Evaluation of the SOFA score: a single-center experience of a medical intensive care unit in 303 consecutive patients with predominantly cardiovascular disorders. Sequential Organ Failure Assessment.

OBJECTIVE: To evaluate the use of the Sequential Organ Failure Assessment (SOFA) score, the total maximum SOFA (TMS) score, and a derived variable, the deltaSOFA (TMS score minus total SOFA score on day 1) in medical, cardiovascular patients as a means for describing the incidence and severity of organ dysfunction and the prognostic value regarding outcome. DESIGN: Prospective, clinical study. SETTING: Medical intensive care unit in a university hospital. PATIENTS: A total of 303 consecutive patients were included (216 men, 87 women; mean age 62 +/- 12.6 years; SAPS II 26.2 +/- 12.7). They were evaluated 24 h after admission and thereafter every 24 h until ICU discharge or death between November 1997 and March 1998. Readmissions and patients with an ICU stay shorter than 12 h were excluded. MAIN OUTCOME MEASURE: Survival status at hospital discharge, incidence of organ dysfunction/failure. INTERVENTIONS: Collection of clinical and demographic data and raw data for the computation of the SOFA score every 24 h until ICU discharge. MEASUREMENTS AND MAIN RESULTS: Length of ICU stay was 3.7 +/- 4.7 days. ICU mortality was 8.3% and hospital mortality 14.5%. Nonsurvivors had a higher total SOFA score on day 1 (5.9 +/- 3.7 vs. 1.9 +/- 2.3, p < 0.001) and thereafter until day 8. High SOFA scores for any organ system and increasing number of organ failures (SOFA score > or = 3) were associated with increased mortality. Cardiovascular and neurological systems (day 1) were related to outcome and cardiovascular and respiratory systems, and admission from another ICU to length of ICU stay. TMS score was higher in nonsurvivors (1.76 +/- 2.55 vs. 0.58 +/- 1.39, p < 0.01), and deltaSOFA/total SOFA on day 1 was independently related to outcome. The area under the receiver-operating characteristic curve was 0.86 for TMS, 0.82 for SOFA on day 1, and 0.77 for SAPS II. CONCLUSIONS: The SOFA, TMS, and deltaSOFA scores provide the clinician with important information on degree and progression of organ dysfunction in medical, cardiovascular patients. On day 1 both SOFA score and TMS score had a better prognostic value than SAPS II score. The model is closely related to outcome and identifies patients who are at increased risk for prolonged ICU stay.

In vitro validation of gastric air tonometry using perfluorocarbon FC 43 and 0.9% sodium chloride.

Monitoring splanchnic perfusion by means of gastric intramucosal tonometry is carried out using saline, or more recently, air tonometry using the Tonocap. The objective of this study was the validation of the Tonocap in saline and perfluorocarbon FC 43. The two methods underestimated the predefined PCO2 value by an average of 10%, with clinically acceptable precision. Accuracy of the Tonocap improved at high PCO2 values (9.33 and 9.94 kPa), whereas saline tonometry was superior at low PCO2 values (3.99 and 3.75 kPa). The Tonocap provides a fast and reliable estimation of the PCO2, and with the revised software requiring only 10 min of equilibration, will increase the comparability of future studies.

Pharmacokinetic and alpha 1-adrenoceptor antagonistic properties of two cyanine-type inhibitors of extraneuronal monoamine transport.

