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Objective: To evaluate the impact of preoperative risk category on metastatic disease and prostate cancer-specific mortality (CSM) in patients with prostate cancer (PCa) with adverse pathology at radical prostatectomy (RP)., Patients and Methods: The records of 6 943 patients who underwent RP at a European tertiary centre were analysed. Biochemical recurrence (BCR), metastatic disease and CSM were assessed for patients with adverse pathology at RP, and stratified according to preoperative low- vs intermediate-/high-risk PCa groups. Kaplan-Meier, cumulative incidence, Cox regression and competing risk regression analyses were performed., Results: In patients with extracapsular extension, the metastatic disease rate was 1.6% vs 8% (P < 0.001) and the CSM rate was 2% vs 5% (P = 0.041) for low vs intermediate-/high-risk patients, respectively, at 10 years. In patients with pathological Gleason score ≥3+4, the metastatic disease rate was 3.0% vs 12% (P < 0.001) and the CSM rate was 3% vs 8%, respectively (P < 0.001). In patients with positive surgical margins (PSMs), the metastatic disease rate was 2.9% vs 15% (P < 0.001) and the CSM rate was 4% vs 10%, respectively (P = 0.0001). Low-risk status was a predictive factor for metastatic disease in patients with pathological Gleason score ≥3+4 (hazard ratio [HR] 0.51), pathological Gleason score ≥4+3 (HR 0.41) and PSMs (HR 0.46) and was a predictive factor for CSM risk in patients with pathological Gleason score ≥3+4 (HR 0.62)., Conclusions: Patients with low-risk PCa were at significantly lower risk of metastatic disease and CSM than their intermediate-/high-risk counterparts, when adverse pathological features were identified at RP. This should be emphasized in the decision-making process after RP., (© 2017 The Authors BJU International © 2017 BJU International Published by John Wiley & Sons Ltd.)

Objective: To determine whether the energy expenditure of mechanically ventilated multiple trauma patients correlates with the severity of injury and illness indices before important systemic infection has complicated the clinical course, and to compare the energy expenditure with the energy expenditure expected from the Harris-Benedict equation adjusted with correction factors for trauma., Design: Prospective, clinical study., Setting: General intensive care unit of a university teaching hospital., Patients: Immediate multiple trauma adult patients who required mechanical ventilation., Interventions: Metabolic cart connected to the ventilator., Measurements and Main Results: Data on admission to the emergency department and during the first 24 hrs of intensive care unit admission were collected for computation of severity of injury and illness indices, respectively. Resting and total energy expenditures were derived at least 48 hrs after intensive care unit admission by continuous indirect calorimetry. Predicted basal energy expenditure was obtained using the Harris-Benedict equation and predicted total energy expenditure was calculated using the Harris-Benedict value adjusted with correction factors for trauma. Twenty-six multiple trauma adult patients completed the study. No statistically significant correlations were observed between both the resting energy expenditure and the total energy expenditure and the Injury Severity Score, Revised Trauma Score, Simplified Acute Physiologic Score II, Acute Physiology and Chronic Health Evaluation II score, and Glasgow Coma Scale score. A regression model of total energy expenditure was developed with the following variables: Harris-Benedict equation, heart rate, and minute ventilation (p = .01; r2 = .74). The resting energy expenditure/predicted basal energy expenditure ratio was 1.17+/-0.2 and the total energy expenditure/predicted total energy expenditure ratio was 0.76+/-0.1., Conclusions: In mechanically ventilated multiple trauma patients the energy expenditure is not correlated to the severity of injury and illness indices but is dependent on the Harris-Benedict equation in addition to heart rate and minute ventilation. Furthermore, this patient population is characterized by a moderate state of hypermetabolism, and the Harris-Benedict prediction modified with correction factors for trauma systematically overestimates the total energy expenditure.

