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B Fontes

Publications and source records attributed to B Fontes.

At least 19 recordsLinked to original sources
PubMed2000

Gut ischemia/reperfusion activates lung macrophages for tumor necrosis factor and hydrogen peroxide production.

BACKGROUND: Gut ischemia followed by reperfusion (I/R) is implicated as a prime initiating event in the mechanism of multiple organ failure after trauma and hemorrhagic shock. Several lines of evidence indicate that macrophages are involved in this prime event. Our purpose was to evaluate hydrogen peroxide (H2O2) and tumor necrosis factor (TNF) production and phagocytosis by lung macrophages in a gut I/R model of multiple organ failure in rats. METHODS: In the experimental group (I/R), Wistar rats (n = 35) were anesthetized and subjected to a median laparotomy, and the superior mesenteric artery was clamped for 45 minutes followed by 60 minutes of reperfusion. In the control group (LAP) (n = 37), animals underwent sham laparotomy. After the period of reperfusion, bronchoalveolar lavage (BAL) was performed and the resulting BAL cells were assayed for H2O2 production using the horseradish peroxidase-mediated red phenol oxidation method. TNF release was determined using the L929 cells bioassay. Zymosan phagocytosis by BAL macrophages was quantitated using phase microscopy. RESULTS: H2O2 release in BAL cells of I/R rats (19.90 +/- 7.98 nmol/L/2 x 10(5) cells) is statistically higher than in the LAP group (10.92 +/- 5.01 nmol/L per 2 x 10(5) cells) (p = 0.0155), and the TNF production by BAL cells of the I/R group (38.09 +/- 20.79 units per 10(6) cells) was significantly higher than that of LAP rats (17.16 +/- 13.35 units per 10(6) cells) (p = 0.0281). Phagocytic activity of BAL mac. Macrophages of I/R rats was not statistically different from LAP animals. CONCLUSION: These results suggest that BAL macrophage play a role in the mechanism of acute lung injury after trauma and hemorrhagic shock.

Animals↗
PubMed2000

Tracheostomy in children: there is a place for acceptable risk.

BACKGROUND: Tracheostomy in children remains controversial regarding the risk of complications. METHODS: Forty-six trauma patients (35 male and 11 female, mean age = 6.8 years) were admitted to the intensive care unit between 1987 and 1991 with severe head injury plus coma. Tracheostomy was performed with standard technique after 5.9 days (range, 2-12 days) of intubation. RESULTS: There were no deaths from tracheostomy, but six deaths resulted from severe head injury. One child was discharged with tracheostomy. The 39 survivors remained with tracheostomy 16.14 days (range, 4-71 days) in the intensive care unit. After cannula removal, 31 remained asymptomatic; 8 had respiratory distress: 2 were normal, 5 had endoscopic treatment for subglottic granulomas/stenosis from intubation, and 1 had tracheomalacia from tracheostomy. In 1997, the 18 patients located for follow-up were asymptomatic. At endoscopy, 8 were normal, 9 had subglottal granulomas from intubation, and 1 had 20% tracheal stenosis from tracheostomy. CONCLUSION: Most complications after tracheostomy result from intubation. Tracheostomy has an acceptable risk in children with severe head injury who need prolonged ventilatory support.

Adolescent↗
PubMed2000

Laparoscopic pneumoperitoneum in acute peritonitis does not increase bacteremia or aggravate metabolic or hemodynamic disturbances.

The use of laparoscopy in generalized peritonitis has become increasingly frequent in recent years. However, CO2 pneumoperitoneum in association with increased intraperitoneal pressure may have deleterious effects in patients with hemodynamic or metabolic disturbances caused by bacterial peritonitis. The purpose of this study was to investigate the effect of CO2 pneumoperitoneum on bacteremia, mean arterial pressure, and blood gas disturbances in an animal model of bacterial peritonitis. Dogs were anesthetized, orally intubated, and subjected to experimental peritonitis by intraperitoneal inoculation of a suspension containing Escherichia coli and sterile dog feces. The animals were randomly assigned to two groups: control animals were maintained under anesthesia, and the insufflated animals were subjected to intraperitoneal CO2 insufflation. Bacterial peritonitis provoked the appearance of bacteremia and a significant decrease in mean arterial pressure, pH, bicarbonate, and base deficit. The induction of bacterial peritonitis did not significantly influence pH in the control group and partial pressure of arterial CO2 in either group. Thirty minutes of CO2 pneumoperitoneum did not influence the effect of bacterial peritonitis on the analyzed variables. These results suggest that laparoscopic CO2 pneumoperitoneum does not aggravate bacteremia or metabolic and hemodynamic disturbances induced by bacterial peritonitis.

Animals↗
PubMed1995

PMNs primed for superoxide release and increased CD11b expression do not sequester in normal lung.

