Variations in the pre-ejection period induced by ventricular extra systoles may be feasible to predict fluid responsiveness.

Monitoring that can predict fluid responsiveness is an unsettled matter for spontaneously breathing patients. Based on the convincing results with dynamic monitoring based on preload variations induced by mechanical ventilation, we hypothesised that the extra systolic post-ectopic beat could constitute a similar intermittent preload shift inducing a brief variation in blood pressure and that the magnitude of this variation could predict the hemodynamic response to volume expansion in sedated pigs. Ten pigs were sedated and hemodynamically monitored and four intravascular volume shifts were made: blood depletion (25% of estimated blood volume; 660 ml), retransfusion (of 500 ml depleted blood), and two sequential volume expansions (500 ml colloid each). Between volume shifts, supraventricular and ventricular extra systoles were induced by a pacemaker. Hemodynamic variables such as pulse pressure (PP) and pre-ejection period (PEP) were determined for each heart beat and the hemodynamic changes in the post-ectopic beats compared to sinus beats was extracted (e.g. ∆PP and ∆PEP) and used to predict fluid responsiveness of subsequent volume expansions which was determined by receiver operating characteristic (ROC) curves. Ventricular extra systoles were generally useful for fluid responsiveness prediction (ROC areas >0.65). ∆PEP variables best predicted fluid responsiveness: ∆PEP derived from arterial pressure curve and ECG had ROC area of 0.84 and sensitivity of 0.77 and specificity of 0.71; ∆PEP derived from plethysmographic curve and ECG had ROC area of 0.79 and sensitivity of 0.71 and specificity of 0.70. However, ∆PP was not a useful variable in this study (ROC area <0.65). Hemodynamic analysis of post ectopic beats may be a feasible method for fluid responsiveness prediction.

Total and high molecular weight (HMW) adiponectin levels and measures of glucose and lipid metabolism following pioglitazone treatment in a randomized placebo-controlled study in polycystic ovary syndrome.

OBJECTIVE: Recent studies suggested that the effect of adiponectin on insulin-stimulated glucose metabolism is mediated primarily by the high molecular weight (HMW) form of adiponectin. In the present study we evaluated total and HMW adiponectin in polycystic ovary syndrome (PCOS) patients and controls and examined possible mechanisms for increased insulin sensitivity during pioglitazone treatment. STUDY SUBJECTS: Thirty PCOS patients randomized to pioglitazone, 30 mg/day, or placebo for 16 weeks and 14 weight-matched healthy females were studied. DESIGN: Total and HMW adiponectin levels were measured, and euglycaemic hyperinsulinaemic clamps and indirect calorimetry were performed. Delta-values denoted changes during pioglitazone treatment (16 weeks--basal). RESULTS: Pretreatment adiponectin levels were decreased in PCOS patients vs. controls (P < 0.05), whereas no significant differences were found in HMW adiponectin levels. Following pioglitazone treatment, total and HMW adiponectin increased (all P < 0.05), whereas no significant changes were observed with placebo. Delta-total adiponectin levels correlated positively with the rate of Delta-insulin-stimulated glucose disposal (R(d)) (r = 0.89) and Delta-oxidative glucose metabolism (r = 0.71) and inversely with Delta-fasting free fatty acid (FFA) levels (r = -0.69) and Delta-lipid oxidation (r = -0.73) during insulin stimulation (all P < 0.01). Weaker correlations were found between Delta-HMW adiponectin levels and Delta-measures of glucose and lipid metabolism during insulin stimulation than with Delta-total adiponectin. CONCLUSION: A close correlation between increased total adiponectin levels and increased insulin-stimulated glucose metabolism during pioglitzone treatment supports the hypothesis that the insulin-sensitizing effect of pioglitazone in PCOS is, at least in part, mediated by adiponectin. Measures of changes in HMW adiponectin did not add further information to this relationship.

Gender differences of oligomers and total adiponectin during puberty: a cross-sectional study of 859 Danish school children.

CONTEXT: Pubertal stages have been shown to influence total adiponectin (ADPN) levels. Furthermore, testosterone has been shown to alter the isomer distribution of ADPN. OBJECTIVE: The goal of this study was to investigate whether pubertal stages and testosterone levels influenced total serum ADPN levels and the distribution of ADPN isomers. DESIGN: This is a cross-sectional study. PATIENTS: The study included 859 children and adolescents (396 males) aged 6-20 yr. MAIN OUTCOME MEASURES: Total ADPN and ADPN isomers were measured using a validated in-house immunofluorometric assay. Fractioning of the ADPN into the three major molecular fractions was performed in representative subgroups of pre- and postpubertal males and females (n = 40, 10 in each group) using a validated fast protein liquid chromatography method. RESULTS: Total ADPN levels before puberty were 13.4 (11.1-15.9) mg/liter (median and interquartile range) and 14.7 (12.3-18.1) mg/liter (P = not significant), in males and females, respectively. After puberty, ADPN levels were significantly reduced in males, 9.7 (8.2-12.0) mg/liter but remained unchanged in females, 12.1 (9.7-15.3) mg/liter (P < 0.0001). Concomitantly, a reduction was seen in the ratio of high-molecular-weight (HMW) isomers to total ADPN (HMW ratio) when comparing prepubertal and postpubertal males. Also, postpubertal males had lower HMW ratios than corresponding females (P = 0.038). Finally, a negative correlation was seen between HMW ratio and testosterone (r = -0.430, P = 0.007). CONCLUSION: Serum total ADPN levels decrease through puberty in males. Also, a reduced HMW ratio is seen in males at the onset of puberty. We speculate that the suppression of HMW ADPN may be caused by testosterone.

Cerebral Effects of Targeted Temperature Management Methods Assessed by Diffusion-Weighted Magnetic Resonance Imaging.

The aim of this randomized porcine study was to compare surface targeted temperature management (TTM) to endovascular TTM evaluated by cerebral diffusion-weighted magnetic resonance imaging (MRI): apparent diffusion coefficient (ADC), and by intracerebral/intramuscular microdialysis. It is well known that alteration in the temperature affects ADC, but the relationship between cerebral ADC values and the cooling method per se has not been established. Eighteen anesthetized 60-kg female swine were hemodynamically and intracerebrally monitored and subsequently subjected to a baseline MRI. The animals were then randomized into three groups: (1) surface cooling (n = 6) at 33.5°C using EMCOOLSpad®, (2) endovascular cooling (n = 6) at 33.5°C using an Icy® cooling catheter with the CoolGard 3000®, or (3) control (n = 6) at 38.5°C using a Bair Hugger™. The swine were treated with TTM for 6 hours followed by a second MRI examination, including ADC. Blood and microdialysate were sampled regularly throughout the experiment, and glucose, lactate, pyruvate, glycerol, and the lactate/pyruvate ratio did not differ among groups, neither intracerebrally nor intramuscularly. Surface cooling yielded a significantly lower median ADC than endovascular cooling: 714 (634; 804) × 10-6 mm2/s versus 866 (828; 927) × 10-6 mm2/s, (p < 0.05). The surface cooling ADC was lowered to a range usually attributed to cytotoxic edema and these low values could not be explained solely by the temperature effect per se. To what extent the ADC is fully reversible at rewarming is unknown and the clinical implications should be further investigated in clinical studies.

The effect of weight loss after gastric banding on the molecular distribution of serum adiponectin.

The above article has been retracted by the authors, as they have withdrawn the data upon which it was based. The retraction was made before the article reached its final form in the publication process. However, the authors' manuscript, prior to copy editing, page layout and proofing, was initially made available online upon acceptance as an Accepted Preprint.