other responses were not significantly different between the two groups. CONCLUSION: The responses to endotoxin in human subjects who received parenteral nutrition were similar compared with subjects who received enteral nutrition, although platelet count and plasma interleukin-6 concentration were diminished.

Adrenocorticotropic Hormone↗

Histochemical and ultrastructural studies of mast cells in the intestinal mucosa and skin of the opossum Didelphis albiventris.

The mast cells located in the intestinal mucosa of a non-eutherian mammal were studied in comparison with those in the skin of the ear. In the intestinal mucosa, the mast cells exhibited a more variable shape, larger cytoplasmic granules and greater sensitivity to fixatives regarding their staining towards Toluidine Blue. Ultrastructurally, these granules were more heterogeneous but lacked the crystalline content found in granules of skin mast cells; lipid body-like organelles were found only in the mucosa-located mast cells. Histochemically, they differed from skin mast cells by the absence of periodic acid-Schiff (PAS)-positive granules. Unlike the mucosal mast cells of the rat, they fluoresced brilliant yellow after berberine treatment, which is evidence of the presence of heparin.

Animals↗

Elaboration of interleukin 1-receptor antagonist is not attenuated by glucocorticoids after endotoxemia.

The body's response to infection/inflammation is initiated by the elaboration of cytokines, such as tumor necrosis factor, interleukin 1-beta (IL-1-beta), IL-6, and IL-8. Cytokines, in turn, stimulate the pituitary-adrenal axis, and it has been suggested that the corticosteroids elaborated serve as negative feedback signals to diminish inflammatory events. To test this hypothesis, we administered hydrocortisone shortly before endotoxin administration to normal volunteers. Steroids greatly reduced the clinical response to endotoxin and attenuated the appearance of tumor necrosis factor, IL-6, and IL-8 in the circulation. In contrast, IL-1-receptor antagonist, a competitive antagonist of the IL-1 receptor, was unaffected by steroid administration. These data suggest that IL-1-receptor antagonist may act in synergism with corticosteroids to reduce inflammation. Elevation of concentrations of these two factors, corticosteroids and IL-1-receptor antagonist, in plasma appears to be the mechanism used by the body to overcome the effects of inflammatory cytokines.

Adult↗