Objective: To evaluate the effect of acute changes in minute ventilation (VE) on oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient, and energy expenditure during volume-controlled mechanical ventilation in the critically ill surgical patient. The effects on some oxygen transport variables were assessed as well., Design: Prospective, randomized clinical study, Setting: Adult surgical intensive care unit of a university teaching hospital., Patients: Twenty adult critically ill surgical patients were studied during volume-controlled mechanical ventilation., Interventions: After a basal period of stability (no changes over time in body temperature, energy expenditure, blood gases, acid-base status, cardiac output, and ventilatory parameters), VE was then randomly either increased or reduced (+/-35%) by a change in tidal volume (VT), while respiratory rate and inspiratory/expiratory ratio were kept constant. Settings were then maintained for 120 mins. During the study, patients were sedated and paralyzed., Measurements and Main Results: VO2, VCO2, and respiratory quotient were measured continuously by a Nellcor Puritan Bennett 7250 metabolic monitor (Nellcor Puritan Bennett, Carlsbad, CA). Hemodynamic and oxygen transport parameters were obtained every 15 mins during the study. Despite large changes in VE, VO2 and energy expenditure did not change significantly either in the increased or in the reduced VE groups. After 15 mins, VCO2 and respiratory quotient changed significantly after ventilator resetting. VCO2 increased by 10.5 +/- 1.1% (from 2.5 +/- 0.10 to 2.8 +/- 0.12 mL/min/kg, p< .01) in the increased VE group and decreased by 12.4 +/- 2.1% (from 2.7 +/- 0.17 to 2.4 +/- 0.16 mL/min/kg, p< .01) in the reduced VE group. Similarly, respiratory quotient increased by 16.2% +/- 2.2% (from 0.87 +/- 0.02 to 1.02 +/- 0.02, p< .01) and decreased by 17.2% +/- 1.8% (from 0.88 +/- 0.02 to 0.73 +/- 0.02, p< .01). VCO2 normalized in the reduced VE group, but remained higher than baseline in the increased VE group. Respiratory quotient did not normalize in both groups and remained significantly different from baseline at the end of the study. Cardiac index, oxygen delivery, and mixed venous oxygen saturation increased, while oxygen extraction index decreased significantly in the reduced VE group. Neither of the mentioned parameters changed significantly in the increased VE group., Conclusions: We conclude that, during controlled mechanical ventilation, the time course and the magnitude of the effect on gas exchange and energy expenditure measurements caused by acute changes in VE suggest that VO2 and energy expenditure measurements can be used reliably to evaluate and quantify metabolic events and that VCO2 and respiratory quotient measurements are useless for metabolic purposes at least for 120 mins after ventilator resetting.

Oxygen consumption (VO2) measured by indirect calorimetry (Nellcor-Puritan-Bennett 7250; Carlsbad, CA, USA) has been compared with VO2 calculated by the Fick method in 22 volume-controlled ventilated general surgical patients in the early post-operative period. For 198 pairs of measurements, VO2 Fick and VO2 indirect calorimetry correlated significantly (y = 1.00x - 35.8, P = 0.0001, r = 0.77). VO2 indirect calorimetry was 212 +/- 32 mL min-1 and VO2 Fick was 177 +/- 41 mL min-1 (P = 0.0001). The bias was 35 +/- 26 mL min-1. This difference represents 16 +/- 13% of the total body VO2. VO2 calculated by the Fick method did not accurately predict VO2 measured by indirect calorimetry, and the two methods were not interchangeable. VO2 calculated by the Fick method underestimated VO2 as measured by indirect calorimetry by a systematic quantity that could be attributed, in part, to VO2 of the lung. Indirect calorimetry should be the preferred method for measuring total body VO2 in mechanically ventilated surgical patients.