1,1'-Diethyl-2,2'-cyanine (decynium22) and 1,1'-diisopropyl-2,4'-cyanine (disprocynium24) are highly potent inhibitors of the extraneuronal monamine transporter. When given as i.v. bolus injections (4 mumol kg-1) to anaesthetized rabbits, both drugs elicited a transient fall in blood pressure without altering heart rate. The observed maximum fall in diastolic blood pressure was 59% after decynium22 and 43% after disprocynium24 administration. The pharmacokinetics of decynium22 and disprocynium24 were similar; they were characterized by short half-lives for elimination (8.2 and 4.5 min, respectively) and very high plasma clearances (173 and 180 ml kg-1 min-1, respectively). The mechanism underlying the blood pressure-lowering effect of decynium22 was explored in the isolated incubated rabbit aorta. Decynium22 antagonized the noradrenaline-induced contraction; the pA2 for this interaction was 7.6, and the slope of the corresponding Schild plot was unity. In a membrane preparation from rat myocardium, decynium22 as well as disprocynium24 inhibited the specific binding of [125I]-2-[beta-(4-hydroxy-3-iodophenyl)-ethylaminomethyl]- tetralone (125I-HEAT), a selective ligand to alpha 1-adrenoceptors. The Ki's were 5.3 and 240 mumol l-1 for decynium22 and disprocynium24, respectively. The type of binding inhibition by decynium22 was competitive. It is concluded that the two inhibitors of extraneuronal monoamine transport decynium22 and disprocynium24 lower blood pressure by blocking alpha 1-adrenoceptors. A comparison of their potencies in blocking extraneuronal monoamine transport and alpha 1-adrenoceptors clearly indicates that disprocynium24 is more suitable for studies designed to determine the role of extraneuronal monoamine transport in vivo. Considering its very fast elimination kinetics, disprocynium24 must be administered by constant rate-infusions in order to avoid large fluctuations of plasma levels.

The ryanodine binding sarcoplasmic reticulum calcium release channel in nonfailing and in failing human myocardium.

The ryanodine-sensitive Ca2+ release channel (RyaCRC) of the sarcoplasmic reticulum plays a key role in the intracellular Ca2+ handling in cardiomyocytes. Altered expression of the RyaCRC has been supposed to contribute to abnormal cellular Ca2+ handling and to myocardial dysfunction in dilated and ischemic cardiomyopathy. In the present study the 3H-ryanodine binding site in human myocardial homogenates was characterized and the density of the RyaCRC (which corresponds to the cardiac ryanodine receptor) was determined in nonfailing and in failing human myocardium. Homogenates were prepared from nonfailing left ventricular myocardium from the hearts of 5 organ donors (NF) and from failing myocardium from 14 explanted hearts of transplant recipients with end-stage heart failure resulting from dilated (DCM, n = 5) or ischemic (ICM, n = 9) cardiomyopathy. Radioligand saturation binding experiments revealed a specific, high-affinity 3H-ryanodine binding site (Kd-values: NF: 0.65 +/- 0.11 nmol/l, DCM: 0.66 +/- 0.09 nmol/l, ICM: 0.88 +/- 0.18 nmol/l; n.s.) in all preparations. Specific 3H-ryanodine binding depended on the free Ca2+ concentration in the assay. It was maximal at 3-100 micro mol/l Ca2+. The binding was inhibited by the RyaCRC antagonists ruthenium red (Ki-value: 0.32 [0.18-0.56] micromol/l, n = 5) and Mg2+ (Ki-value: 2.95 [1.23-7.11] mmol/l, n = 5). The RyaCRC density was 103.5 +/- 11.9 fmol/mg protein in nonfailing myocardium. There was no significant change in the RyaCRC density in dilated or ischemic cardiomyopathy (112.4 +/- 17.1 and 122.7 +/- 13.9 fmol/mg protein) compared to nonfailing control myocardium. In summary, 3H-ryanodine binds specifically and with high-affinity to the RyaCRC in human myocardium. There is no change in the RyaCRC density in failing myocardium of patients with DCM or ICM in comparison to non-failing controls.

Investigation of some enzymatic activities contributing to the biosynthesis of galactolipid precursors in Vicia faba.

Assay conditions, intracellular distribution and change of activity during greening of etiolated seedlings of Vicia faba L. have been investigated for aldose reductase (EC 1.1.1.21), UDP-glucose pyrophosphorylase (EC 2.7.7.9), UDP-glucose 4-epimerase (EC 5.1.3.2) and phosphatidate phosphatase (EC 3.1.3.4). The first three enzymes were found to be soluble proteins of the cytoplasm, whereas phosphatidate phosphatase was found in the soluble and a sedimentable (15000 Xg) fraction.