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Metabolic and hormonal profile in relation with TNF and IL1 levels in patients with sepsis (S) and septic shock (SS)
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METABOLIC AND HORKO:'AL PROFILE IN RELATION 'riITHTNF AND TLl LEVELS IN PATIENTS WITH SEPSIS (S) AND SEPTIC SHOCK (%).A. LEPAPE, B. QUINET, J. BIENVENU, P. ARMANET, C. DOCHE, M. BARRIER, Y. BARRIER, .I.P. PERDRIX, V.BANSSILLON. Departments of anesthesiology, immunochemistry and nuclear medicine - LYON - FRANCE. In infusion experiments,TNF and TLl have been shown to have various effects on hormonal secretions (e.g. stimulation of ACTH secretion by TNF), substrates metabolism (e.g. inhibition of lipolysis by TNF) and acute phase proteins synthesis. The present study was undertaken in order to examine wether such relationships can be demonstrated during clinical infections. Method : In 16 patients, 22 determinations of various parameters were made, 11 during a sepsis and 11 during a septic shock. The samples were collected at the admission and repeated the following day in 5 patients of the septic group. SS : n = 11 Results (mean ZSJJ): methods S : n+= 11 t-test 98 _+108 19 ; 16 p <0.05 TNF (pg/ml) (1) 0.24 ; 0.30 IL 1 (ng/ml) 0.11 NS 0.09 (2) ; 44.4 ACTH (ng/l) 36 20 5 p co.05 (2) ; ; 47 38 INSULIN (mu/l) 54 ; 24 NS (2) ; 5.5 CPEPTIDE (mmol/l) 3.1 ; 2.3 NS 5.1 (2) 9.58 5 GLYCEMIA (mmol/l) 4.75 10.9 NS 2.5 (3) TRIGLYCERIDES (mmol/l) (3) 1.58 ; 2.57 2.04 i 1.46 NS NEFA (mmol/l) 0.43 0.14 0.33 ; 0.15 NS (3) CR? (mg/l) 242 ; 112 188 NS - 36 (4) LACTATE (m-d/l) 7.5 3.4 2.60 + 1.70 p co.01 (3) 1 : IRMA, 2 : RIA, 3 : enzymatic method, 4 : immunonephelometry. TNF positively correlates with ACTH (pcO.01) and lactic acid (p
0.32 BILXKAGE OF STRHSS HORMONES ABOLISHES POSTOPERATIVE CATABOLISM. Hans Eeindorff, S. Schulze, T. Mogensen, T. Almdal, H. Kehlet & H. Vilstrup. Divison of Hepatology, Rigshospitalet, Denmark. Changes in hepatic kinetics of amino-N conversion are partly responsible for postop. stress catabolism. The role of catecholamines, cortisol, and glucagon in mediating this response were studied in eight cholecystectomized patients where the hormones were blocked from the start of surgery continuing for 30 hours. Ten patients identical apart from hormonal blockage were controls. Hormonal blockage. Catecholamines: Stable epidural analgesia (Th7-8). Bolus injection of 2+7 ml of 0.5% bupivacain + 4mg morphine, followed by 5 ml of 0.5% bupivacain + 0.5 mg morphine/hour. Cortisol: Ethomidate 0.3mg/kgBW followed by lOug/kgBW/min until end of operation. Glucagon: Somatostatin, bolus 6ng/kgBW followed by 6ng/kgBW/min. Hepatic amino-N conversion was quantified the Functional Hepatic Nitrogen Clearance (FHNC) calculated as the slope of the relation between blood amino-N cont. and urea synthesis rate. Results. Hormonal changes normally induced by surgery were abolished by the blockage. Preop. l.postop.day Horm. block. 91 FHNC (ml/s). 9+1 Cholecystec. 9:2 16;s' Values: mean+sem. * (pt0.05). Conclusion. Combined blockage of the major stress hormones normalizes postop. hepatic amino-N conversion. This favours the suggestion that interaction among the stress hormones is responsible for the hepatic part of postop. catabolism.