Objective: To calculate cardiac ouptut from dual oximetry with carbon dioxide production (VCO2) and oxygen consumption (VO2) measured by a new metabolic monitor, and to compare these values with measurements made simultaneously using the thermodilution method during the steady state condition., Design: Prospective, comparative clinical study., Setting: The adult postsurgical intensive care unit (ICU) of a University Hospital., Patients: Twenty mechanically ventilated postsurgical patients (70.7 +/- 7.8 years of age; range 50-84)., Measurements and Results: A new metabolic monitor (Puritan-Bennett 7250, Carlsbard, USA) connected to a ventilator (Puritan-Bennett 7200) was used to measure VCO2 and VO2. Measurements of arterial (SaO2) and mixed venous (SvO2) oxygen saturations were made using pulse and venous fiberoptic oximeters. Cardiac output starting from VCO2 (COVCO2) was obtained according to Mahutte's formula: COVCO2 = VCO2/[k (SaO2-SvO2)], where k represents a constant. The value for each patient was determined from the initial measurements of thermodilution cardiac output (COtd), VCO2, SaO2 and SvO2. COVCO2 calculated from the previous equation was compared to the COtd. Cardiac output calculated from the traditional O2 Fick equation (COVO2) was compared to the COtd. All patients were studied over a period of 120 min at 15-min intervals in reasonably stable conditions. COVCO2 was closely related to COtd (r = 0.94; SEE = 0.79; p = 0.0001; n = 180) with a bias of -0.10 and a precision of 0.45 l/min. The mean percent difference between the two methods was -2.2 +/- 8.3%. COVO2 was related to COtd (r = 0.77; SEE = 0.79; p = 0.0001; n = 180) with a bias of -0.57 and precision of 0.86 l/min. The mean percent difference between the two methods was -10.8 +/- 16.0%., Conclusions: In stable patients, cardiac output measurements obtained from dual oximetry with VO2 and VCO2 measured by this new metabolic monitor, show good correlation with measurements made using the thermodilution method. The values of cardiac output calculated from VCO2 are more accurate and precise than values from VO2. The validity of these measurements in hemodynamically unstable patients and during various modes of mechanical ventilation seems warranted.

Indirect calorimetry is the method by which metabolic rate and substrate utilization are estimated in human beings starting from respiratory gas exchange measurements and urinary nitrogen excretion. This method is based on some models and assumptions that must be known and taken into consideration to correctly interpret the results obtained. Recent advances in technology and the availability of precise and portable metabolic carts have made this technique practical at the beside even in critically ill patients. It must be considered that, particularly in the ICU, there may be several sources of error and many technical difficulties in applying this methodology. Taking into account the relevant clinical studies related to the outcomes of critically ill patient, this article defines when the assessment of energy expenditure by indirect calorimetry may provide useful and valid information. Review of the literature suggests that the clinical application of indirect calorimetry in critically ill patients, although promising, requires further evaluation. Currently, the potential useful clinical applications of indirect calorimetry in this category of patients can be summarized as follows: (1) assessment of energy expenditure in patients who fail to adequately respond to the estimated nutritional needs; (2) assessment of energy expenditure in patients with single- or multiple-organ dysfunction who need prolonged ICU care and artificial nutritional support; (3) assessment of the effects induced by artificial nutrition on the cardiocirculatory and respiratory systems in mechanically ventilated patients with acute respiratory failure; and (4) monitoring of VO2 during weaning from mechanical ventilation.

Study Objective: To determine the effect of elective thoracic surgery on energy metabolism and gas exchange and to evaluate whether the 30-degree sitting position would affect these variables., Design: Prospective, unblinded, controlled study., Setting: Surgical ICU in a university hospital., Patients: Twenty-two adult patients undergoing elective pulmonary resection., Interventions: Posture change from supine to 30-degree sitting position., Measurements and Results: Oxygen consumption (VO2), carbon dioxide production (VCO2), respiratory quotient (RQ), and energy expenditure (EE) were measured by means of computerized indirect calorimetry before and after surgery. Heart rate and respiratory frequency were measured continuously during gas exchange measurement. Blood gases were analyzed with an automated blood gas analyzer. Preoperatively, altering position did not affect energy metabolism, gas exchange, and cardiopulmonary variables. Postoperatively, the measured EE was 116% of the expected value. Mean EE and VO2 values for each position were higher than the preoperative values for the corresponding postures (p<0.05 for each position), while VCO2 increased only in the supine position (p<0.05). Mean percent increases in EE, VO2, and VCO2 were significantly lower in the 30-degree sitting position than in the supine position (EE: 7.9+/-2.7% vs 14.4+/-2.3%; p<0.001; VO2: 9.0+/-3.0% vs 16.4+/- 2.6%; p<0.001; VCO2: 3.2+/-2.1% vs 6.5+/-1.4%: p<0.05). Arterial oxygen tension and all the physiologic indexes of gas exchange for each position were worse than the preoperative values for the corresponding postures (p<0.05 for each position). Mean arterial pressure, heart rate, and respiratory frequency for each position were higher than the preoperative values for the corresponding postures (p<0.05 for each position). No changes in mean values of these variables occurred between the two positions postoperatively., Conclusions: The early postoperative period of patients undergoing elective thoracic surgery is characterized by a condition of impaired gas exchange and by a hypermetabolic state. Hypermetabolism can be partly mitigated by assuming the 30-degree sitting position.