Our previous work has implicated platelet activating factor (PAF)-induced neutrophil (PMN) priming and increased CD11b/CD18 receptor expression in the pathogenesis of lung injury following gut ischemia/reperfusion (I/R). In this model CD11b blockade abrogates lung injury but does not alter PMN priming or pulmonary leukosequestration. We, therefore, hypothesized that PAF-stimulated PMN priming and CD11b expression are insufficient to promote lung PMN sequestration. Normal rat PMNs, labeled with 51Cr, were incubated with PAF (10 ng/ml) to induce priming for superoxide (O2-) generation and enhance CD11b expression. Gut I/R animals underwent superior mesenteric artery occlusion for 45 min. 51Cr-labeled PMNs (2 x 10(7)) were injected iv. Study groups, consisting of (a) normal/control, (b) sham/laparotomy, and (c) gut I/R, were given either normal or PAF-treated PMNs. PAF-primed PMNs had increased 2- release and CD11b expression, but did not sequester in the lungs of normal rats. However, following gut I/R PAF-treated PMNs sequestered in the pulmonary bed. These data suggest that PAF priming for O2- generation and increased CD11b expression are insufficient alone to promote PMN sequestration in the lung. Rather, additional factors generated by gut I/R are necessary for this process.

Animals↗
PubMed1995

Reperfused gut elaborates PAF that chemoattracts and primes neutrophils.

Our in vivo model of mesenteric ischemia/reperfusion (I/R) has shown that the gut serves as a priming bed for neutrophils (PMN). Activation of phospholipase A2 (PLA2) during ischemia temporally precedes PMN sequestration in the gut and the appearance of primed PMN in the portal circulation. Therefore, we hypothesized that reperfused gut secretes platelet activating factor (PAF) via PLA2 activation that is responsible for increased PMN chemotaxis and priming for superoxide (O2-) generation. Sprague-Dawley rats underwent gut ischemia/reperfusion (45 min SMA occlusion/2 hr reperfusion) or sham laparotomy. Distal ileum was harvested, rinsed with bacteriostatic saline/neomycin, and incubated for 1 hr at 37 degrees C in RPMI 1640 and the cell-free supernatant was collected. Normal human PMNs, isolated by plasma-Percoll gradients, were pretreated with or without a PAF receptor antagonist (WEB 2170). Chemotaxis toward gut supernatant was then measured by the agarose method. Additionally, PMNs were preincubated with or without WEB 2170 and their O2- release in response to 1 microM FMLP was measured by the Vmax of SOD-inhibitable cytochrome c reduction. Reperfused gut produced a chemotactic index of 2.1 +/- 0.1 compared to 0.2 +/- 0.9 following sham laparotomy (P < 0.05); this was reduced to 0.4 +/- 0.9 with PAF receptor blockade. Similarly, gut I/R supernatant primed PMNs for O2- (P < 0.05) compared to laparotomy, and this effect was abrogated by a PAF antagonist. These data suggest that reperfused gut can elaborate PAF which chemoattracts and primes PMNs for O2- generation.

Animals↗
PubMed1995

CD11b blockade prevents lung injury despite neutrophil priming after gut ischemia/reperfusion.

Gut ischemia/reperfusion (I/R) provokes lung injury via a mechanism that involves neutrophils [polymorphonuclear neutrophils (PMNs)]. CD11b/CD18 (alpha mB2) is the integrin receptor on PMNs critical for adhesion-dependent oxidative burst. The purpose of this study was to investigate the mechanistic role of CD11b in the process of gut I/R-induced lung injury. Sprague-Dawley rats underwent 45 minutes of superior mesenteric artery (SMA) occlusion with and without CD11b monoclonal antibody treatment (IB6) (1 mg/kg, i.v.), before SMA clamping. At 2-hour reperfusion, PMN presence in tissue was quantitated by myeloperoxidase activity and circulating PMN priming determined by the difference in superoxide production with and without N-formyl-methionyl-leucyl-phenylalanine, whereas lung leak was assessed by 125I-albumin lung/blood ratio. In sum, CD11b blockade prevented gut I/R-induced lung leak, but did not attenuate gut I/R-induced PMN priming or tissue PMN accumulation. In conclusion, gut I/R promotes PMN priming and PMN adhesion in both local and distant beds via receptors other than CD11b, but this B2 integrin receptor is critical for PMN-mediated endothelial injury.

Animals↗
PubMed1995

Postinjury neutrophil priming and activation states: therapeutic challenges.

Both hyperactivity and hypoactivity of neutrophils (PMNs) have been implicated in the pathogenesis of postinjury multiple organ failure. In this paper, the cellular and molecular mechanisms involved in the regulation of PMN O2- production are reviewed. In addition, relevant research laboratory techniques for measuring both intracellular and extracellular O2- release are outlined. In a pilot study PMN O2- release in response to a battery of PMN agonists was determined, and four functional states of the NADPH were defined: resting, primed, activated, and unresponsive. PMNs from normal adult volunteers are in the resting state. In contrast, PMNs from patients with severe torso trauma are primed and activated in the first 24 h postinjury, but, after 48 h, become unresponsive to both receptor-dependent (platelet activating factor and N-formyl-methyl-leucyl-phenylalanine) and receptor-independent (phorbol 12-myristate 13-acetate) activation. The ability to identify at-risk patients and provide a rationale for ameliorating PMN-mediated tissue injury in patients with hyperinflammation syndromes are discussed. In addition, the importance of identifying patients with PMNs that are unresponsive, and the necessity for increasing PMN function in these patients in order to reduce the risk of sepsis, are also discussed.