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METABOLIC AND HORKO:'AL PROFILE IN RELATION 'riITHTNF AND TLl LEVELS IN PATIENTS WITH SEPSIS (S) AND SEPTIC SHOCK (%).A. LEPAPE, B. QUINET, J. BIENVENU, P. ARMANET, C. DOCHE, M. BARRIER, Y. BARRIER, .I.P. PERDRIX, V.BANSSILLON. Departments of anesthesiology, immunochemistry and nuclear medicine - LYON - FRANCE. In infusion experiments,TNF and TLl have been shown to have various effects on hormonal secretions (e.g. stimulation of ACTH secretion by TNF), substrates metabolism (e.g. inhibition of lipolysis by TNF) and acute phase proteins synthesis. The present study was undertaken in order to examine wether such relationships can be demonstrated during clinical infections. Method : In 16 patients, 22 determinations of various parameters were made, 11 during a sepsis and 11 during a septic shock. The samples were collected at the admission and repeated the following day in 5 patients of the septic group. SS : n = 11 Results (mean ZSJJ): methods S : n+= 11 t-test 98 _+108 19 ; 16 p <0.05 TNF (pg/ml) (1) 0.24 ; 0.30 IL 1 (ng/ml) 0.11 NS 0.09 (2) ; 44.4 ACTH (ng/l) 36 20 5 p co.05 (2) ; ; 47 38 INSULIN (mu/l) 54 ; 24 NS (2) ; 5.5 CPEPTIDE (mmol/l) 3.1 ; 2.3 NS 5.1 (2) 9.58 5 GLYCEMIA (mmol/l) 4.75 10.9 NS 2.5 (3) TRIGLYCERIDES (mmol/l) (3) 1.58 ; 2.57 2.04 i 1.46 NS NEFA (mmol/l) 0.43 0.14 0.33 ; 0.15 NS (3) CR? (mg/l) 242 ; 112 188 NS - 36 (4) LACTATE (m-d/l) 7.5 3.4 2.60 + 1.70 p co.01 (3) 1 : IRMA, 2 : RIA, 3 : enzymatic method, 4 : immunonephelometry. TNF positively correlates with ACTH (pcO.01) and lactic acid (p
0.32 BILXKAGE OF STRHSS HORMONES ABOLISHES POSTOPERATIVE CATABOLISM. Hans Eeindorff, S. Schulze, T. Mogensen, T. Almdal, H. Kehlet & H. Vilstrup. Divison of Hepatology, Rigshospitalet, Denmark. Changes in hepatic kinetics of amino-N conversion are partly responsible for postop. stress catabolism. The role of catecholamines, cortisol, and glucagon in mediating this response were studied in eight cholecystectomized patients where the hormones were blocked from the start of surgery continuing for 30 hours. Ten patients identical apart from hormonal blockage were controls. Hormonal blockage. Catecholamines: Stable epidural analgesia (Th7-8). Bolus injection of 2+7 ml of 0.5% bupivacain + 4mg morphine, followed by 5 ml of 0.5% bupivacain + 0.5 mg morphine/hour. Cortisol: Ethomidate 0.3mg/kgBW followed by lOug/kgBW/min until end of operation. Glucagon: Somatostatin, bolus 6ng/kgBW followed by 6ng/kgBW/min. Hepatic amino-N conversion was quantified the Functional Hepatic Nitrogen Clearance (FHNC) calculated as the slope of the relation between blood amino-N cont. and urea synthesis rate. Results. Hormonal changes normally induced by surgery were abolished by the blockage. Preop. l.postop.day Horm. block. 91 FHNC (ml/s). 9+1 Cholecystec. 9:2 16;s' Values: mean+sem. * (pt0.05). Conclusion. Combined blockage of the major stress hormones normalizes postop. hepatic amino-N conversion. This favours the suggestion that interaction among the stress hormones is responsible for the hepatic part of postop. catabolism.
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