Objective: To investigate the venous-arterial PCO2 gradient, and the mixed venous blood acid-base status together with the oxygen transport variables in a group of acutely ill postsurgical patients., Design: Retrospective, descriptive study of hemodynamic and acid-base data collected immediately after the patients' admission to the Postsurgical Intensive Care Unit., Setting: Eight-bed, Postsurgical Intensive Care Unit in a University Hospital., Patients: A total of one hundred and one postsurgical patients (87 male, 14 female; 14 to 86 years)., Interventions: None immediately before the first measurement., Measurements and Main Results: Hemodynamic, oxygen transport variables, and arterial and mixed venous acid-base status measurements obtained immediately after the admission to the Postsurgical Intensive Care Unit. The venous-arterial PCO2 gradient was elevated (> 6 torr) in 23 patients and normal (< or = 6 torr) in 78 patients (respectively 9.1 +/- 3.3 vs 4.4 +/- 1.0 torr, p < 0.001). Patients with an increased venous-arterial PCO2 gradient had a higher arterial-venous pH gradient (0.05 +/- 0.03 vs 0.03 +/- 0.01 Unit, p < 0.001) and mixed venous PCO2 (47.5 +/- 8.0 vs 42.1 +/- 5.6 torr, p < 0.001). These patients had a lower cardiac index, oxygen delivery, mixed venous oxygen saturation, and a higher oxygen extraction index than the patients with normal venous-arterial PCO2 and pH gradients. For all the measurements, there was an inverse non linear significant relation between oxygen delivery, venous-arterial PCO2 (r = 0.74, p < 0.001) and pH (r = 0.57, p < 0.01) gradients., Conclusions: This study suggests that in acutely ill postoperative patients increased venous-arterial PCO2 and pH gradients are directly and principally related to the reduction in blood flow and are both suggestive of low-flow state.

Objective: To investigate if there were differences between bench central oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2) in a group of acutely ill postsurgical patients., Design: A prospective comparative study of two sampling sites., Setting: Postsurgical ICU at a University Hospital., Patients: 39 acutely ill postsurgical patients, requiring perioperative invasive hemodynamic monitoring, studied during their stay in a postsurgical ICU., Interventions: Routine care for acutely ill postsurgical patients., Measurements and Main Results: Blood was simultaneously sampled, according to the clinical course, both from the distal and central port of a pulmonary artery catheter (n = 296 each). Oxygen saturation and blood gas analysis were immediately measured with a CO-oxymeter and a blood gas analyzer. We investigated the relationship and the agreement between the two measures. To assess if bench ScVO2 could give information on time related variations of bench SvO2 we evaluated the absolute sequential changes of the two measures during the period of observation, by analyzing the relationship and the agreement of their absolute changes (n = 1817). There was a significant difference between bench SvO2 and bench ScvO2 (71.8 +/- 8.2 vs 72.7 +/- 8.6% mean +/- SD, p < 0.001). The relationship between the two measures showed a significant correlation (r = 0.90, p < 0.001, and SEE 3.8%). The bias was -0.93 +/- 3.8%, and the limits of agreement were +6.6 and -8.5%. The changes in bench ScvO2 correlated with the respective changes in bench SvO2 (r = 0.86, p < 0.001, and SEE 4.4%). The bias was 0.79 +/- 4.7% and the limits of agreement were +9.4 and -7.8%., Conclusions: SvO2 cannot be predicted well from bench ScvO2, nor changes in ScO2 can be predicted wel from changes in bench ScvO2. Therefore, in this category of patients, the clinical usefulness of monitoring bench ScvO2 is strongly limited and we must still rely on the SvO2.

The breath-by-breath monitoring of anesthetic gases can provide information, beyond the usual safety control. The study of the decay and concentration effects along the circuit can be useful to evaluate their kinetics. The presence of unexpected gases coming from the patient's tissues is another important topic. By means of gas monitoring devices we can study the physiologic changes consequent to the modifications to the patient position, or the respiratory variations due to V/Q mismatching. The end-expired fraction of the anesthetic (FE') is not so close to MAC as first proposed in the 1960s, but it remains the most precise index of the depth of anesthesia. The traditional concept of quantitative anesthesia is still sufficiently actual to be considered in the design of new anesthesia machines.

