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H J Sugerman

Publications and source records attributed to H J Sugerman.

At least 19 recordsLinked to original sources
PubMed1997

Delayed administration of inhaled nitric oxide preserves alveolar-capillary membrane integrity in porcine gram-negative sepsis.

OBJECTIVE: To determine the effect of delayed administration of inhaled nitric oxide (NO) on acute lung injury after the onset of gram-negative sepsis. DESIGN: Nonrandomized controlled study. SETTING: University medical center laboratory. SUBJECTS: Yorkshire swine. INTERVENTIONS: Five groups of swine were anesthetized, mechanically ventilated, and studied for 5 hours. After surgical preparation, control (n = 10) and NO-treated control (n = 6) animals received a 1-hour infusion of sterile saline solution. Sepsis was induced with a 1-hour intravenous infusion of live Pseudomonas aeruginosa. Untreated animals with sepsis (n = 10) received no treatment. Inhaled NO at 20 ppm was administered to NO30-treated animals with sepsis (n = 7) and NO60-treated animals with sepsis (n = 8) beginning at 30 and 60 minutes after bacterial infusion was begun, respectively. MAIN OUTCOME MEASURES: Systemic and pulmonary hemodynamics, arterial blood gas determination, bronchoalveolar lavage protein and neutrophil content, neutrophil oxidant burst, lung myeloperoxidase content, and scanning electron micrographic studies. RESULTS: A progressive, significant (P < .05) decline in PaO2 developed in untreated animals with sepsis, which was prevented in NO30- and NO60-treated animals with sepsis. A significant (P < .05) increase in bronchoalveolar lavage protein and neutrophil counts compared with baseline values was observed in untreated animals with sepsis, indicating acute lung injury. These variables exhibited no notable increase in NO30- and NO60-treated animals with sepsis and were significantly (P < .05) reduced compared with untreated animals with sepsis. The lung myeloperoxidase content was significantly (P < .05) elevated at 5 hours in all groups with sepsis compared with baseline values and the control and NO-treated control groups. The total phorbol myristate acetate-induced polymorphonuclear leukocyte oxidant burst at 5 hours was significantly (P < .05) decreased in the NO30- and NO60-treated animals with sepsis compared with untreated animals with sepsis. Untreated and NO30- and NO60-treated animals with sepsis showed a significant (P < .05) increase in pulmonary artery pressure at 30 minutes, followed by a progressive decline. These changes were significant (P < .05) compared with baseline values and the control groups. No significant (P < .05) difference in pulmonary artery pressure or systemic arterial pressure was found at any time between untreated and NO30- and NO60-treated animals with sepsis. CONCLUSIONS: The delayed administration of inhaled NO preserves alveolar-capillary membrane integrity in this porcine model of gram-negative sepsis. The inhibition of neutrophil transendothelial migration, rather than neutrophil rolling or tight adhesion, may be a critical mechanism by which inhaled NO produces this effect. Decreased oxidant production by activated neutrophils may be a secondary mechanism by which inhaled NO reduces acute lung injury.

Animals↗
PubMed1997

Protective role of synthetic sialylated oligosaccharide in sepsis-induced acute lung injury.

Proper engagement of leukocyte and endothelial cell selectins with their counterreceptors is an initial step in neutrophil trafficking to sites of inflammation. Certain fucosylated carbohydrate determinants such as sialyl Lewis-x are proposed to act as these counterreceptors. We studied the effects of a synthetic sialyl Lewis-x analog, CY-1503, on the course of hemodynamic derangements and acute lung injury during experimental gram-negative sepsis. Anesthetized ventilated swine were made septic with an infusion of live Pseudomonas aeruginosa. A treatment group received an initial bolus of CY-1503 (60 mg/kg) before sepsis, followed by continuous infusion of CY-1503 (15 mg.kg-1.h-1). Treatment with CY-1503 did not prevent the development of pulmonary hypertension, systemic hypotension, decline in cardiac output, or severe neutropenia. However, CY-1503 significantly attenuated lung injury, demonstrated by decreased bronchoalveolar lavage protein content and neutrophil influx, lowered lung myeloperoxidase activity, and improved arterial oxygenation. Neutrophils from septic and CY-1503 animals showed significant activation, reflected by upregulated CD18 expression and priming for oxidant burst compared with control animals. This study suggests blockade of selectin interactions as a potential therapeutic intervention in sepsis-induced lung injury.

