Objectives. To determine relationship of intraabdominal pressure to central obesity and the comorbidity of obesity. Design. Non‐randomized, prospective. Setting. University hospital, operating room. Subjects. Eighty‐four anaesthetized consecutive patients prior to gastric bypass for morbid obesity and five non‐obese patients before colectomy for ulcerative colitis. Main outcome measures. Weight, body mass index (BMI), co‐morbid history, sagittal abdominal diameter, waist:hip (W∶H) ratio and urinary bladder pressure, as an estimate of intra‐abdominal pressure. Results. Urinary bladder pressure was greater in the obese than the non‐obese (18±0.7 vs. 7±1.6 cm H2O, P < 0.001), correlated with sagittal abdominal diameter (r = +0.67, P < 0.001) and was greater (P < 0.05) in patients with, than those without, morbidity probably (hypoventilation, gastroesophageal reflux, venous stasis, stress incontinence, incisional hernia) or possibly (hypertension, diabetes) due to increased abdominal pressure. W∶H ratio correlated with urinary bladder pressure in men (r = +0.6, P < 0.05) but not women (r = −0.3). Conclusions. Increased sagittal abdominal diameter was associated with increased intraabdominal pressure which contributed to obesity‐related comorbidity. W∶H ratio was not a reliable indicator of intraabdominal pressure for women who often have both peripheral and central obesity. Further studies are needed to evaluate the relationship between intraabdominal pressure and Type II diabetes and hypertension.

OBJECTIVE: Evaluate the effects of surgically induced weight loss on intra-abdominal pressure at one year, re¯ected in urinary bladder pressure, central obesity, measured by sagittal abdominal diameter and obesity co-morbidity. DESIGN: Prospective, non-randomized trial. SETTING: University Hospital, Operating Room, In-patient, Outpatient Clinics. SUBJECTS: Gastric bypass in 15 severely obese patients. MEASUREMENTS: Patients underwent pre-operative assessment of weight, body mass index (BMI), co-morbid history, urinary bladder pressure and sagittal abdominal diameter. Patients were reassessed one year after gastric bypass with repeat measurement of weight, bladder pressure, and sagittal abdominal diameter and assessment of co-morbidity. RESULTS: There were signi®cant (P`0.001) decreases in weight (140 AE 8±87 AE 6 kg), BMI (52 AE 3±33 AE 2 kg/m 2 ), sagittal abdominal diameter (32 AE 1±20 AE 2 cm), urinary bladder pressure (17 AE 2±10 AE 1 cm H 2 O) and obesity related problems per patient (2.9 AE 0.4±1 AE 0.2) one year after gastric bypass, with 69 AE 4% loss of excess weight. CONCLUSIONS: Increased sagittal abdominal diameter is associated with increased intra-abdominal pressure which contributes to obesity related co-morbidity. Weight loss following gastric bypass decreases abdominal pressure, sagittal abdominal diameter and obesity co-morbidity.

Tumor necrosis factor (TNFa), both by direct action and by trafficking cells of the immune system, is implicated in cardiopulmonary derangements and PMN-mediated microvascular injury associated with gram-negative sepsis. We examined the effects of pretreatment with a monoclonal antibody to TNFa on PMN function, hemodynamic derangements, and alveolar capillary membrane damage in a septic porcine model. Anti-TNFa profoundly improved hemodynamic consequences in this model. Reduction in PMN CD11 / 18 receptor expression, lung myeloperoxidase activity, and attenuation of peripheral neutropenia (all P < 0.05) indicate that pretreatment significantly reduced lung sequestration of PMNs seen in septic controls. In contrast, PMN oxygen radical (02-) generation was not significantly different from unprotected septic animals. Despite the presence of circulating PMNs primed for 0°-burst, alveolar capillary membrane damage, assessed by bronchoalveolar lavage protein content and arterial Po2 was markedly attenuated in the treatment group (P < 0.05). We conclude that antiTNFa suppresses systemic hemodynamic actions of TNFa. Further, it prevents upregulation of PMN adhesion receptors inhibiting PMN/endothelial cell interaction. This prevents formation of a "microenvironment," protected from circulating oxidant scavengers, into which sepsis-activated PMNs release their toxic products. Pretreatment with anti-TNFa monoclonal antibody thus affords global protection in porcine Gram-negative sepsis. (J. Clin. Invest. 1993. 91:1459-1468

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