Aim: To evaluate the effect of noradrenaline infusion in a case of hyperdynamic septic shock refractory to volume loading, dopamine and dobutamine, on hemodynamic parameters, oxygen transport, lactate and pyruvate levels., Design: Description of a clinical case., Setting: Postsurgical Intensive Care Unit in a University Hospital., Patient: A 48-year-old woman with symptoms of peritonitis due to Enterobacter Agglomerans and refractory hyperdynamic septic shock., Interventions: Administration of noradrenaline in doses ranging from 0.03 to 0.14 micrograms/kg/min., Measurements and Results: Before and after noradrenaline infusion the following were evaluated: hemodynamic (parameters) and oxygen transport acid-base status, arterial blood levels of lactate and pyruvate, and lactate/pyruvate ratio. During the administration of noradrenaline an increase was observed over time in oxygen consumption (from 110 +/- 16 to 164 +/- 19 mL/min/m2; p < 0.01), peripheral vascular resistance (from 509 +/- 95 to 1172 +/- 384 dynes.sec.cm-5, p < 0.01) and the oxygen extraction index (from 12.9 +/- 2.1 to 21.2 +/- 2.9%, p < 0.01), together with reduced lactate (from 24.4 +/- 1.5 to 4.9 +/- 5.1 mmol/L) and pyruvate levels (from 945 +/- 62 to 357 +/- 174 mumol/L; p < 0.01) and a reduced lactate/pyruvate ratio (from 26.2 +/- 1.2 to 11.8 +/- 5.9, p < 0.01). No significant increases were found in cardiac output and oxygen delivery., Conclusions: In the case observed here the infusion of noradrenaline induced an increase in oxygen consumption and the oxygen extraction index associated with a reduction in the lactate/pyruvate ratio and the normalisation of the acid-base status. These changes were not associated with an increase in oxygen which remained delivery > or = 600 mL/min/m2.

1. Stress is associated with a severe, yet reversible, form of insulin resistance. The aim of this study was to quantify the kinetics of insulin action (sensitivity and responsiveness) on intermediary metabolism during post-surgical stress. 2. We studied nine patients 6-8 h after major uncomplicated surgery, and eight healthy subjects matched for age, weight, glucose tolerance and duration of fast. A three-step isoglycaemic insulin clamp was combined with indirect calorimetry, [6-3H]glucose infusion and the forearm technique. 3. The following significant (P < 0.05 or less) abnormalities were found in the patients. Hepatic glucose production was higher at baseline, and less suppressed by insulin. Whole-body glucose disposal was impaired at all insulin doses (by 33-60%). Glucose oxidation was depressed throughout the dose range but its increments in response to insulin were normal. In contrast, non-oxidative glucose disposal was essentially unresponsive. At all insulin levels, forearm glucose extraction was markedly depressed and forearm lactate release was in excess of concurrent glucose uptake, suggesting ongoing glycogenolysis despite insulin. Total lipolysis (plasma free fatty acid and glycerol levels) promptly responded to insulin but remained higher than in the control subjects throughout. In the forearm, even the highest insulin dose could not suppress net free fatty acid and glycerol release. Total lipid oxidation was increased throughout the insulin range, and calculated direct free fatty acid (as opposed to plasma free fatty acid) oxidation was virtually unaffected by insulin. Protein oxidation was slightly (35%) increased, but was suppressed normally in response to insulin. Energy expenditure was 20% higher at baseline, and failed to rise with insulin. Arterial blood pH values were consistently (if slightly) lower, and net forearm proton release was higher, both at baseline and during insulin infusion. 4. Post-surgical insulin resistance is characterized by normal sensitivity but decreased responsiveness of glucose oxidation, lipolysis and plasma free fatty acid oxidation, whereas glycogen synthesis and direct free fatty acid oxidation are virtually unresponsive. For both glucose and lipid metabolism, the insulin resistance is particularly severe in forearm tissues, in which mild metabolic acidosis may play an additional role.