Animals↗
PubMed1996

Pulmonary artery endothelial cell function in swine pseudomonas sepsis.

A substantial increase in pulmonary vascular resistance is associated with sepsis and its sequelae (sepsis syndrome and septic shock). It is postulated that increased resistance may result from sepsis-induced endothelial cell injury or altered vasoreactivity secondary to pulmonary hypertension. We, therefore, tested the hypothesis that sepsis causes endothelial cell injury and that increased pulmonary pressure alters vascular reactivity. Young swine (15-25 kg) were anesthetized and ventilated. Septic animals received a 1-hr infusion of live Pseudomonas aeruginosa (n = 11), and the control cohort received 0.9% NaCl (n = 7). All animals were studied for 300 min following the infusion. Postmortem branches of peripheral pulmonary arteries were prepared and tested in a vessel myograph. Ring segments were set to 90% of the circumference the vessels would have at pressures of 20, 30, 40, or 50 mmHg (L90), corresponding to varying pulmonary pressures observed in sepsis. A high dose of potassium was used to obtain maximum possible contraction. Prostaglandin was used to precontract the vessels before testing endothelial cell responses to acetylcholine or bradykinin. Sodium nitroprusside was added at the end of each experiment to obtain maximum possible smooth muscle relaxation. No differences in contraction or relaxation were observed when vessels were set to different pressures (i.e., 20 vs 50 mmHg). Maximum possible contraction to KCl was significantly decreased after 300 min of sepsis compared to control. No differences between groups were found in contractility to prostaglandin. Bradykinin-induced EDRF/NO production, mediated by BK2 receptors, was not altered in Pseudomonas sepsis (97-98% of total relaxation control and 91-95% septic cohort). Response to acetylcholine was significantly decreased after sepsis (89-95% of total relaxation control and 51-61% of septic cohort relaxation). Decreased response to acetylcholine could not be attributed to decreased smooth muscle sensitivity to nitric oxide because the response to bradykinin plus sodium nitroprusside was not altered following sepsis. Vessel reactivity was not altered by increasing pressure settings reflective of changing pulmonary pressure in vivo. These results strongly suggest a sepsis-induced alteration in pulmonary artery endothelial cell receptor sensitivity to acetylcholine, independent of changing pulmonary arterial pressures. This is the first time this decrease has been shown in pseudomonas sepsis.

Animals↗
PubMed1996

Conversion of failed or complicated vertical banded gastroplasty to gastric bypass in morbid obesity.

BACKGROUND: Previous studies have documented a significantly better we weight loss for gastric bypass (GBP) than for vertical banded gastroplasty (VGB). Additional problems associated with VBG include intractable vomiting or gastroesophageal (GE) reflux, intragastric migration of the polypropylene band, staple line disruption, or inadequate weight loss due to excessive ingestion of high-calorie liquid or soft carbohydrates. PATIENTS AND METHODS: Fifty-eight morbidly obese patients underwent conversion from VBG to GBP for either weight-loss failure (15) or complications of VBG (43), including 2 who where referred with anastomotic leaks and peritonitis, 3 with band erosion, 15 with staple line disruption, and 23 with stomal stenosis, of whom 6 had severe GE reflux, with a Barrett's esophagus in 1. RESULTS: Percentage of excess weight loss in the 53 patients followed up for at least 1 year after conversion increased from 36% +/- 24% to 67% +/- 18%, and in the 15 "sweets eaters" from 20% +/- 19% to 70% +/- 19% (both P <0.001), was equal to weight loss after primary GBP, and was reasonably constant over 8 years in those patients who could be contacted for follow-up, although average follow-up after 5 years was only 45% All patients had resolution of GE reflux symptoms immediately after surgery and for at least 1 year or at last contact. Complications of conversion included 2 anastomotic leaks with major wound infections (1 in a referred patient requiring emergency subtotal gastrectomy following a VBG leak), 3 staple line disruptions (2 subclinical), 3 small-bowel obstructions, and 20 marginal ulcers or stomal stenoses (all responded to endoscopic balloon dilation or acid reduction therapy). Hemoglobin, calcium, and vitamin B12 levels remained within normal levels with prophylactic supplementation in patients who returned for follow-up evaluation. CONCLUSIONS: These data support the efficacy of conversion to GBP in morbidly obese patients with a failed or complicated VBG.