Humans↗
PubMed1994

Gut ischemia induces bone marrow failure and increases risk of infection.

Hemorrhagic shock leads to bone marrow (BM) failure and renders the host susceptible to infection. We hypothesized that splanchnic hypoperfusion may play a mechanistic role in this process. BM was harvested from normal rats and, on Postprocedure Days 1 and 3, from rats that had undergone laparotomy (LAP) or gut ischemia/reperfusion (I/R; 45 min superior mesentery artery occlusion). Granulocyte-macrophage colony-forming unit (CFU-GM) proliferation, a measure of BM myeloid progenitors, was quantitated using a standard soft agar culture technique. On Postprocedure Days 1 and 3, BM proliferation of CFU-GM was depressed in gut I/R rats, compared to control and LAP animals (P < 0.05). Next, six rats were subjected to I/R, LAP, ANEST (anesthesia control), or no treatment (NL, normal control); 1 day later, 3.5 x 10(7) Staphylococcus aureus, suspended in 0.25 ml of saline, were injected subcutaneously in four sites on the back of each animal. Five days later, the NL rats had developed 23 abscesses, ANEST 23, and LAP 22, while the gut I/R rats had 24. The abscesses were excised, weighed, and measured. The weight and size of abscesses were greater in the gut I/R animals (P < 0.05). In summary, gut I/R depressed BM proliferation and rendered animals susceptible to infection in a manner similar to that observed following hemorrhagic shock. These data suggest that splanchnic hypoperfusion, a common sequela of hemorrhagic shock, may play a mechanistic role in BM failure and infection after hemorrhage.

Abscess↗
PubMed1988

The efficacy of loop colostomy for complete fecal diversion.

In an attempt to evaluate the real efficacy of loop colostomy for fecal diversion, the authors studied 62 patients previously colostomized under emergency conditions. Radiologic series of the abdomen were taken after 200 gm of barium meal. The results showed that the colostomy provided complete diversion of the radiologic contrast in 53 patients (85 percent) and incomplete diversion in nine patients (15 percent). Analysis of the results revealed that incomplete fecal diversion was: 1) observed as of the 86th postoperative day, with a significantly higher frequency following the 10th postoperative month, and 2) significantly correlated with either colostomy retraction or prolapse. The authors present a diagram showing a possible interaction of factors responsible for incomplete fecal diversion in loop colostomy and conclude that: 1) retraction is probably the basic contributing factor for colostomy failure; 2) the prolapse, once reduced, propitiates sinking of the stoma, facilitating colostomy failure; 3) the common assumption that loop colostomy eventually fails to provide complete fecal diversion is further supported; 4) loop colostomy assures, over its usual duration, a satisfactory defunctionalization of the colon; and 5) use of improved techniques of colostomy construction may prolong complete fecal diversion.

Abdominal Muscles↗
PubMedDate not supplied

Cardiac herniation mimics cardiac tamponade in blunt trauma. Must early resuscitative thoracotomy be done?

Blunt rupture of the pericardium is a rare injury. Strangulated cardiac hernia following blunt trauma is one cause of reversible cardiac arrest. Traumatic pericardial tears usually have delayed diagnoses and carry high mortality rates (64%). Clinical signs mimic cardiac tamponade during the primary survey. We report here two cases of blunt trauma. Both patients arrived alive in the emergency room and presented signs of cardiac tamponade caused by pericardial rupture.

Accidents, Traffic↗
PubMedDate not supplied

Percutaneous catheterization of the subclavian vein in hemophiliac patients: report of 47 cases.

Hemophiliac patients frequently require venous access, but usually their peripheral veins are collapsed and not puncturable. Several procedures employed to overcome this difficulty present a high complication rate. The authors report 47 cases of percutaneous subclavian vein catheterization (PSC) in hemophiliacs with an overall complication rate of 23%. Six patients (13%) had complications attributed to the coagulation disorder. The complications attributed to the coagulopathy and presenting major clinical importance occurred early in the series. After the improvement of the coagulation control with a routine AHG administration policy, the authors observed that among the last 22 patients there were 3 complications related to the coagulopathy, all of them without major clinical importance. The authors conclude that, in the lack of a safer access, PSC seems to be an acceptable procedure in hemophiliac patients, if employed with strict indication, accurate technique and rigorous control of the coagulopathhy.

Adolescent↗
PubMedDate not supplied

[The role of the polymorphonuclear neutrophil in the failure of multiple organs and systems].

The role of the polymorphonuclear neutrophil (PMN) on MOF is analyzed either as PMN activation for superoxide and enzyme release, or as PMN function depression after trauma and surgery. The authors stress: 1) the signal transduction pathway from the PMN membrane receptors to the effector response; 2) the PMN-NADPH system structure and function; 3) the functional states of the PMN (quiescente, primed, activated, non-responsive) in terms of the NADPH system activation; 4) the mechanism of tissue injuiry by the PMN. Clinical investigations on the PMN activation state, and therapeutical goals based on recent clinical investigations are also discussed.

Animals↗