Lactate has been suggested to interfere with intermediary metabolism by restricting both lipolysis and glucose utilization. To test this hypothesis, in paired studies in healthy volunteers, sodium lactate (25 mumol.min-1 x kg-1) or saline was infused for 1 h in the fasting state and during 2 h of euglycemic (4.75 mM) hyperinsulinemia (approximately 400 pmol/l). Hyperlactatemia (approximately 2 mM) had no inhibitory effect on fasting free fatty acid or glycerol levels nor did it alter the suppressive action of insulin on these substrates. Likewise, sodium lactate infusion did not influence hepatic glucose production ([3-3H]glucose technique) or its suppression by insulin. During the clamp, hyperlactatemia was associated with a small increase in whole body glucose disposal (34.9 +/- 4.1 vs. 30.3 +/- 3.7 mumol.min-1 x kg-1, P < 0.05) with no major change in the pattern of substrate (carbohydrate vs. lipid) oxidation. By simultaneously measuring arteriovenous gradients across the deep tissues of the forearm (forearm technique), it was found that hyperlactatemia did not impede insulin-mediated glucose uptake; furthermore, it could be estimated that muscle tissues were responsible for the disposal of roughly one-fifth of the lactate load. Whole body energy expenditure was stimulated above the level achieved with hyperinsulinemia when lactate was also infused. Thus, under the present experimental conditions, physiological hyperlactatemia did not interfere with lipolysis, hepatic glucose production, or whole body or forearm muscle glucose utilization, or with insulin action on these processes, and was accompanied by a strong thermogenic effect.

To test whether carnitine availability is rate-limiting for fat oxidation under conditions of augmented oxidative use of fatty substrates, two series of studies were performed. In study no. 1, L-carnitine (1 g + 0.5 g/h intravenously [i.v.]) or saline was given to eight volunteers during a 4-hour infusion of a 10% triglyceride emulsion, thereby increasing plasma free-carnitine levels from 38 +/- 4 to 415 +/- 55 mumol/L. Fat infusion increased plasma triglyceride levels (80%) and lipid oxidation (30%), and decreased (28%) carbohydrate oxidation (as measured by indirect calorimetry); hypercarnitinemia had no influence on these responses. In study no. 2 in 12 healthy subjects a bolus of L-carnitine (3 g) or saline was administered 40 minutes before aerobic exercise (bicycling for 40 minutes at 60 W), followed by 2 minutes of anaerobic exercise (250 W) and 50 minutes of recovery. Oxygen consumption (VO2), increased to 18.3 +/- 0.7 mL.min-1 x kg-1 during aerobic exercise, reached a maximum of 46.0 +/- 0.8 mL.min-1 x kg-1 during the anaerobic bout, and returned to baseline within a few minutes, with no difference between control and carnitine. At virtually identical mean energy expenditure rates (196 +/- 7 v 197 +/- 7 J.min-1 x kg-1, saline v carnitine), after carnitine administration the entire exercise protocol was sustained by a lower mean carbohydrate oxidation rate (42.1 +/- 3.6 v 36.5 +/- 2.3 mumol.min-1 x kg-1, P < .03) and a higher mean lipid oxidation rate (6.7 +/- 1.0 v 8.3 +/- 0.7 mumol.min-1 x kg-1, P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Objective: To compare a method of measuring energy expenditure and gas exchange using the Fick principle with the standard indirect calorimetry technique., Design: Prospective study of a consecutive sample of postoperative patients. Oxygen consumption (VO2), CO2 production (VCO2), respiratory quotient, and energy expenditure were derived from measurements of variables, including oxygen content and cardiac output. Energy expenditure and gas exchange were measured simultaneously by continuous indirect calorimetry over a 60-min period., Setting: Surgical ICU in a university hospital., Patients: Twenty-six consecutive patients (45 to 80 yrs) who underwent sustained surgical trauma. Excluded from the study entry were patients with time-related fluctuations of hemodynamic variables, poor cooperation, patients who required supplemental oxygen, or mechanical ventilation., Interventions: None., Measurements and Main Results: While the measurements of VO2 and VCO2 by calorimetry and thermodilution were significantly correlated with one another (for VO2, r2 = .93, p less than .001; for VCO2, r2 = .26, p less than .01), VO2 and VCO2 values by indirect calorimetry were consistently greater than VO2 and VCO2 values by the Fick method (p less than .01). The respiratory quotient calorimetric measurements ranged between 0.69 and 0.99, whereas the corresponding thermodilution measurements spread to impossible values, from 0.24 to 1.30 (0.821 +/- 0.07 vs. 0.740 +/- 0.24, p less than .05). There was an insignificant relationship (r2 = .06, p = .21) between the values of respiratory quotient by the two methods. A strong, positive correlation between energy expenditure measured by indirect calorimetry and energy expenditure measured by the Fick method was observed (r2 = .92, p less than .001). The limit of agreement between the two methods was -0.24 +/- 73 kcal/day/m2 (-1.00 +/- 305 kJ/day/m2)., Conclusions: In postoperative patients, while VO2 and energy expenditure measurements by thermodilution are easy to perform and accurate for clinical purposes, VCO2, and respiratory quotient measurements are too imprecise and inaccurate to serve any useful function. Therefore, in those clinical situations in which an evaluation of respiratory quotient and substrate utilization may be useful for purposes of metabolic care of the surgical patient, precise measurements of gas exchange with indirect calorimetry are mandatory.