Gastric Bypass↗
PubMed1996

Greater risk of incisional hernia with morbidly obese than steroid-dependent patients and low recurrence with prefascial polypropylene mesh.

BACKGROUND: Incisional hernia is a serious complication of abdominal surgery. We compared incisional hernia frequency following gastric bypass (GBP) for morbid obesity versus total abdominal colectomy and ileal pouch-anal anastomosis (IPAA) for ulcerative colitis. A prefascial polypropylene mesh repair was also evaluated. PATIENTS AND METHODS: All patients had midline incisions, xiphoid to umbilicus in GBP patients and midepigastrium to pubis in IPAA patients. Fascia were closed with running No. 2 polyglycolic acid suture. Ninety-eight patients underwent prefascial polypropylene mesh repair; 80 were GBP patients, 46 had 1 previous repair, and 17 had 2 to 9 previous repairs (6 with properitoneal mesh). RESULTS: Incisional hernia occurred in 20% (198/968) of GBP patients (19% without versus 41% with a previous hernia, P < 0.001) versus 4% (7/171) of the IPAA patients (P < 0.001), of whom 102 (60%) were taking prednisone (32 +/- 2 mg/d) and 5 were quite obese (body mass index > or = 30 kg/m2). Additional risk factors for hernia in GBP patients included wound infection, diabetes, sleep apnea, and obesity hypoventilation. For the 98 patients who underwent prefascial polypropylene mesh repair, the mean follow-up was 20 +/- 2 months (range 6 to 104), and complications occurred in 35% of patients, including minor wound infection (12%), major wound infection (5%), seroma (5%), hematoma (3%), chronic pain (6%), and recurrent hernia (4%). CONCLUSIONS: Severe obesity is a greater risk factor for incisional hernia and hernia recurrence than chronic steroid use in nonobese colitis patients. A prefascial polypropylene mesh repair minimizes recurrence.

Abdomen↗
PubMed1996

Effects of increased intra-abdominal pressure upon intracranial and cerebral perfusion pressure before and after volume expansion.

OBJECTIVE: To study the effects of elevated intra-abdominal pressure (IAP) upon intracranial (ICP) and cerebral perfusion pressure (CPP) before and after intravascular volume resuscitation. MATERIALS AND METHODS: Intra-abdominal pressure was increased in five anesthetized swine by inflating an intraperitoneal balloon until the IAP was 25 mm Hg above baseline. Intravascular volume was then expanded and finally abdominal decompression was performed. Changes in ICP and systemic and pulmonary hemodynamic parameters secondary to increasing IAP were measured. The effect upon CPP was derived from these measurements. PaO2 and PaCO2 were maintained relatively constant by increasing ventilatory rate. MEASUREMENTS AND MAIN RESULTS: Elevated IAP significantly increased ICP (7.6 +/- 1.2 vs. 21.4 +/- 1.0), pleural pressure and central venous pressure; whereas cardiac index and CPP (82.2 +/- 6.3 vs. 62.0 +/- 10.0) decreased significantly. Intravascular volume expansion further significantly increased ICP (27.8 +/- 1.0), and significantly increased both mean arterial pressure (83.4 +/- 14.0 versus 103.4 +/- 8.9) and CPP (75.6 +/- 9.0). Abdominal decompression returned ICP (11.2 +/- 1.8) toward baseline and further increased CPP (79.8 +/- 9.7). CONCLUSIONS: Elevated IAP increases ICP and decreases CPP and cardiac index. Volume expansion further increases ICP yet improves CPP via its greater positive effect upon mean arterial pressure (*p < 0.05, analysis of variance. All measurements are mean +/- SEM in mm Hg).