The relation between the renin-angiotensin-aldosterone (RAA) system and carbohydrate metabolism and insulin sensitivity in essential hypertension has not been investigated systematically. Twenty nondiabetic patients (age, 49 +/- 1 years; body mass index (BMI), 26.1 +/- 0.4 kg/m2) with essential hypertension (blood pressure, 155 +/- 3/105 +/- 1 mm Hg) received an oral glucose tolerance test (OGTT) at the end of a 1-month placebo period and again monthly during 3 months of angiotensin converting enzyme (ACE) inhibition (cilazapril, 5 mg/day). Furthermore, a two-step euglycemic insulin clamp was performed after placebo and again at the end of treatment. Blood pressure fell by 7 +/- 4/10 +/- 3 mm Hg (p less than 0.001), while BMI remained stable. On the euglycemic clamp, insulin-mediated (plasma insulin, 470 pM) whole body glucose use averaged 42.5 +/- 1.6 mumol.min-1.kg-1 before and 43.6 +/- 1.9 after ACE inhibition (p = NS). Substrate concentrations and oxidative rates and energy expenditure (as estimated by indirect calorimetry) were not altered by ACE inhibition, either in the fasting state or in response to insulin. In contrast, oral glucose tolerance was significantly (p less than 0.05) improved after treatment (area under OGTT curve (AUC), 240 +/- 24 versus 282 +/- 23 mmol 2 hr.l-1). The latter change was associated with enhanced (+16%, p less than 0.05) insulin responsiveness to glucose (estimated as the insulin AUC divided by the glucose AUC) throughout the 3 months of ACE inhibition. At baseline, both the OGTT and the clamp had a marked hypokalemic effect (mean decrements in plasma potassium of 0.75 +/- 0.05 and 0.92 +/- 0.05 mmol/l, respectively) in association with plasma aldosterone reductions of 30% and 50%. Chronic ACE inhibition caused a further 20% (p less than 0.03) lowering of plasma aldosterone concentrations but attenuated insulin-induced hypokalemia. Plasma sodium, which was unaltered by the pretreatment tests, fell during the posttreatment tests (by 3 mmol/l, p less than 0.001). In the urine, the ratio of the fractional excretion of potassium to that of sodium was decreased by both oral glucose (-22%, p less than 0.01) and ACE inhibition (-21%, p less than 0.001). Higher plasma potassium levels before treatment predicted a better blood pressure response to ACE inhibition (r = 0.60, p less than 0.005).(ABSTRACT TRUNCATED AT 400 WORDS)