Abdomen↗
PubMed1995

Sepsis-induced acute lung injury is attenuated by selectin blockade following the onset of sepsis.

OBJECTIVE: To determine the effect of infusion with a dual-binding antibody to E- and L-selectin, EL-246, in a postonset model of sepsis. DESIGN: Nonrandomized controlled study. STUDY SUBJECTS: Young Yorkshire swine. INTERVENTIONS: Three groups were studied. Controls (n = 8) received saline solution only. Untreated animals with sepsis (n = 8) received a 1-hour intravenous infusion of live Pseudomonas aeruginosa. Animals treated with EL-246 (n = 6) received the same bacterial infusion and a 2-mg/kg bolus of EL-246 at 30 minutes. OUTCOME MEASURES: Systemic and pulmonary hemodynamics, arterial blood gas determination, bronchoalveolar lavage protein and neutrophil content, neutrophil integrin and selectin expression, neutrophil oxidant burst, and organ myeloperoxidase content. RESULTS: Treatment with EL-246 significantly reduced lung injury, as indicated by improved bronchoalveolar lavage protein and neutrophil content, resulting in a significant improvement in arterial oxygenation. This reduction in lung injury was produced by a reduction in lung myeloperoxidase content. Treatment with EL-246 failed to prevent the development of pulmonary hypertension and systemic hypotension. Neutrophils from animals with sepsis exhibited significant activation and upregulation of CD18, shedding of L-selectin, and production of increased levels of oxidants compared with controls. CONCLUSION: Treatment of animals with EL-246 soon the onset of sepsis produced significant protection against acute lung injury but failed to attenuate hemodynamic derangements associated with sepsis.

Animals↗
PubMed1995

Tumor necrosis factor-alpha and interleukin-6 selectively regulate neutrophil function in vitro.

The neutrophil is an important effector cell of the host response to sepsis. Tumor necrosis factor-alpha (TNF-alpha), a cytokine mediator of the septic response, is rapidly released following endotoxemia or gram-negative bacteremia. Interleukin-6 (IL-6) is another cytokine mediator of the host response to sepsis whose role is less well understood than that of TNF-alpha. It is known to be elevated in gram-negative sepsis, where peak levels have been correlated with mortality. This study examined the effect of IL-6 alone and in combination with TNF-alpha on three neutrophil functions--CD18 adhesion receptor expression, phagocytosis, and superoxide anion generation. Neutrophils from human volunteers were incubated with amounts of IL-6 ranging from 10 to 1000 ng/ml. At a concentration of 1000 ng/ml, IL-6 increased neutrophil phagocytosis of opsonized bacteria (826 +/- 255 x 10(3) MESF vs 552 +/- 103 MESF, P < 0.05) and also increased neutrophil superoxide anion generation (18.41 +/- 1.86 vs 12.6 nmol O2-/10(6) PMN/10 min, P < 0.05). Lesser amounts of IL-6 had no effect on phagocytosis or superoxide generation. IL-6 did not increase neutrophil CD18 adhesion receptor expression. Combining IL-6 with TNF-alpha at doses of 100 ng/ml and 100 U/ml, respectively, neutrophil phagocytosis (221 +/- 455 MESF vs 552 +/- 103 MESF) and superoxide generation (23.18 +/- 1.86 vs 12.6 nmol O2-/10(6) PMN/10 min) were significantly (P < 0.05) increased above control by an amount similar to that seen with 1000 U/ml TNF-alpha alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Effect of NSAIDs on gallbladder bile composition.

Secretion of gallbladder mucin is an important step in gallstone pathogenesis. Previous studies have demonstrated that aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) can both inhibit gallbladder mucin secretion and prevent gallstone formation in animal models of cholesterol gallstone disease. The present study was performed to determine if chronic NSAID use was associated with a reduction in the mucin content or affected the lipid components of human gallbladder bile. Four groups of patients were identified retrospectively from a cohort of 230 morbidly obese patients who underwent gastric bypass surgery. The index group consisted of 18 patients who were found to have gallstones at gastric bypass surgery and had a history of chronic NSAID use. Three other patient groups were identified from the cohort by matching this index population for sex, race, and age according to the following criteria: (1) patients with gallstones who had not utilized NSAIDs, (2) patients without gallstones but with chronic NSAID use, and (3) patients without gallstones and without a history of NSAID use. Gallbladder bile was obtained from all patients by direct aspiration from the gallbladder at the time of surgery. Patients with gallstones had a significantly (P < 0.02) greater concentration of gallbladder mucin in their gallbladder bile compared to patients without gallstones (0.897 +/- 0.226 vs 0.173 +/- 0.039 mg/ml). Among gallstone patients, gallbladder mucin was reduced in those patients with a history of chronic NSAID use (1.18 +/- 0.43 vs 0.74 +/- 0.19 mg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

A multicenter, placebo-controlled, randomized, double-blind, prospective trial of prophylactic ursodiol for the prevention of gallstone formation following gastric-bypass-induced rapid weight loss.

BACKGROUND: Previous studies have documented a high incidence of gallstone formation following gastric-bypass (GBP)-induced rapid weight loss in morbidly obese patients. This study was designed to determine if a 6-month regimen of prophylactic ursodiol might prevent the development of gallstones. METHODS: A multicenter, randomized, double-blind, prospective trial evaluated 3 oral doses of ursodiol: 300, 600, and 1,200 mg versus placebo beginning within 10 days after surgery and continuing for 6 months or until gallstone development, for patients with a body mass index (BMI) > or = 40 kg/m2. All patients had normal intraoperative gallbladder sonography. Transabdominal sonography was obtained at 2, 4, and 6 months following surgery, or until gallstone formation. RESULTS: Of 233 patients with at least one postoperative sonogram, 56 were randomized to placebo, 53 to 300 mg ursodiol, 61 to 600 mg ursodiol, and 63 to 1,200 mg ursodiol. Preoperative age, sex, race, weight, BMI, and postoperative weight loss were not significantly different between groups. Gallstone formation occurred at 6 months in 32%, 13%, 2%, and 6% of the patients on the respective doses. Gallstones were significantly (P < 0.001) less frequent with ursodiol 600 and 1,200 mg than with placebo. CONCLUSION: A daily dose of 600 mg ursodiol is effective prophylaxis for gallstone formation following GBP-induced rapid weight loss.

Adolescent↗
PubMed1995

Beneficial effects of a bradykinin antagonist in a model of gram-negative sepsis.