1. Injury is known to be associated with variable degrees of tissue insensitivity to insulin. We measured insulin resistance in a group of non-obese, glucose-tolerant patients undergoing major elective surgery with an uncomplicated post-operative course. 2. Shortly after surgery, hyperglycaemia (7.3 +/- 0.6 versus 4.2 +/- 0.3 mmol/l glucose pre-surgery, mean +/- SEM, P less than 0.01) with normal insulin concentrations (73 +/- 15 versus 64 +/- 18 pmol/l) suggested the presence of insulin resistance. Counter-regulatory hormones were raised, whole-body protein oxidation was doubled (P less than 0.01) and energy expenditure was up by 18% (P less than 0.01). 3. Insulin sensitivity was quantified by clamping plasma glucose concentrations at 5.6 mmol/l during 24 h of total parenteral nutrition (15% protein, 55% glucose and 30% fat, supplying 1.25 times the measured resting energy expenditure) with a variable infusion of exogenous insulin. After surgery, eight times more insulin was needed than before surgery (14.14 +/- 1.15 versus 1.78 +/- 0.29 pmol min-1 kg-1, P less than 0.001) to maintain euglycemia. 4. After surgery, stimulation of net carbohydrate oxidation (18.8 +/- 1.4 versus 17.2 +/- 1.8 mumol min-1 kg-1 preoperatively, not significant), suppression of lipolysis and lipid oxidation and inhibition of ketogenesis occurred to the same extent as before surgery. Of the infused nutrients, the glucose was all oxidized, amino acids replaced endogenous protein losses (= neutral nitrogen balance) and lipids were stored. Insulin administration caused no further increment in oxygen consumption or energy expenditure.(ABSTRACT TRUNCATED AT 250 WORDS)

It has been suggested that the insulin resistance of non-insulin-dependent diabetes mellitus (NIDDM) may be caused by substrate competition between glucose and free fatty acids (FFAs) (Randle's cycle). We measured substrate oxidation and energy metabolism in 10 nonobese untreated NIDDM patients with fasting glucose levels of 7-8 mM with indirect calorimetry in the basal state and during an isoglycemic-hyperinsulinemic (approximately 100 mU/L) clamp without (control) and with a concomitant infusion (approximately 0.35 mmol/min) of Intralipid, a triglyceride emulsion. In the control study, fasting rates of total glucose turnover [( 3-3H]glucose) and glucose and lipid oxidation (9.4 +/- 1.4, 7.3 +/- 1.3, and 3.0 +/- 0.4 mumol.kg-1.min-1, respectively) were comparable with those of nondiabetic individuals. After insulin administration, lipid oxidation was normally suppressed (to 1.3 +/- 0.3 mumol.kg-1.min-1, P less than 0.01), as were the circulating levels of FFA, glycerol, and beta-hydroxybutyrate, whereas glucose oxidation doubled (14.1 +/- 1.8 mumol.kg-1.min-1, P less than 0.01). Because glycemia was clamped at 7.5 mM, endogenous glucose production (EGP) was completely suppressed, and total glucose disposal was stimulated (to 25.7 +/- 5.2 mumol.kg-1.min-1, P less than 0.01 vs. baseline), but glucose clearance (3.6 +/- 0.8 ml.kg-1.min-1) was 30% reduced compared with normal. With concomitant lipid infusion, FFA, glycerol, and beta-hydroxybutyrate all rose during the clamp; correspondingly, lipid oxidation was maintained at fasting rates (3.6 +/- 0.2 mumol.kg-1.min-1, P less than 0.01 vs. control).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of surgery on TSH secretion, with particular regard to the nocturnal TSH surge, were evaluated in 10 consecutive patients followed for 6 days after surgery. Surgical trauma was associated in all patients with significant decreases in serum total and free T3 and a significant increase in serum rT3 levels, with no variations in serum total and free T4 concentrations. A marked increase in serum cortisol levels was observed, with higher values at night than in the morning. Serum cortisol levels and circadian rhythm normalized on the fifth day. Serum TSH values in the morning significantly decreased on the first day after surgery and returned to normal on the second day. Serum TSH values at night (2400-0200 h) were higher than in the morning preoperatively, but the nocturnal surge was abolished from days 1-5 after surgery and was restored only on the sixth day. Thus, surgery was associated with a prolonged loss of the nocturnal serum TSH surge. This effect on TSH secretion was more marked than predictable on the basis of serum TSH measurements in the morning alone. An inverse relationship was found between serum cortisol and serum TSH values at night, suggesting that the excessive endogenous cortisol secretion might play a role in the derangement of TSH secretion.

A case of recurrent renovascular hypertension is described in a patient with a solitary kidney successfully treated as an emergency for acute renal failure and unresponsive hypertension, by renal autotransplantation in the right iliac fossa. The results suggests that renal autotransplantation is a safe and reliable procedure in correcting particularly difficult renal vascular diseases where, due to the presence of a solitary kidney, all possible causes of technical failure of revascularization should be avoided.