UNLABELLED: Activation of the kallikrein-kinin system in sepsis has long been recognized, but its role, beneficial or pathologic, has not been determined. Recently, however, specific bradykinin (BK) antagonists have become available and we sought to determine the effects of a BK antagonist, NPC17731, in a model of sepsis-induced acute lung injury (ALI). METHODS: Anesthetized swine were studied for 5 hours, receiving a 1-hour infusion of saline (Controls) or live Pseudomonas aeruginosa (Septic untreated). Treatment groups received a 5 mg/kg bolus of NPC17731 followed by a 1 mg/kg bolus hourly commencing either just before sepsis (Pretreatment) or 30 minutes following the onset of sepsis (Posttreatment). RESULTS: Septic untreated animals showed a rapid, progressive decline in arterial PaO2 compared to controls, and this was significantly improved in both treatment groups. Bronchoalveolar lavage at 5 hours in both treatment groups also showed significant decreases in neutrophil (PMN) counts and protein content compared to untreated septic animals, indicating decreased PMN migration and alveolar-capillary membrane damage. Both treatment groups also showed reduced PMN sequestration in the lung compared to untreated animals, although PMNs did exhibit significant upregulation of PMN CD18 receptor expression and superoxide generation. CONCLUSIONS: These data imply a significant role for BK in the pathogenesis of sepsis-induced ALI. Use of a competitive BK antagonist significantly attenuated the development of ALI without inhibiting PMN activation. BK antagonists may be a useful adjunct in the armamentarium against sepsis-induced ALI.

Animals↗
PubMed1995

Cardiopulmonary effects of raised intra-abdominal pressure before and after intravascular volume expansion.

The cardiopulmonary effects of acutely elevated intra-abdominal pressure (IAP) were studied in a porcine model to help define more clearly IAP effects in patients with trauma. IAP was increased in six anesthetized swine by intra-abdominal instillation of isotonic ethylene glycol up to an IAP of 25 mm Hg above baseline. Systemic and pulmonary hemodynamic parameters were measured, as well as the effects on bladder pressure, pleural pressure, and pulmonary function. At IAP of 25 mm Hg above baseline, intravascular volume expansion with saline was administered to return the cardiac index (CI) to baseline. Raising IAP correlated with measured bladder pressures (r = 0.9, p = 0.001). At IAP of 25 mm Hg, CI was significantly decreased (p < 0.05, analysis of variance (ANOVA); 3.6 +/- 0.3 vs. 2.2 +/- 0.3 L/min/m2); whereas wedge, pulmonary arterial, and pleural pressures were all elevated (p < 0.05, ANOVA). However, transarterial wedge pressure (wedge--pleural pressure) declined nonsignificantly with increasing IAP. Raised IAP caused impaired pulmonary function with a decreased (p < 0.05, ANOVA) PaO2 and increased (p < 0.05, ANOVA) PaCO2. Despite the elevated wedge pressure, fluid resuscitation returned CI to baseline. These data clarify the hemodynamic changes associated with raised IAP and indicate that care must be taken in interpreting hemodynamic measurements to determine intravascular fluid status in patients with elevated IAP.

Abdomen↗
PubMed1995

Treatment of increasing intracranial pressure secondary to the acute abdominal compartment syndrome in a patient with combined abdominal and head trauma.

Acute abdominal compartment syndrome has recently been shown to raise intracranial pressure (ICP). This may increase the risk of ischemic neuronal damage by decreasing cerebral perfusion pressure. We report the successful management of a patient with severe multisystem injury in whom abdominal decompression dramatically reduced high ICP unresponsive to medical measures.

Abdomen↗
PubMed1995

Circulating ICAM-1 is increased in septic shock.

Adhesion molecules play a critical role in the interaction of circulating neutrophils with vascular endothelium during inflammation. Increased quantities of soluble, circulating intercellular adhesion molecule-1 (cICAM-1) are present in various inflammatory conditions. The purpose of this investigation was to measure cICAM-1 levels in septic adults, as well as to examine the relationship between this potential marker of endothelial-cell activation and the consequences of sepsis (i.e., multiple organ failure and death). Using a sandwich-type enzyme-linked immunosorbent assay (ELISA), we measured cICAM-1 in blood samples obtained within 12 h of admission to an intensive care unit (ICU) for sepsis and other conditions. We found cICAM-1 levels to be increased in 25 septic patients (1,259 +/- 159 ng/ml, mean +/- SEM) as compared with 12 healthy volunteers (355 +/- 41 ng/ml, p < 0.0001) and four ICU patients without systemic inflammatory response syndrome (SIRS) (585 +/- 76 ng/ml, p < 0.001). Twenty-five patients with SIRS but no evidence of causative infection also had elevated levels of cICAM-1 (937 +/- 144 ng/ml, p = 0.12 versus sepsis). Serial measurements over the first week of sepsis demonstrated persistent elevation in most patients. Day 1 cICAM-1 levels were higher (p = 0.017, ANOVA) in 16 patients with septic shock than in seven with severe sepsis and two with sepsis but without hypotension or hypoperfusion. There was a positive correlation (r = 0.50, p = 0.009) between Day-1 cICAM-1 measurements and severity of shock as determined by the presence of hypotension and vasopressor use.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

A dual-binding antibody to E- and L-selectin attenuates sepsis-induced lung injury.

Many studies indicate a pivotal role for neutrophil adhesion in sepsis-associated lung injury. Neutrophil adhesion to endothelium depends on activation and expression of selectin and integrin adhesion receptors. We studied the effects of pretreatment with a dual-binding porcine anti-E- and anti-L-selectin monoclonal antibody (EL-246) on a porcine model of sepsis-induced lung injury. Four groups were studied for 5 h. Group 1 (control animals) received intravenous saline only. Group 2 (septic) received a 1-h infusion of Pseudomonas aeruginosa. Group 3 (EL-246 pretreatment) received EL-246 (1 mg/kg) prior to Pseudomonas infusion. Group 4 (EL-246 controls) received EL-246 infusion only. Group 2 animals showed rapid, significant decline in arterial pH and oxygen tension whereas, in Group 3, physiologic deterioration was significantly attenuated. Bronchoalveolar lavage at 5 h showed a significant increase in neutrophil count and protein content in Group 2. Group 3, however, showed no significant differences in these parameters compared with control animals. Despite severe neutropenia, lung myeloperoxidase content at 5 h was significantly reduced in Group 3 compared with Group 2. There was no significant difference in pulmonary and systemic hemodynamics between Groups 2 and 3. Group 4 animals exhibited a transient neutropenia, but otherwise no other differences in measured parameters were found compared with Group 1 control animals. In conclusion, EL-246 significantly reduced neutrophil accumulation in lung and attenuated sepsis-induced lung injury, but failed to attenuate deranged pulmonary and systemic hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Effects of surgically induced weight loss on idiopathic intracranial hypertension in morbid obesity.

BACKGROUND: The effect on CSF pressures and symptoms of weight loss induced by gastric surgery was studied in morbidly obese patients with idiopathic intracranial hypertension (IIH). METHODS: Gastric weight reduction surgery was performed in eight morbidly obese women (49 +/- 3 kg/m2 body mass index) who had IIH and elevated CSF pressures. Each had been treated medically for IIH. Two had ventriculoperitoneal shunts, with occlusion in both and hemorrhage and hemiparesis in one. Post--weight-reduction measurement of CSF pressures, signs and symptoms of IIH, and obesity co-morbidity were evaluated. RESULTS: CSF pressures decreased in all eight patients, from a mean of 353 +/- 35 to a mean of 168 +/- 12 mm H2O (p < 0.001), following mean weight loss of 57 +/- 5 kg (p < 0.001) when measured at 34 +/- 8 months after surgery. At follow-up no patient had papilledema, all eight patients had resolution or marked reduction of headache, and resolution of tinnitus occurred in all six patients with this symptom. Neuroimaging was unchanged at 27 +/- 6 months after surgery in six patients. There was also resolution or clinical improvement of additional obesity-related co-morbidity, including diabetes, hypertension, sleep apnea, obesity hypoventilation, joint pains, stress urinary incontinence, and gastroesophageal reflux. CONCLUSIONS: Although several complications occurred following obesity surgery over the 11 years of this study, the current low morbidity and mortality with gastric bypass make this a primary option in the severely obese patient with IIH.

Adult↗